Coronary Artery Disease (CAD)

 

By: Health Treatise Editorial Board and Contributors

✅ Medically Reviewed By: William N. P. Kwateng, MD, MPH

Coronary Artery Disease: An Overview

You’ve likely heard the term “Coronary Artery Disease” (CAD) more than once. But do you know what it really means? Here’s an accessible guide to understanding CAD, free from medical jargon, aimed at helping you to comprehend its nature and implications.

Imagine your heart as a powerhouse. It is working day and night, beat after beat, pumping blood to every corner of your body. Now, consider the arteries as the highways that transport this blood, rich in oxygen and nutrients, to your cells and organs. In CAD, these highways, or more specifically, your coronary arteries, start to narrow. This narrowing process doesn’t happen overnight but rather over years, even decades, due to the buildup of fatty substances and cholesterol. This buildup is often referred to as plaque, but think of it like rust in a pipe, slowing down the flow. This is CAD in its simplest form and, sadly, it’s one of the leading causes of death globally.1National Library of Medicine – National Center for Biotechnology Information. (2023, February 9). Coronary artery disease – statpearls – NCBI bookshelf. Coronary Artery Disease. https://www.ncbi.nlm.nih.gov/books/NBK564304/

Picture this. You’re in a very active city during rush hour and roads are congested. As a result, less traffic can flow, causing delays and sometimes even a complete standstill. CAD operates similarly. As your arteries narrow, less blood can reach parts of your heart. This might not seem like an issue when you’re relaxed or sleeping, as your heart doesn’t need as much oxygen. But during physical activity or stress, your heart works harder, and it craves more oxygen. When your arteries can’t deliver the necessary oxygen due to their narrowed state, your heart protests. This protest is typically experienced as chest pain, often described as a heaviness or tightness in the chest. This is a condition known as angina, which serves as a crucial warning sign.2Gulati M, Levy P, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. J Am Coll Cardiol. 2021 Nov, 78 (22) e187–e285.

Now, imagine the worst-case scenario. What if one of these “rusty pipes” becomes entirely blocked? The traffic comes to a standstill, right? In terms of your heart, this means a certain section won’t receive any oxygen or nutrients, causing heart muscle cells to die. This catastrophic event is what we commonly call a heart attack (or myocardial infarction). CAD is the leading cause of heart attacks, making it a disease that should not be taken lightly.3U.S. Department of Health and Human Services. (2022, March 25). Causes and risk factors. National Heart Lung and Blood Institute. https://www.nhlbi.nih.gov/health/heart-attack/causes 4Ojha N, Dhamoon AS. Myocardial Infarction. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537076/5Ambrose JA, Singh M. Pathophysiology of coronary artery disease leading to acute coronary syndromes. F1000Prime Rep. 2015 Jan 14;7:08. doi: 10.12703/P7-08. PMID: 25705391; PMCID: PMC4311268.

So, what makes your arteries start to rust? Well, several factors can contribute. These include unhealthy habits like smoking, a diet rich in saturated fats, a lack of physical activity, and being overweight. Apart from these, age, family history, diabetes, high blood pressure, and high cholesterol levels can also play a role in the development of CAD.6Said MA, van de Vegte YJ, Zafar MM, van der Ende MY, Raja GK, Verweij N, van der Harst P. Contributions of Interactions Between Lifestyle and Genetics on Coronary Artery Disease Risk. Curr Cardiol Rep. 2019 Jul 27;21(9):89. doi: 10.1007/s11886-019-1177-x. PMID: 31352625; PMCID: PMC6661028.7Khera AV, Emdin CA, Drake I, Natarajan P, Bick AG, Cook NR, Chasman DI, Baber U, Mehran R, Rader DJ, Fuster V, Boerwinkle E, Melander O, Orho-Melander M, Ridker PM, Kathiresan S. Genetic Risk, Adherence to a Healthy Lifestyle, and Coronary Disease. N Engl J Med. 2016 Dec 15;375(24):2349-2358. doi: 10.1056/NEJMoa1605086. Epub 2016 Nov 13. PMID: 27959714; PMCID: PMC5338864.8Yoriko Heianza , Lu Qi, Impact of Genes and Environment on Obesity and Cardiovascular Disease, Endocrinology, Volume 160, Issue 1, January 2019, Pages 81–100, https://doi.org/10.1210/en.2018-00591

Living with CAD is no easy feat, and it places a significant burden on those affected and their families. The constant monitoring of symptoms, frequent medical appointments, and lifestyle modifications can make life seem like an uphill battle. But remember, it’s not a fight you’re alone in. With support from healthcare providers, family, and friends, managing CAD becomes a shared journey, not a solitary struggle.

CAD is a common but severe condition that affects the highways of your heart. By understanding its nature and risk factors, you’re taking a step towards prevention and better management. After all, health is a shared responsibility, and knowledge is the first step on the road to well-being.

Historical Overview of Coronary Artery Disease (CAD)

Coronary Artery Disease (CAD) seems like a modern problem, doesn’t it? It feels linked to today’s less active lives and processed food. However, CAD has been lurking around much longer than you might think.

Imagine you’re stepping into a time machine, whirling back to ancient Egypt over 3,500 years ago. The mummies there, silent as they may be, can still tell us a story about clogged arteries. Yes, a buildup of fats and cholesterol, what doctors would call ‘atherosclerosis’, is a sign of CAD.9American College of Cardiology. (2011, April 5). Earliest case of coronary artery disease found in Egyptian princess. Earliest Case Of Coronary Artery Disease Found In Egyptian Princess. https://www.acc.org/about-acc/press-releases/2011/04/05/16/22/mummies

As we spin forward to the 18th and 19th centuries, doctors began to piece together the puzzle. They identified chest pain or ‘angina pectoris’, laying the foundation for our modern understanding of CAD. But it wasn’t until the 20th century that the term CAD began to make waves, signaling a significant leap in our understanding.10Hajar R. Coronary Heart Disease: From Mummies to 21st Century. Heart Views. 2017 Apr-Jun;18(2):68-74. doi: 10.4103/HEARTVIEWS.HEARTVIEWS_57_17. PMID: 28706602; PMCID: PMC5501035.11Nabel, E. G., & Braunwald, E. (2012). A tale of coronary artery disease and myocardial infarction. New England Journal of Medicine, 366(1), 54–63. https://doi.org/10.1056/nejmra1112570

During the 20th century, the perception of CAD changed dramatically. No longer was it seen as just another fact of getting older. Instead, it started to be recognized as a preventable and treatable disease. Two key studies during this time painted a clearer picture of CAD for us. The first was the Framingham Heart Study in 1948. This pioneering work identified factors that could lead to heart disease, linking CAD to high blood pressure, smoking, and high cholesterol levels.12Mahmood SS, Levy D, Vasan RS, Wang TJ. The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective. Lancet. 2014 Mar 15;383(9921):999-1008. doi: 10.1016/S0140-6736(13)61752-3. Epub 2013 Sep 29. PMID: 24084292; PMCID: PMC4159698.13Gallestey, J. Bacallao (2016, April 22). Framingham Heart Study. Encyclopedia Britannica. https://www.britannica.com/event/Framingham-Heart-Studay14O’Donnell, C. J., & Elosua, R. (2008). Cardiovascular risk factors. insights from Framingham Heart Study. Revista Española de Cardiología (English Edition), 61(3), 299–310. https://doi.org/10.1016/s1885-5857(08)60118-8

Not long after came the Seven Countries Study in the 1950s. This research highlighted the strong bond between our diet and CAD, warning us that diets high in saturated fats could increase the risk of CAD.15Yngve A. A Historical Perspective of the Understanding of the Link between Diet and Coronary Heart Disease. Am J Lifestyle Med. 2009;3(1 Suppl.):35S-38S. doi: 10.1177/1559827609334887. PMID: 20046857; PMCID: PMC2790142.16Katherine D Pett, MS, MEd, RDN and others, The Seven Countries Study, European Heart Journal, Volume 38, Issue 42, 07 November 2017, Pages 3119–3121, https://doi.org/10.1093/eurheartj/ehx603 These findings shifted the narrative from merely managing CAD to preventing its onset. Despite these strides, CAD remains a leading cause of death globally, a harsh reminder of the long-standing and ongoing fight against this disease.

Understanding the past of CAD isn’t just about knowledge; it’s about the human story that’s been unfolding for millennia. This tale connects our past, present, and future in a shared quest for healthier hearts. By recognizing the journey CAD has taken, you’re better equipped to understand its current standing and the need for continued efforts. CAD’s history emphasizes the importance of healthy lifestyle choices. After all, every beat of your heart is a note in the symphony of human history.

Current Global Burden of Coronary Artery Disease (CAD)

Can you grasp the enormity of Coronary Artery Disease (CAD)? It’s a phrase that many have heard, but few truly comprehend. When you think of CAD, remember that it’s more than just a diagnosis; it’s a global burden that dramatically affects lives all around the world. Here’s something to consider: Each year, CAD claims more lives than any other condition in the United States. It is the third leading cause of mortality worldwide.17Brown JC, Gerhardt TE, Kwon E. Risk Factors for Coronary Artery Disease. 2023 Jan 23. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 32119297. This fact alone underscores the grave importance and immediate attention this disease demands.

Now, let’s imagine a very active city with about 18 million people. It’s overwhelming, isn’t it? Sadly, this staggering figure represents the approximate number of people CAD snatches away from us every year.18Brown JC, Gerhardt TE, Kwon E. Risk Factors for Coronary Artery Disease. [Updated 2023 Jan 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554410/ Each loss is a story cut short, a family in despair, and a community losing a cherished member.

Yet, CAD’s impact extends beyond the grim shadow of death. Frequently, CAD doesn’t necessarily end lives; it transforms them. Picture living with persistent chest discomfort, gasping for breath after climbing just a few stairs, or the constant fear of a looming heart attack. For many, this isn’t a hypothetical scenario; it’s a daily reality. And by the year 2030, it is estimated that almost 23.6 million people could be wrestling with this reality.19Amini, M., Zayeri, F. & Salehi, M. Trend analysis of cardiovascular disease mortality, incidence, and mortality-to-incidence ratio: results from global burden of disease study 2017. BMC Public Health 21, 401 (2021). https://doi.org/10.1186/s12889-021-10429-0

While it’s true that CAD generally affects those over 65, an alarming trend is on the rise. CAD is no longer just an ‘old person’s disease’. It’s reaching into the lives of younger individuals at an escalating pace.20American College of Cardiology . (2019, March 7). Heart attacks increasingly common in young adults. Heart Attacks Increasingly Common in Young Adults. https://www.acc.org/about-acc/press-releases/2019/03/07/08/45/heart-attacks-increasingly-common-in-young-adults This development intensifies the urgency of tackling CAD.

But let’s not overlook the unequal distribution of CAD across the globe. Certain regions, particularly low-income countries, bear the brunt of CAD due to inadequate healthcare access, high rates of tobacco use, and other factors.21Gaziano TA, Bitton A, Anand S, Abrahams-Gessel S, Murphy A. Growing epidemic of coronary heart disease in low- and middle-income countries. Curr Probl Cardiol. 2010 Feb;35(2):72-115. doi: 10.1016/j.cpcardiol.2009.10.002. PMID: 20109979; PMCID: PMC2864143.22Wurie HR, Cappuccio FP. Cardiovascular disease in low- and middle-income countries: an urgent priority. Ethn Health. 2012;17(6):543-50. doi: 10.1080/13557858.2012.778642. PMID: 23534502; PMCID: PMC7613448.

Does cardiovascular disease discriminate based on gender? You might assume it’s mainly a men’s health issue, but the truth is cardiovascular disease doesn’t play favorites. It’s an equal opportunity ailment and stands as the leading cause of death in women worldwide.23Garcia M, Mulvagh SL, Merz CN, Buring JE, Manson JE. Cardiovascular Disease in Women: Clinical Perspectives. Circ Res. 2016 Apr 15;118(8):1273-93. doi: 10.1161/CIRCRESAHA.116.307547. PMID: 27081110; PMCID: PMC4834856. Often, women are diagnosed late in the disease course, which perpetuates a hidden crisis in women’s health.

It’s a sobering reality. CAD’s reach is vast and its touch, indiscriminate. Yet, in understanding its breadth and depth, we find the motivation to act. Remember, knowledge empowers us to make lifestyle changes, advocate for public health measures, and push for wider healthcare access. It’s not just about surviving CAD; it’s about living with dignity and quality of life.

The fight against CAD is collective, fought in the hearts of millions worldwide. When you take a step forward in this battle, you are not just a spectator; you become part of the solution. So, let’s not just understand CAD; let’s act on this understanding and share it with the world. In doing so, you can turn CAD from a devastating disease into a challenge that humanity can and will overcome.

Predicted Future Trends of Coronary Artery Disease (CAD)

When you picture the future, what do you see? A world of technological advancement, new opportunities, and hopefully, improved health? Well, if you’ve been following the saga of Coronary Artery Disease (CAD), you might be wondering what the future holds for this notorious health culprit.

Let’s start with a fact that might surprise you: experts are warning that we may see a significant surge in CAD cases in the coming decades.24Heidenreich, P. (2011). Forecasting the future of cardiovascular disease in the United States: A policy statement from the American Heart Association. American Heart Association, 2011, 12–13. https://doi.org/10.1016/j.yane.2012.01.067 How so? With the growing rates of obesity and diabetes worldwide, more people could be at risk. You see, these conditions don’t just affect your waistline or your blood sugar, they could pave the way to CAD.

Take a moment to consider the millions dealing with obesity and diabetes. For each of these individuals, the risk of developing CAD increases.25 Powell-Wiley, T. M., Poirier, P., Burke, L. E., Després, J.-P., Gordon-Larsen, P., Lavie, C. J., Lear, S. A., Ndumele, C. E., Neeland, I. J., Sanders, P., & St-Onge, M.-P. (2021). Obesity and cardiovascular disease: A scientific statement from the American Heart Association. Circulation, 143(21). https://doi.org/10.1161/cir.0000000000000973 And it’s not just adults; kids and teens with obesity are more likely to carry this excess weight into adulthood and eventually face the prospect of CAD. This makes fighting obesity and diabetes today an essential part of the battle against CAD tomorrow.

What about our ever-advancing world of technology? Surely, this must have a positive impact. The answer is both yes and no. On the one hand, technological advancements promise new ways to diagnose and treat CAD. This means people living with CAD might have a better shot at managing their condition.26Cassar A, Holmes DR Jr, Rihal CS, Gersh BJ. Chronic coronary artery disease: diagnosis and management. Mayo Clin Proc. 2009 Dec;84(12):1130-46. doi: 10.4065/mcp.2009.0391. PMID: 19955250; PMCID: PMC2787400.27Kandaswamy E, Zuo L. Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology. Int J Mol Sci. 2018 Jan 31;19(2):424. doi: 10.3390/ijms19020424. PMID: 29385089; PMCID: PMC5855646.

However, on the flip side, our increasingly digital lifestyle is creating a generation more sedentary than ever before. More hours spent in front of screens means less time for physical activity, a crucial factor in maintaining heart health. So while technology might provide new solutions, it could also contribute to the problem.28Warren TY, Barry V, Hooker SP, Sui X, Church TS, Blair SN. Sedentary behaviors increase risk of cardiovascular disease mortality in men. Med Sci Sports Exerc. 2010 May;42(5):879-85. doi: 10.1249/MSS.0b013e3181c3aa7e. PMID: 19996993; PMCID: PMC2857522.

A key point here is that future trends in CAD aren’t solely about numbers. They’re also about our understanding of the disease. As research progresses, we’re learning more about the genetic factors of CAD. 29Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.30Roberts R. Genetics of coronary artery disease: an update. Methodist Debakey Cardiovasc J. 2014 Jan-Mar;10(1):7-12. doi: 10.14797/mdcj-10-1-7. PMID: 24932356; PMCID: PMC4051327. This could lead to more personalized treatment approaches, potentially transforming the way we manage CAD.

Reflecting on these trends, it’s clear that the future of CAD is a mix of challenges and opportunities. Remember, you’re not just a spectator in this story; you’re an essential part of it. In the face of these predicted trends, it’s crucial that you don’t lose hope. Each step towards a healthier lifestyle, each conscious decision to prioritize your heart health, contributes to a future where CAD does not hold the reins.

Together, by spreading awareness and understanding, encouraging healthy habits, and advocating for research, we can shape a future where CAD is no longer a dominant health threat but a battle humanity is poised to win. Because, in the end, the story of CAD is not just about a disease, it’s about the people it affects – people like you, your loved ones, and millions around the globe. And it’s a story that we can change, one heart at a time.

Impact of Coronary Artery Disease (CAD) on Quality of Life 

Have you ever tried to carry a heavy load for an extended period? If you have, you know how exhausting it can be, and after a while, the burden starts to affect all aspects of your life. This is similar to the journey that you or your loved ones may experience when living with Coronary Artery Disease (CAD). It’s not just a physical condition; CAD casts a broad shadow, affecting much more than just your heart. It affects your whole body.

To begin with, let’s talk about the physical toll CAD takes. When your heart isn’t working as it should, you might find yourself feeling tired more often. Those routine tasks that you used to do without a second thought, like climbing a flight of stairs or walking the dog, suddenly become more challenging.31van Rosendael AR, Bax AM, van den Hoogen IJ, Smit JM, Al’Aref SJ, Achenbach S, Al-Mallah MH, Andreini D, Berman DS, Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Chinnaiyan K, Chow BJW, Cury RC, DeLago A, Feuchtner G, Hadamitzky M, Hausleiter J, Kaufmann PA, Kim YJ, Leipsic JA, Maffei E, Marques H, de Araújo Gonçalves P, Pontone G, Raff GL, Rubinshtein R, Villines TC, Gransar H, Lu Y, Peña JM, Lin FY, Shaw LJ, Narula J, Min JK, Bax JJ. Associations between dyspnoea, coronary atherosclerosis, and cardiovascular outcomes: results from the long-term follow-up CONFIRM registry. Eur Heart J Cardiovasc Imaging. 2022 Jan 24;23(2):266-274. doi: 10.1093/ehjci/jeaa323. PMID: 33538308; PMCID: PMC8932389. If you’re living with CAD, you might find that these limitations impact your ability to enjoy hobbies or activities that you once loved.

But it’s not only about the physical effects. Imagine always having to think twice before making any plans, fearing a sudden flare-up of chest pain or discomfort. This anxiety can become a constant companion for those living with CAD.32Celano CM, Daunis DJ, Lokko HN, Campbell KA, Huffman JC. Anxiety Disorders and Cardiovascular Disease. Curr Psychiatry Rep. 2016 Nov;18(11):101. doi: 10.1007/s11920-016-0739-5. PMID: 27671918; PMCID: PMC5149447.33Askin L, Uzel KE, Tanrıverdi O, Kavalcı V, Yavcin O, Turkmen S. The relationship between coronary artery disease and depression and anxiety scores. North Clin Istanb. 2020 Aug 5;7(5):523-526. doi: 10.14744/nci.2020.72602. PMID: 33163893; PMCID: PMC7603855.. You see, the disease can create a sense of uncertainty, impacting emotional health and contributing to feelings of stress or depression.

When we talk about CAD, we can’t ignore the changes that it necessitates in your lifestyle. Adapting to a heart-healthy diet, integrating regular exercise, and keeping up with medical appointments and treatments – it’s a lot to juggle, and it can feel overwhelming.34Gaudel P, Neupane S, Koivisto AM, Kaunonen M, Rantanen A. Effects of intervention on lifestyle changes among coronary artery disease patients: A 6-month follow-up study. Nurs Open. 2022 Jul;9(4):2024-2036. doi: 10.1002/nop2.1212. Epub 2022 Apr 17. PMID: 35434911; PMCID: PMC9190674.35Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.

Let’s not forget the financial aspect of this journey. Treating and managing CAD can be expensive, with costs ranging from medication and regular doctor’s visits to potentially requiring expensive procedures or hospitalizations.36Bauersachs R, Zeymer U, Brière JB, Marre C, Bowrin K, Huelsebeck M. Burden of Coronary Artery Disease and Peripheral Artery Disease: A Literature Review. Cardiovasc Ther. 2019 Nov 26;2019:8295054. doi: 10.1155/2019/8295054. PMID: 32099582; PMCID: PMC7024142.37Ekinci G. Economic Impacts of Cardiovascular Diseases: An Econometric Evaluation in Turkey. Iran J Public Health. 2023 Jan;52(1):118-127. doi: 10.18502/ijph.v52i1.11673. PMID: 36824237; PMCID: PMC9941436. If you’re grappling with these costs, you’re not alone. This financial stress can further detract from the quality of life.

CAD also has a ripple effect, impacting not only those diagnosed but also their loved ones. Family members often step in to provide care, which can lead to significant emotional and physical strain.38Reid RD, McDonnell LA, Riley DL, Mark AE, Mosca L, Beaton L, Papadakis S, Blanchard CM, Mochari-Greenberger H, O’Farrell P, Wells GA, Slovinec D’Angelo ME, Pipe AL. Effect of an intervention to improve the cardiovascular health of family members of patients with coronary artery disease: a randomized trial. CMAJ. 2014 Jan 7;186(1):23-30. doi: 10.1503/cmaj.130550. Epub 2013 Nov 18. PMID: 24246588; PMCID: PMC3883820.

Yet, even amidst these challenges, there are countless stories of resilience. While CAD might change your life in many ways, it does not define it. If you or someone you know is living with CAD, remember that support is available. There are communities of other people who have gone through the same journey, healthcare professionals dedicated to helping you manage this condition, and loved ones who are rooting for you.

Moreover, each day brings new research, new treatments, and new hope for those living with CAD.39Kandaswamy E, Zuo L. Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology. Int J Mol Sci. 2018 Jan 31;19(2):424. doi: 10.3390/ijms19020424. PMID: 29385089; PMCID: PMC5855646.

Remember, having CAD is part of your life’s journey, but it doesn’t have to steer your path. It might mean taking a few more pit stops, perhaps taking the scenic route, but the destination? That’s still in your hands. And in this journey, you’re not alone. There are millions of others navigating life with CAD, turning their challenges into opportunities for growth, connection, and advocacy.

When viewed from the outside, CAD may appear to be ‘just’ a heart condition. But when you delve deeper, it’s clear that its impact is far-reaching, touching every aspect of life. However, amid these challenges lies resilience and hope, a testament to the human spirit’s strength. For anyone dealing with CAD, this is your journey, and with each step, you’re showing the world what it truly means to have a heart full of courage. Your experience of CAD is much like a story, with its ebbs and flows, its moments of victory, and its struggles. It’s a story only you can tell in full because it’s deeply personal and unique to you.40Khatib R, Marshall K, Silcock J, Forrest C, Hall AS. Adherence to coronary artery disease secondary prevention medicines: exploring modifiable barriers. Open Heart. 2019 Jul 3;6(2):e000997. doi: 10.1136/openhrt-2018-000997. PMID: 31354954; PMCID: PMC6615814.

Let’s imagine, just for a moment, the chapters of this story. One might begin with the diagnosis. The moment when you first heard the words “Coronary Artery Disease”. You may have felt fear, confusion, or disbelief. This chapter might narrate the shock, the questions that raced in your mind, the information overload.41Coping with feelings. www.heart.org. (n.d.). https://www.heart.org/en/health-topics/cardiac-rehab/taking-care-of-yourself/coping-with-feelings

Then comes a chapter on adjustment. This phase is a bit like getting used to a new pair of shoes. It pinches at first, and every step is uncomfortable. Gradually though, you learn to walk in them. You learn about your condition, about the medical terminology that seemed like a foreign language at first. You learn to recognize your body’s signs, the warning signals it sends you.42Gomes L, Liébana-Presa C, Araújo B, Marques F, Fernández-Martínez E. Heart Disease, Now What? Improving Quality of Life through Education. Int J Environ Res Public Health. 2021 Mar 17;18(6):3077. doi: 10.3390/ijerph18063077. PMID: 33802701; PMCID: PMC8002524.

There might be a chapter on lifestyle changes – the heart-healthy diet, and the prescribed exercise regime. This is when you realize that managing CAD is a team effort. You, your doctors, your loved ones – you’re all in this together. Each decision, each change, is a step toward taking control of CAD rather than letting it control you.43Sharifi-Rad J, Rodrigues CF, Sharopov F, Docea AO, Can Karaca A, Sharifi-Rad M, Kahveci Karıncaoglu D, Gülseren G, Şenol E, Demircan E, Taheri Y, Suleria HAR, Özçelik B, Nur Kasapoğlu K, Gültekin-Özgüven M, Daşkaya-Dikmen C, Cho WC, Martins N, Calina D. Diet, Lifestyle and Cardiovascular Diseases: Linking Pathophysiology to Cardioprotective Effects of Natural Bioactive Compounds. Int J Environ Res Public Health. 2020 Mar 30;17(7):2326. doi: 10.3390/ijerph17072326. PMID: 32235611; PMCID: PMC7177934.44Chiuve, S. E., McCullough, M. L., Sacks, F. M., & Rimm, E. B. (2006). Healthy lifestyle factors in the primary prevention of coronary heart disease among men. Circulation, 114(2), 160–167. https://doi.org/10.1161/circulationaha.106.621417

Don’t forget about the chapter on support. It’s the one where you find strength in places you didn’t expect – a sympathetic doctor, a helpful support group, a friend who’s always just a call away. It’s the chapter that reminds you, you’re not alone on this journey. There’s a community of people who understand and are ready to help.45Compare A, Zarbo C, Manzoni GM, Castelnuovo G, Baldassari E, Bonardi A, Callus E, Romagnoni C. Social support, depression, and heart disease: a ten year literature review. Front Psychol. 2013 Jul 1;4:384. doi: 10.3389/fpsyg.2013.00384. PMID: 23847561; PMCID: PMC3696881.46Wenn P, Meshoyrer D, Barber M, Ghaffar A, Razka M, Jose S, Zeltser R, Makaryus AN. Perceived Social Support and its Effects on Treatment Compliance and Quality of Life in Cardiac Patients. J Patient Exp. 2022 Feb 4;9:23743735221074170. doi: 10.1177/23743735221074170. PMID: 35141401; PMCID: PMC8819762.

But perhaps the most important chapter is the one on hope. It’s the chapter that’s still being written. It’s about the daily victories, the good days when you feel stronger and more in control. It’s about the advances in medical science that promise better management strategies, and better outcomes. It’s about looking to the future, not with fear, but with cautious optimism.47Rakhshan M, Toufigh A, Dehghani-Firouzabadi A, Yektatalab S. Effect of Cardiac Rehabilitation on Hope Among Cardiac Patients After Coronary Artery Bypass Graft Surgery. Risk Manag Healthc Policy. 2020 Aug 25;13:1319-1326. doi: 10.2147/RMHP.S262656. PMID: 32922100; PMCID: PMC7457873.

Your story of living with CAD is not yet complete. Each day adds a few more lines, a few more experiences. It’s a tale of strength and resilience, of challenges faced and battles won. And while CAD is a significant part of your story, it’s not the only one. There are other parts too – your passions, your loved ones, your dreams. CAD may have changed the course of your story, but it’s you who’s holding the pen, writing each word, each sentence, and shaping the story as you live it. And that’s what truly matters.

Basics of Coronary Arteries

Anatomy and Physiology of the Coronary Arteries 

Macroscopic Anatomy of the Coronary Arteries

Think about your heart for a moment. It’s not just the poetic center of emotion as depicted in the books and movies, but it’s a marvelous, intricate piece of machinery right inside you, tirelessly working, beat after beat, day after day. Today, let’s get to know one crucial part of it – the coronary arteries. They’re a bit like the highways that fuel your heart.48Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/49Chaudhry R, Rahman S, Law MA. Anatomy, Thorax, Heart Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470522/

Your heart is a muscle and like any other muscle in your body, it needs a steady supply of oxygen and nutrients to keep functioning. This is where your coronary arteries come into play. These two small vessels branch off from the main artery, the aorta, right when it leaves your heart, and they envelop the heart in a beautiful, intricate network.50Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/

Now, imagine for a moment, holding an apple in your hand. The size of your heart is roughly similar to this apple and the coronary arteries would be like the winding roads around a mountain, only that in this case, the mountain is the heart itself.51Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/52Chaudhry R, Rahman S, Law MA. Anatomy, Thorax, Heart Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470522/

Picture this: there are two main highways – the left and the right coronary arteries. The right one heads towards the, you guessed it right, the right side of your heart. It supplies the right atrium and ventricle, and also runs a service to the lower part of the left ventricle and the heart’s own electrical system.53Saxton A, Chaudhry R, Manna B. Anatomy, Thorax, Heart Right Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537357/

Now, let’s talk about the left one. It’s like a massive expressway as it branches into two major routes shortly after its origin – the left anterior descending artery and the circumflex artery. These routes service the left part of your heart and the bulk of your left ventricle, which is the main pump pushing blood out to your body.54Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/

These highways and roads are critical for the life and health of your heart. If they’re clear and traffic is moving smoothly, everything is good. But, in coronary artery disease, these arteries get narrow, almost like a roadblock. This interrupts the smooth flow of blood, and that’s when problems start.55InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. Coronary artery disease: Overview. 2013 Feb 13 [Updated 2017 Jul 27]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK355313/

Remember, coronary arteries are your heart’s lifeline. They work 24/7, no weekends, no holidays, ensuring your heart gets what it needs. The more you know about them, the more amazed you’ll be at this incredible system within you. And with knowledge comes power – the power to take better care of your heart and your health. So, let’s appreciate these vital highways that keep your heart fueled and ready for all of life’s beautiful moments.

There’s more to the story of your heart’s intricate roadway system. While we’ve traced the main routes, let’s delve a bit deeper to understand the less-trodden paths. And remember, in the context of your heart, every bit of detail is vital. Knowledge here isn’t just power, it’s the key to healthy living.

So, let’s embark on this journey together, with your heart as our destination.

Imagine for a moment, you’re inside your heart, a spectacular and intricate world. Here, every tiny alleyway is as significant as the wide, bustling highways. These are your smaller, but equally vital, arterial branches, snaking through your heart muscle.56Goodwill AG, Dick GM, Kiel AM, Tune JD. Regulation of Coronary Blood Flow. Compr Physiol. 2017 Mar 16;7(2):321-382. doi: 10.1002/cphy.c160016. PMID: 28333376; PMCID: PMC5966026.

These arteries are like a miniature model of your highway system, seamlessly branching out, creating a network of life-sustaining routes. They dive deeper into your heart muscle, carrying oxygen-rich blood to even the remotest cells of your heart. Remember, in the heart’s universe, no cell is insignificant.57Pittman RN. Regulation of Tissue Oxygenation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Chapter 2, The Circulatory System and Oxygen Transport. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54112/58InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. How does the blood circulatory system work? 2010 Mar 12 [Updated 2019 Jan 31]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279250/

What’s even more fascinating is that this intricate arterial network doesn’t stop at just one layer. Your heart muscle is essentially composed of three layers, each with its own supply of these arterial roadways. Picture them as multilayered, interconnecting highways, spanning the entirety of your heart.59Sharma B, Chang A, Red-Horse K. Coronary Artery Development: Progenitor Cells and Differentiation Pathways. Annu Rev Physiol. 2017 Feb 10;79:1-19. doi: 10.1146/annurev-physiol-022516-033953. Epub 2016 Dec 9. PMID: 27959616; PMCID: PMC5513160.

Now, let’s take a slight detour and focus on the heart’s unsung heroes – the capillaries. These tiny blood vessels are the endpoint of your coronary circulation. They’re like the local streets that take you right to your doorstep, or in this case, the individual heart cells.60Tucker WD, Arora Y, Mahajan K. Anatomy, Blood Vessels. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470401/

Even though they are tiny, capillaries are of huge importance. They form a vast network within your heart muscle, ensuring each and every cell gets its required supply of oxygen and nutrients. This way, every single cell contributes to the overall function of your heart. Isn’t that just amazing?61Pittman RN. Regulation of Tissue Oxygenation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Chapter 2, The Circulatory System and Oxygen Transport. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54112/

Think about it – the health of your heart relies heavily on this elaborate, beautiful network. When everything works in harmony, your heart beats uninterrupted, powering you through life. But, things can, and do go wrong. In coronary artery disease, it’s these very highways and byways that get affected.62Falk, E., Shah, P. K., & Fuster, V. (1995). Coronary plaque disruption. Circulation, 92(3), 657–671. https://doi.org/10.1161/01.cir.92.3.657

Like a roadblock causing a traffic jam, the arteries get narrowed, affecting the smooth flow of blood. And when the heart cells don’t receive enough oxygen, they struggle to work, causing discomfort and pain, often known as angina. And if an artery gets completely blocked, it’s like a significant road closure. The result can be quite severe – a heart attack.63Saleh M, Ambrose JA. Understanding myocardial infarction. F1000Res. 2018 Sep 3;7:F1000 Faculty Rev-1378. doi: 10.12688/f1000research.15096.1. PMID: 30228871; PMCID: PMC6124376.

Understanding the workings of your heart is not only fascinating but also empowering. It allows you to comprehend the importance of heart health and the factors that can potentially disrupt it. Keeping your heart’s highways clear is your duty. Regular check-ups, a balanced diet, regular exercise, and an overall healthy lifestyle are the maintenance crew for your heart’s roadway system. They help to ensure smooth traffic, prevent roadblocks, and ultimately, keep your heart happy and healthy.64Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.

With each heartbeat, let’s appreciate this intricate system, this marvel of nature, and pledge to take good care of it. Because your heart, in every sense, is at the heart of your life. Now that you’re acquainted with your heart’s vast and vital roadway system, let’s talk about what’s actually flowing on these routes – the blood. You’ve often heard the phrase, ‘Life is in the blood’, haven’t you? Let’s explore why that’s absolutely spot-on.

Blood, as you know, is the vehicle that carries vital passengers – oxygen and nutrients, to the heart. Picture it like a stream of red, life-giving trucks, all filled to the brim with everything your heart cells need to do their job.65Pittman RN. Regulation of Tissue Oxygenation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Chapter 2, The Circulatory System and Oxygen Transport. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54112/

The bloodstream isn’t a one-way street, though. As it winds its way through your heart, it picks up passengers for the return journey as well – the waste materials from the heart cells. Just like your city’s garbage trucks, these elements are swiftly transported away for disposal, ensuring your heart stays clean and efficient.66InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. How does the blood circulatory system work? 2010 Mar 12 [Updated 2019 Jan 31]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279250/

Let’s go a bit deeper now. The walls of your arteries, those vital highways, aren’t just passive bystanders. They’re active players in this journey. These walls can expand and contract, adjusting the arterial diameter and controlling the blood flow, much like how traffic lights manage vehicle flow.67Chaudhry R, Miao JH, Rehman A. Physiology, Cardiovascular. [Updated 2022 Oct 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493197/

When your body needs more oxygen – let’s say, during a workout – the arterial walls relax, widening the highway, allowing more blood to flow. On the flip side, when you’re resting, the arterial walls contract, slowing down the blood flow. It’s an intricate dance, perfectly choreographed to match your body’s needs.68Joyner MJ, Casey DP. Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiol Rev. 2015 Apr;95(2):549-601. doi: 10.1152/physrev.00035.2013. PMID: 25834232; PMCID: PMC4551211.

However, in the case of coronary artery disease, this natural flow is disrupted. The arterial walls thicken, the highways narrow down, and the heart cells are left gasping for oxygen. The smooth-flowing stream turns into a trickle, and your heart struggles to keep up.69Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/

This is why you may experience chest pain or discomfort during physical activity or emotional stress, times when your heart needs more blood. Your heart is literally signaling to you that it’s not getting enough oxygen.70Pimple P, Hammadah M, Wilmot K, Ramadan R, Al Mheid I, Levantsevych O, Sullivan S, Garcia EV, Nye J, Shah AJ, Ward L, Mehta P, Raggi P, Bremner JD, Quyyumi AA, Vaccarino V. Chest Pain and Mental Stress-Induced Myocardial Ischemia: Sex Differences. Am J Med. 2018 May;131(5):540-547.e1. doi: 10.1016/j.amjmed.2017.11.026. Epub 2017 Dec 7. PMID: 29224740; PMCID: PMC5910270.

It’s a cry for help, a plea for attention. Your heart’s asking you to make some changes, to switch to healthier highways, to open up the blockages. It’s asking you to ensure that the stream of life-giving trucks keeps flowing smoothly.71Pinckard K, Baskin KK, Stanford KI. Effects of Exercise to Improve Cardiovascular Health. Front Cardiovasc Med. 2019 Jun 4;6:69. doi: 10.3389/fcvm.2019.00069. PMID: 31214598; PMCID: PMC6557987.72Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495. Remember, your heart is your body’s lifeline. It tirelessly pumps blood, day in, day out, never asking for a break. But it does ask for your care, your attention. So, let’s answer its call.

As we end this part of our journey, we hope you’ve gained a deeper understanding of your heart’s wonderful world. The arterial highways, the life-giving blood, the flexible walls, and their role in your heart’s well-being. We hope it’s inspired you to take better care of your heart, and by extension, your health. Because in the grand story of life, every beat counts.

Microscopic Anatomy of the Coronary Arteries

So, you’ve been on this enlightening journey with us, discovering the macroscopic world of your coronary arteries – the wide highways that carry life’s sustenance to your heart. But now, let’s dive even deeper. Let’s zoom in a bit more, and look at what makes these roads. It’s time to explore the microscopic structure of your coronary arteries. Imagine looking at a cross-section of a tree trunk, where you see all the different layers of its growth. The coronary arteries aren’t much different. They have layers too. You can think of them as layers of an onion, each with a unique role.73Holzapfel, G. A., Sommer, G., Gasser, C. T., & Regitnig, P. (2005). Determination of layer-specific mechanical properties of human coronary arteries with nonatherosclerotic intimal thickening and related constitutive modeling. American Journal of Physiology-Heart and Circulatory Physiology, 289(5). https://doi.org/10.1152/ajpheart.00934.2004

The innermost layer is the tunica intima. It’s the smooth, inner road surface that allows blood to flow swiftly and efficiently. It’s like the smooth asphalt on a highway, facilitating your life-giving trucks – the blood cells – to rush past without any hindrance.74OpenStax, L. L. &. (n.d.). Anatomy and Physiology II. Structure and Function of Blood Vessels | Anatomy and Physiology II. https://courses.lumenlearning.com/suny-ap2/chapter/structure-and-function-of-blood-vessels/  It’s so thin, you’d need a microscope to see it. But, this fine lining has a critical role in your heart’s health. It’s made of endothelial cells which are like the traffic cops of your artery highway. They regulate what can enter or exit the blood, like nutrients, oxygen, and waste. Just imagine, these cells keep everything running smoothly despite the torrent of blood that’s constantly rushing past.75Milutinović, A., Šuput, D. ., & Zorc-Pleskovič, R. (2020). Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries: An updated review. Biomolecules and Biomedicine, 20(1), 21–30. https://doi.org/10.17305/bjbms.2019.4320 Now, right under the tunica intima is the basement membrane. This tough, flexible layer is what holds the endothelial cells in place, allowing them to function efficiently.76Khalilgharibi N, Mao Y. To form and function: on the role of basement membrane mechanics in tissue development, homeostasis, and disease. Open Biol. 2021 Feb;11(2):200360. doi: 10.1098/rsob.200360. Epub 2021 Feb 17. PMID: 33593159; PMCID: PMC8061686.

The middle layer, the tunica media, is the artery’s muscle. Composed primarily of smooth muscle cells and elastic fibers, it’s the tunica media that dictates how wide or narrow your arterial highway will be. 77Imo E. Hoefer and others, Biomechanical factors as triggers of vascular growth, Cardiovascular Research, Volume 99, Issue 2, 15 July 2013, Pages 276–283, https://doi.org/10.1093/cvr/cvt089 Now, it’s not enough for this muscle layer to be strong – it needs to be flexible too. That’s where the elastic fibers come in. They give your arteries the ability to stretch and recoil with each heartbeat, maintaining a steady flow of blood.78Vatner, S. F., Zhang, J., Vyzas, C., Mishra, K., Graham, R. M., & Vatner, D. E. (2021). Vascular stiffness in aging and disease. Frontiers in Physiology, 12. https://doi.org/10.3389/fphys.2021.762437

Lastly, the outer layer, the tunica adventitia, is the support structure. It’s like the guardrails on your highways, offering structural strength and stability to your arterial roads.79Majesky MW, Dong XR, Hoglund V, Mahoney WM Jr, Daum G. The adventitia: a dynamic interface containing resident progenitor cells. Arterioscler Thromb Vasc Biol. 2011 Jul;31(7):1530-9. doi: 10.1161/ATVBAHA.110.221549. PMID: 21677296; PMCID: PMC3382115.

Together, these three layers work in perfect harmony, ensuring that your heart always gets the oxygen and nutrients it needs. But here’s where coronary artery disease comes into the picture. This harmony can be disrupted. The smooth tunica intima may get damaged, resulting in plaque build-up. This narrows the road, leading to less blood reaching your heart.80Belhoul-Fakir, H., Wu, J., Yeow, Y. L., Musk, G. C., Kershaw, H., Ingley, E., Zhao, B. S., Reid, C. M., Lagat, C., Evans, B., Thompson, P. L., Brown, M. L., Hamzah, J., & Jansen, S. (2023). Injury to the Tunica Media Initiates Atherogenesis in the presence of Hyperlipidemia. Frontiers in Cardiovascular Medicine, 10. https://doi.org/10.3389/fcvm.2023.1152124  It’s like when a road undergoes construction. The traffic slows down, right? The same happens in your arteries. The flow of life-giving trucks slows down, your heart receives less oxygen and nutrients, and that’s when you start experiencing symptoms like chest pain.

Last but not least, let’s look at the outermost layer, the tunica adventitia. If the tunica media is the muscle, then the tunica adventitia is the skeleton. It gives your artery its structure and shape. Composed mostly of collagen, a strong and flexible protein, the tunica adventitia ensures your artery can withstand the high-pressure flow of blood without tearing.81Chow MJ, Turcotte R, Lin CP, Zhang Y. Arterial extracellular matrix: a mechanobiological study of the contributions and interactions of elastin and collagen. Biophys J. 2014 Jun 17;106(12):2684-92. doi: 10.1016/j.bpj.2014.05.014. PMID: 24940786; PMCID: PMC4070071.

But that’s not all. The tunica adventitia also houses tiny blood vessels called vasa vasorum. These “vessels of the vessels” have an essential task – they supply blood to the outer layers of your coronary arteries. Even the highways need their own supply routes.82Majesky MW, Dong XR, Hoglund V, Mahoney WM Jr, Daum G. The adventitia: a dynamic interface containing resident progenitor cells. Arterioscler Thromb Vasc Biol. 2011 Jul;31(7):1530-9. doi: 10.1161/ATVBAHA.110.221549. PMID: 21677296; PMCID: PMC3382115.

Remember how we talked about coronary artery disease and how the smooth tunica intima could get damaged leading to plaque build-up? Well, it’s often these microscopic players – the endothelial cells, the smooth muscle cells, the collagen – that are affected first. And understanding their role can help us figure out how to protect them and, in turn, protect our heart.83Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/

To sum it up, your coronary arteries aren’t just passive tubes carrying blood. They are complex, living structures, teeming with cells and proteins, each performing a delicate balancing act to keep your heart nourished and healthy. It’s a testament to the marvel that is the human body – a marvel that we are only beginning to understand.

When the tunica intima gets damaged, it’s like a pothole opening up on a smooth road. The body then sends a cleanup crew to fix this “pothole”. These crews are your white blood cells, who, under normal circumstances, are your body’s first line of defense against foreign invaders. But in the case of artery damage, they can unintentionally make things worse.84Swirski FK, Nahrendorf M. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Science. 2013 Jan 11;339(6116):161-6. doi: 10.1126/science.1230719. PMID: 23307733; PMCID: PMC3891792. When these white blood cells arrive at the site of damage, they try to gobble up cholesterol present in your blood. Over time, they get filled with so much cholesterol that they morph into what are known as foam cells.85Swirski FK, Nahrendorf M. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Science. 2013 Jan 11;339(6116):161-6. doi: 10.1126/science.1230719. PMID: 23307733; PMCID: PMC3891792.

Now, imagine if your city’s maintenance crew, while trying to fix a pothole, ended up creating a mound of debris right in the middle of the road. That wouldn’t be very helpful, would it? Similarly, these foam cells end up forming a fatty streak in your artery – the earliest visible sign of plaque buildup and the beginning of coronary artery disease.86Javadifar A, Rastgoo S, Banach M, Jamialahmadi T, Johnston TP, Sahebkar A. Foam Cells as Therapeutic Targets in Atherosclerosis with a Focus on the Regulatory Roles of Non-Coding RNAs. Int J Mol Sci. 2021 Mar 3;22(5):2529. doi: 10.3390/ijms22052529. PMID: 33802600; PMCID: PMC7961492.

Biochemistry of Coronary Artery Disease (CAD)

Role of Lipids in Coronary Artery Disease (CAD)

We’ve been on an amazing journey through your body’s superhighways, your coronary arteries. But what’s a trip without getting to know the locals, right? So, let’s get up close and personal with the key players that call your arteries home, specifically the lipids or fats. Think of lipids as those tiny, invisible particles whizzing through your bloodstream. They’re like the cars and trucks zooming down the arterial highways. They’re essential, providing energy, but when they get out of control, they’re like reckless drivers causing havoc.87Dong J, Yang S, Zhuang Q, Sun J, Wei P, Zhao X, Chen Y, Chen X, Li M, Wei L, Chen C, Fan Y, Shen C. The Associations of Lipid Profiles With Cardiovascular Diseases and Death in a 10-Year Prospective Cohort Study. Front Cardiovasc Med. 2021 Nov 25;8:745539. doi: 10.3389/fcvm.2021.745539. PMID: 34901209; PMCID: PMC8655628.

You may have heard of cholesterol, a type of lipid, and its notorious reputation. There are two main types of cholesterol: the good (HDL) and the bad (LDL). HDL is like the cleanup crew, while LDL is the troublemaker.88Wilson PW. High-density lipoprotein, low-density lipoprotein and coronary artery disease. Am J Cardiol. 1990 Sep 4;66(6):7A-10A. doi: 10.1016/0002-9149(90)90562-f. PMID: 2203248.

When LDL cholesterol is too high, it’s like a bunch of unruly drivers causing mayhem on your arterial highways. These ‘bad cholesterol’ particles can sneak into the arterial wall; and remember our cleanup crew, the white blood cells? They see this as an emergency and rush to the scene.89Tall AR, Yvan-Charvet L. Cholesterol, inflammation and innate immunity. Nat Rev Immunol. 2015 Feb;15(2):104-16. doi: 10.1038/nri3793. PMID: 25614320; PMCID: PMC4669071. But instead of helping, they get transformed into foam cells, contributing to the fatty streaks we talked about earlier. It’s a bit like having a block party that gets way out of hand.90Ilhan F, Kalkanli ST. Atherosclerosis and the role of immune cells. World J Clin Cases. 2015 Apr 16;3(4):345-52. doi: 10.12998/wjcc.v3.i4.345. PMID: 25879006; PMCID: PMC4391004.91Parthasarathy S, Raghavamenon A, Garelnabi MO, Santanam N. Oxidized low-density lipoprotein. Methods Mol Biol. 2010;610:403-17. doi: 10.1007/978-1-60327-029-8_24. PMID: 20013192; PMCID: PMC3315351.

Sometimes, your body might start ignoring insulin, the hormone that helps keep your blood sugar levels in check. This can cause a sudden rise in the population of triglycerides and LDL, while HDL decreases. Think of insulin as a traffic cop, keeping everything flowing smoothly. When the cop is ignored, chaos ensues.92Bjornstad P, Eckel RH. Pathogenesis of Lipid Disorders in Insulin Resistance: a Brief Review. Curr Diab Rep. 2018 Oct 17;18(12):127. doi: 10.1007/s11892-018-1101-6. PMID: 30328521; PMCID: PMC6428207.

Let’s clear the air about LDL, the supposed ‘bad guy’. He’s not all bad. LDL plays a big part in the building of your body, laying the foundation of cells, and also helping out in creating some hormones. However, like any good character with a tragic flaw, when LDL starts to multiply and hang around too much, that’s when the plot thickens. It’s a bit like that buddy of yours who can’t hold his drinks and starts causing a ruckus at a party.93Ference BA, Ginsberg HN, Graham I, Ray KK, Packard CJ, Bruckert E, Hegele RA, Krauss RM, Raal FJ, Schunkert H, Watts GF, Borén J, Fazio S, Horton JD, Masana L, Nicholls SJ, Nordestgaard BG, van de Sluis B, Taskinen MR, Tokgözoglu L, Landmesser U, Laufs U, Wiklund O, Stock JK, Chapman MJ, Catapano AL. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017 Aug 21;38(32):2459-2472. doi: 10.1093/eurheartj/ehx144. PMID: 28444290; PMCID: PMC5837225.

Now, what about the hero, HDL? Well, think of HDL as your body’s personal clean-up crew, always ready to pick up the rowdy LDLs and send them back to the liver. But even our hero has limits. When the LDLs get too unruly, even a high HDL level might not be enough to handle the situation. Imagine having a top-of-the-range vacuum cleaner, but the mess you’re dealing with is just too vast.94Mann S, Beedie C, Jimenez A. Differential effects of aerobic exercise, resistance training and combined exercise modalities on cholesterol and the lipid profile: review, synthesis, and recommendations. Sports Med. 2014 Feb;44(2):211-21. doi: 10.1007/s40279-013-0110-5. PMID: 24174305; PMCID: PMC3906547.

Then there are triglycerides, another type of lipid. They’re your body’s main form of stored energy. But when there’s too much of them, they’re like those huge trucks that clog up the highway. And guess what? They too can contribute to the buildup of plaque.95Sarwar, N., Danesh, J., Eiriksdottir, G., Sigurdsson, G., Wareham, N., Bingham, S., Boekholdt, S. M., Khaw, K.-T., & Gudnason, V. (2007). Triglycerides and the risk of coronary heart disease. Circulation, 115(4), 450–458. https://doi.org/10.1161/circulationaha.106.637793

The next lipids are VLDL and IDL. VLDL stands for Very Low-Density Lipoprotein, and IDL stands for Intermediate Density Lipoprotein. They’re like the delivery drivers in our body’s transportation system.96Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/ Let’s imagine VLDL as the big, fully loaded delivery trucks departing from the warehouse (which is our liver, by the way). These trucks are full of triglycerides, a type of fat that the body uses for energy.97Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/

As these trucks start their delivery routes, they drop off triglycerides to cells around the body. As they make these deliveries, they start to shrink, becoming our friend, IDL. You can think of IDL as the smaller delivery vans that make the neighborhood rounds.98Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/

The smaller vans (IDL) can be picked up again by the liver or further processed into Low-Density Lipoprotein (LDL), the ‘bad’ cholesterol. LDL is like the last delivery of the day – it needs to find a home. Unfortunately, if LDL levels become too high, these packages start to get left in places they don’t belong – like our artery walls.99Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/

Coronary artery disease may seem like a complex and daunting issue, but understanding how lipids like LDL, HDL, IDL, and VLDL play their part makes it easier to navigate. By making informed choices, you can support your body in maintaining a healthy lipid balance and keep the party going strong.

Role of Glucose and Insulin in Coronary Artery Disease (CAD) 

Imagine you’re at a party, and the party represents your body’s complex system. The guests at the party are the nutrients from the food you eat, and the star attractions are glucose and insulin. We’re going to get up close and personal with these two, understanding their dance and how it directly impacts your heart, specifically in the context of coronary artery disease.

Glucose, the main energy source for your body, is like the life of the party. Every cell in your body needs glucose to function. From the delicious pasta you had for dinner to the apple you snacked on, all carbs you eat are broken down into glucose.100Holesh JE, Aslam S, Martin A. Physiology, Carbohydrates. [Updated 2023 May 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459280/101Ludwig D S, Hu F B, Tappy L, Brand-Miller J. Dietary carbohydrates: role of quality and quantity in chronic disease BMJ 2018; 361 :k2340 doi:10.1136/bmj.k2340

But for glucose to really light up the party, it needs a partner, and that’s where insulin comes in. Insulin is the much-needed chaperone, produced by your pancreas, that helps glucose get from your bloodstream into your cells. It’s as if insulin takes glucose by the hand and leads it to the dance floor, i.e., the body’s cells.102Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005 May;26(2):19-39. PMID: 16278749; PMCID: PMC1204764.103Chang, L., Chiang, SH. & Saltiel, A.R. Insulin Signaling and the Regulation of Glucose Transport. Mol Med 10, 65–71 (2004). https://doi.org/10.2119/2005-00029.Saltiel

However, when this harmonious dance gets disrupted, that’s when problems arise. Picture insulin trying to lead glucose to the dance floor, but the door is jammed. This condition is what we call insulin resistance, where your cells resist the efforts of insulin, causing glucose to build up in your blood.104Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005 May;26(2):19-39. PMID: 16278749; PMCID: PMC1204764.105Freeman AM, Pennings N. Insulin Resistance. [Updated 2022 Sep 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507839/ Prolonged insulin resistance leads to higher glucose levels in the blood, a condition known as hyperglycemia.106Ormazabal, V., Nair, S., Elfeky, O. et al. Association between insulin resistance and the development of cardiovascular disease. Cardiovasc Diabetol 17, 122 (2018). https://doi.org/10.1186/s12933-018-0762-4

So, why should you, as someone curious about coronary artery disease, care about a disrupted dance at a party inside your body? Here’s why: this build-up of glucose can, over time, damage the walls of your arteries, making them more susceptible to the accumulation of fatty materials. This can lead to a condition called atherosclerosis, a major contributor to coronary artery disease.107Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/

Now, where does our heart fit into this busy city scene? High blood glucose levels can cause damage to the blood vessels, including those that supply blood to the heart. This damage may start off as minor, like a small pothole in a city street. But over time, as the damage increases, this can lead to a buildup of plaque, narrowing the arteries – a scenario akin to road construction causing lane closures. When this happens in the arteries supplying your heart, we call this coronary artery disease.108Aronson D, Edelman ER. Coronary artery disease and diabetes mellitus. Cardiol Clin. 2014 Aug;32(3):439-55. doi: 10.1016/j.ccl.2014.04.001. Epub 2014 Jun 10. PMID: 25091969; PMCID: PMC4672945.

And the story doesn’t end here. You see, hyperglycemia can also cause inflammation and changes in your blood that can lead to clotting. It’s as if this traffic jam and road construction now have an added problem of fallen trees blocking the way. Blood clots in your coronary arteries can completely block the blood supply to parts of your heart, causing a heart attack.109Undas A, Wiek I, Stêpien E, Zmudka K, Tracz W. Hyperglycemia is associated with enhanced thrombin formation, platelet activation, and fibrin clot resistance to lysis in patients with acute coronary syndrome. Diabetes Care. 2008 Aug;31(8):1590-5. doi: 10.2337/dc08-0282. Epub 2008 May 16. PMID: 18487475; PMCID: PMC2494657.110Liu X, Li T, Xu H, Wang C, Ma X, Huang H, Hu Y, Chu H. Hyperglycemia may increase deep vein thrombosis in trauma patients with lower limb fracture. Front Cardiovasc Med. 2022 Sep 8;9:944506. doi: 10.3389/fcvm.2022.944506. PMID: 36158801; PMCID: PMC9498976.

Understanding this narrative can empower you to take control of the situation. Managing your blood sugar levels, watching your diet, and staying physically active is like being a city planner who ensures smooth traffic flow and timely road repairs, preventing severe congestion and blockages.

Normal Function of the Coronary Arteries

Picture yourself at the heart of a very active city – not just any city, but one known for its efficient, tireless flow of traffic. This city represents your heart; and the vehicles? They are oxygen-rich blood. The highways that keep the city moving are your coronary arteries, responsible for ensuring that each corner of your heart-city remains lively and vibrant. The primary function of the coronary arteries is simple yet crucial: they deliver oxygenated blood to the heart muscle.111Chaudhry R, Rahman S, Law MA. Anatomy, Thorax, Heart Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470522/ Imagine the highways funneling cars into the city center. Each vehicle delivers what’s needed to keep the city operating smoothly – just as each droplet of blood supplies the heart muscle with vital oxygen and nutrients.

As you visualize this, remember that the heart isn’t just another organ; it’s the life-sustaining hub that tirelessly pumps blood to the entire body. It’s the downtown district, the heart of the city that never sleeps. The responsibility resting on the coronary arteries is thus immense, ensuring the ceaseless beat of life itself112Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/

In a city, smooth traffic flow depends on well-maintained roads, efficient traffic signals, and responsible drivers. In the case of the coronary arteries, the smooth flow of blood depends on the health of the artery walls and the consistency of the blood itself.113Rehman S, Khan A, Rehman A. Physiology, Coronary Circulation. [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482413/ A balanced diet, regular exercise, and good lifestyle habits, like avoiding smoking, help maintain this.

At the heart of understanding coronary artery disease is understanding the critical role of these arterial highways in our bodies. These arteries are not just static tubes; they are dynamic, living tissues that respond to the body’s needs. When the heart needs more oxygen during physical activity, these arteries can widen to increase blood flow – much like how city authorities might open additional lanes during peak hours.114Duncker DJ, Bache RJ. Regulation of coronary blood flow during exercise. Physiol Rev. 2008 Jul;88(3):1009-86. doi: 10.1152/physrev.00045.2006. PMID: 18626066.

However, imagine if there’s construction on a city highway, leading to lane closures. Suddenly, traffic slows down, causing delays and disruptions. In your heart, such “construction” or blockages can happen when plaque builds up in the arteries, a condition we call atherosclerosis, which is a primary cause of coronary artery disease.115Sandy N Shah, D. (2023, July 20). Coronary artery atherosclerosis. Practice Essentials, Background, Anatomy. https://emedicine.medscape.com/article/153647-overview?form=fpf .

Pathophysiology of Coronary Artery Disease (CAD)

The Development of Atherosclerosis in Coronary Artery Disease (CAD)

Atherosclerosis starts innocently enough, like that first soda can floating in the river. When you have too much low-density lipoprotein (LDL), the “bad” cholesterol, in your blood, it can start to stick to the walls of your arteries. Now, your body, being the clean-up crew that it is, sends white blood cells to gobble up this cholesterol, but instead of clearing the problem, these cells get stuck in the arterial walls too. This gathering – cholesterol, cells, and other substances – forms a streak of plaque.

Plaque is a bit like a zit. It starts small but can grow larger over time, and like a zit, it can rupture. When that happens, it’s like knocking over a beehive – the body freaks out and forms a blood clot around the rupture. This clot can block the flow of blood entirely. If that clot blocks an artery supplying blood to the heart, it’s a heart attack. If it blocks an artery supplying blood to the brain, it’s a stroke.116Fang J, Luncheon C, Ayala C, Odom E, Loustalot F. Awareness of Heart Attack Symptoms and Response Among Adults – United States, 2008, 2014, and 2017. MMWR Morb Mortal Wkly Rep. 2019 Feb 8;68(5):101-106. doi: 10.15585/mmwr.mm6805a2. PMID: 31851653; PMCID: PMC6366680.117Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. Int J Mol Sci. 2020 Oct 15;21(20):7609. doi: 10.3390/ijms21207609. PMID: 33076218; PMCID: PMC7589849.

It’s important to remember that not all plaque is the same. Some is soft and more likely to rupture; other plaque is hard and more likely to narrow the arteries over time. Either way, it’s trouble for your river, affecting the smooth flow of blood and potentially leading to serious health problems down the line. Atherosclerosis isn’t something that happens overnight. It’s a slow process, and it often starts quietly, without symptoms. With each fatty meal, with each puff of smoke, the plaque builds up on your arterial walls, the bug inside the violin continues to gnaw.

But, as it often happens with villains, atherosclerosis doesn’t work alone. Its partners in crime are hypertension and diabetes. High blood pressure is akin to tightening the strings of the violin too much, putting undue strain on it. Diabetes, on the other hand, can be likened to a moth eating away at the violin’s wooden structure, weakening it from the inside. With these two factors joining the party, the plaque’s impact is magnified and the risk of a heart event skyrockets.

In some scenarios, the plaque that lines the arteries triggers the body’s repair mechanisms, resulting in the thickening of the arterial wall over time. It’s like adding layer upon layer of duct tape on the violin’s strings. Sure, it might hold for a while, but it’s not a real solution and it significantly alters the sound. In the same way, this thickening process, known as stenosis, disrupts the flow of blood in the artery, causing the heart to work harder, and possibly leading to chest pain, shortness of breath, or even heart attack.

The Role of Inflammation in Coronary Artery Disease (CAD) 

Inflammation isn’t entirely bad. Normally, it’s your body’s way of protecting itself, much like the water rising in a canal to wash away unwanted debris. But when inflammation becomes a chronic visitor, it’s like the canal water rising too much, too often. The water starts to erode the canal walls, much like chronic inflammation damaging your artery walls.

Imagine you’re living in a house beside this canal, and you notice that the water has started to rise more frequently than it used to. Wouldn’t you be concerned? Would you just watch as the water slowly erodes your property? Or would you take action?

When it comes to inflammation in your arteries, you might not be able to see it, but its effects are just as real. High levels of inflammation can lead to atherosclerosis, which is like a stubborn plaque that sets up shop on your artery walls. It’s like having unwanted graffiti on the canal wall that restricts the water flow.

This graffiti (atherosclerosis) isn’t just an eyesore; it’s a hazard. The graffiti artist (inflammation) isn’t done yet. It continues to work, adding more and more layers to the plaque, which bulges into the artery, making it harder for blood to flow.

Now, imagine a day when the canal water rises exceptionally high. It hits the graffiti hard, causing a piece to break off. The detached piece starts to float downstream, causing havoc as it goes, potentially leading to a blockage—a heart attack.118Fang J, Luncheon C, Ayala C, Odom E, Loustalot F. Awareness of Heart Attack Symptoms and Response Among Adults – United States, 2008, 2014, and 2017. MMWR Morb Mortal Wkly Rep. 2019 Feb 8;68(5):101-106. doi: 10.15585/mmwr.mm6805a2. PMID: 31851653; PMCID: PMC6366680.

Remember, you’re not a helpless observer. Just as you’d call city officials to clean up the graffiti and repair the canal, there are things you can do about inflammation. Healthy lifestyle changes, like a balanced diet and regular exercise, are a great start. It’s like building up a strong barrier to prevent the water from rising too high and making sure that there’s no place for the graffiti artist to cause damage.

You might not have a visual representation like a canal outside your window, but you do have tests that can detect inflammation levels in your body. So, it’s essential to keep regular check-ups with your doctor.

Have you ever bumped your shin and noticed how your body leaps into action? Your skin gets red and warm, and it might even swell up a bit. This is inflammation doing its job – rushing to protect and heal you. In this sense, inflammation is your body’s superhero, always on standby to swoop in and save the day whenever you’re hurt.119Punchard NA, Whelan CJ, Adcock I. The Journal of Inflammation. J Inflamm (Lond). 2004 Sep 27;1(1):1. doi: 10.1186/1476-9255-1-1. PMID: 15813979; PMCID: PMC1074343.

Sometimes, though, harmful substances like LDL cholesterol (the bad kind), toxins from cigarettes, or excessive sugar in your bloodstream may invade these highways. It’s as if you suddenly found debris or potholes on your drive, threatening your smooth journey. Your body recognizes these invaders as harmful and sends in the inflammation superheroes, its natural response to any injury or threat.

It’s a bit like calling in a road repair crew. But what if the crew never leaves, and their repair work never ends? Instead of a quick patch-up, they keep working, causing long-term traffic and chaos on the highway. The endless work – or in the case of your arteries, chronic inflammation – isn’t productive.120Pahwa R, Goyal A, Jialal I. Chronic Inflammation. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493173/121Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019 Dec;25(12):1822-1832. doi: 10.1038/s41591-019-0675-0. Epub 2019 Dec 5. PMID: 31806905; PMCID: PMC7147972. The constant action irritates your artery walls and results in plaques, sort of like unwanted speed bumps. This is atherosclerosis, a key player in coronary artery disease.

Living with coronary artery disease, or working to prevent it, doesn’t have to feel like a never-ending battle. It’s more like an ongoing dialogue with your body. Listen to it, understand its signals, and respond in the best way you can.

The Role of Endothelial Dysfunction in Coronary Artery Disease (CAD)

Let’s explore the significance of endothelial dysfunction in coronary artery disease.

Endothelial cells are like traffic managers. These tireless little cells also release substances that control the size of the blood vessels. When things are normal, they ensure a perfect balance – your arteries are neither too loose nor too tight. But imagine what might happen if this function goes awry. This is precisely what occurs in endothelial dysfunction. The result? Your arteries can’t relax properly. You know how tense you feel when you can’t relax, right? Your arteries feel the same way.122Rajendran P, Rengarajan T, Thangavel J, Nishigaki Y, Sakthisekaran D, Sethi G, Nishigaki I. The vascular endothelium and human diseases. Int J Biol Sci. 2013 Nov 9;9(10):1057-69. doi: 10.7150/ijbs.7502. PMID: 24250251; PMCID: PMC3831119.

This state of tension in your arteries is known as vasoconstriction, and it reduces the supply of oxygen-rich blood to your heart. Doesn’t sound too good, does it? It’s not. It is one of the key stages in the development of coronary artery disease.123Rajendran P, Rengarajan T, Thangavel J, Nishigaki Y, Sakthisekaran D, Sethi G, Nishigaki I. The vascular endothelium and human diseases. Int J Biol Sci. 2013 Nov 9;9(10):1057-69. doi: 10.7150/ijbs.7502. PMID: 24250251; PMCID: PMC3831119.

Furthermore, when endothelial cells aren’t at their best, they produce less nitric oxide, a molecule that acts like peacekeeper, preventing inflammation and clotting. With less nitric oxide on the scene, these destructive processes can take root, contributing to the progression of coronary artery disease.124Sharma JN, Al-Omran A, Parvathy SS. Role of nitric oxide in inflammatory diseases. Inflammopharmacology. 2007 Dec;15(6):252-9. doi: 10.1007/s10787-007-0013-x. PMID: 18236016.125Iwata M, Inoue T, Asai Y, Hori K, Fujiwara M, Matsuo S, Tsuchida W, Suzuki S. The protective role of localized nitric oxide production during inflammation may be mediated by the heme oxygenase-1/carbon monoxide pathway. Biochem Biophys Rep. 2020 Jul 24;23:100790. doi: 10.1016/j.bbrep.2020.100790. PMID: 32760814; PMCID: PMC7390790.

Your endothelial cells, when functioning properly, are quite like that efficient traffic officer on a good day. They manage the traffic of your bloodstream – directing the flow of oxygen and nutrients to where they are needed, signaling when to slow down or speed up, and maintaining a delicate, vital balance.126Chiu JJ, Chien S. Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives. Physiol Rev. 2011 Jan;91(1):327-87. doi: 10.1152/physrev.00047.2009. PMID: 21248169; PMCID: PMC3844671.

Now, imagine if these cells become less efficient, like that distracted traffic officer. The consequences are not pretty. This is exactly what happens during endothelial dysfunction. The cells lose their ability to control blood vessel diameter. They struggle to regulate inflammation, and they can’t prevent the blood from clotting unnecessarily. The result? A rise in the risk of coronary artery disease.127Park KH, Park WJ. Endothelial Dysfunction: Clinical Implications in Cardiovascular Disease and Therapeutic Approaches. J Korean Med Sci. 2015 Sep;30(9):1213-25. doi: 10.3346/jkms.2015.30.9.1213. Epub 2015 Aug 13. PMID: 26339159; PMCID: PMC4553666.

But it doesn’t stop there. As endothelial dysfunction progresses, it leads to the formation of plaques in your arteries. Picture these as roadblocks on our highway analogy. These roadblocks gradually get bigger, further disrupting the blood flow to your heart.128Gimbrone MA Jr, García-Cardeña G. Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis. Circ Res. 2016 Feb 19;118(4):620-36. doi: 10.1161/CIRCRESAHA.115.306301. PMID: 26892962; PMCID: PMC4762052.

Risk Factors for Coronary Artery Disease (CAD)

Genetic Factors in Coronary Artery Disease (CAD)

Peek into your family album. Notice any striking resemblances? The same smile, the same eyes, perhaps even the same mannerisms. You inherited all those traits from your ancestors. And in a similar way, there’s something unseen that may also be passed down through generations: susceptibility to coronary artery disease.129Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.

Think of your genes as a blueprint, an instruction manual of sorts, that designs and guides the functioning of your body. Sometimes, this manual contains minor errors or variations, which can affect your body in various ways, including making you more likely to develop certain diseases. This includes coronary artery disease.130Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.

In fact, your risk of coronary artery disease increases significantly if your parents or siblings have this disease, especially if they were diagnosed at a young age. It’s as if there’s a familial echo of the disease, reverberating through generations.131Semaev S, Shakhtshneider E. Genetic Risk Score for Coronary Heart Disease: Review. J Pers Med. 2020 Nov 20;10(4):239. doi: 10.3390/jpm10040239. PMID: 33233501; PMCID: PMC7712936.132Chow CK, Pell AC, Walker A, O’Dowd C, Dominiczak AF, Pell JP. Families of patients with premature coronary heart disease: an obvious but neglected target for primary prevention. BMJ. 2007 Sep 8;335(7618):481-5. doi: 10.1136/bmj.39253.577859.BE. PMID: 17823190; PMCID: PMC1971158.

But just because heart disease runs in your family, it doesn’t mean it’s your destiny. Imagine it as you’re hiking a mountain trail. The genes you’ve inherited have set the path, but whether you reach the top depends on various factors, like your diet, your level of physical activity, and whether you smoke or drink alcohol. It’s this interplay between your genes and your lifestyle that determines your health journey.133Virolainen, S.J., VonHandorf, A., Viel, K.C.M.F. et al. Gene–environment interactions and their impact on human health. Genes Immun 24, 1–11 (2023). https://doi.org/10.1038/s41435-022-00192-6134Said, M.A., van de Vegte, Y.J., Zafar, M.M. et al. Contributions of Interactions Between Lifestyle and Genetics on Coronary Artery Disease Risk. Curr Cardiol Rep 21, 89 (2019). https://doi.org/10.1007/s11886-019-1177-x

You might wonder, “How do we know all this?” Well, some of this understanding comes from studying identical twins. Why twins, you ask? Identical twins share the same genetic blueprint, so by comparing their health outcomes, we can see the impact of different environmental factors on people who start with the same genetic material.135Sahu M, Prasuna JG. Twin Studies: A Unique Epidemiological Tool. Indian J Community Med. 2016 Jul-Sep;41(3):177-82. doi: 10.4103/0970-0218.183593. PMID: 27385869; PMCID: PMC4919929.136Prescott CA, Kendler KS. Twin Study Design. Alcohol Health Res World. 1995;19(3):200-205. PMID: 31798103; PMCID: PMC6875762.

These twin studies have shown that if one identical twin has coronary artery disease, the other twin has a significantly higher risk of also having the disease compared to the general population. It’s like two houses built with the same blueprint in different locations. If one house develops a certain problem, there’s a good chance the other might develop the same issue, especially if they’re exposed to similar weather conditions.137Smith MC, Baker JR, Gleaves E, Singh A, Kazimuddin M. Twinning: Coronary Artery Disease in Monozygotic Twins. Cureus. 2021 Jul 3;13(7):e16139. doi: 10.7759/cureus.16139. PMID: 34367763; PMCID: PMC8330499.138Drobni, Z. D., Kolossvary, M., Karady, J., Jermendy, A. L., Tarnoki, A. D., Tarnoki, D. L., Simon, J., Szilveszter, B., Littvay, L., Voros, S., Jermendy, G., Merkely, B., & Maurovich-Horvat, P. (2022). Heritability of coronary artery disease: Insights from a classical twin study. Circulation: Cardiovascular Imaging, 15(3). https://doi.org/10.1161/circimaging.121.013348

What’s interesting is that, while we know that coronary artery disease can run in families, it’s usually not due to a single faulty gene, but a combination of several minor genetic variations coupled with lifestyle factors. It’s a complex puzzle of genetics and environment that scientists are still trying to solve.139Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.

Understanding your family’s heart health history can help you and your healthcare provider determine your risk and plan strategies to reduce it. Just like how knowing a storm is coming allows you to prepare and protect your house.

Yet, it’s important to remember, having a family history doesn’t seal your fate. It just gives you the power of knowledge, the chance to adjust your sails and navigate your journey to heart health. Because ultimately, your health story is not just about where you come from, but where you’re heading and how you choose to get there.140Acheson LS, Wang C, Zyzanski SJ, Lynn A, Ruffin MT 4th, Gramling R, Rubinstein WS, O’Neill SM, Nease DE Jr; Family Healthware Impact Trial (FHITr) Group. Family history and perceptions about risk and prevention for chronic diseases in primary care: a report from the family healthware impact trial. Genet Med. 2010 Apr;12(4):212-8. doi: 10.1097/GIM.0b013e3181d56ae6. PMID: 20216073; PMCID: PMC4037165.

In essence, you’re not just a product of your genes. You’re also a product of your actions. So, make each step count on your journey towards a heart-healthy life.

Now, let’s delve deeper into your genes, not the denim kind, but the ones that help create the unique individual you are. These tiny molecules can tell us more about your risk of developing coronary artery disease. But to understand this, we must first demystify some genetic concepts.141McPherson, R., & Tybjaerg-Hansen, A. (2016). Genetics of coronary artery disease. Circulation Research, 118(4), 564–578. https://doi.org/10.1161/circresaha.115.306566

You see, genes are like tiny chapters in the grand book of you. They tell the story of your traits, from the color of your eyes to your love for music, and yes, even your likelihood of developing diseases. Now, within these chapters, there are certain sections or sentences, known as genetic variants, which can have an impact on the plot of your life story. Sometimes, they can even lead to plot twists, like an increased risk of coronary artery disease.142McPherson, R., & Tybjaerg-Hansen, A. (2016). Genetics of coronary artery disease. Circulation Research, 118(4), 564–578. https://doi.org/10.1161/circresaha.115.306566

Genetic Polymorphisms in Coronary Artery Disease (CAD)

Let’s continue our journey into the world of genetics, where a plot twist called ‘genetic polymorphisms’ lies. You see, our bodies are incredibly complex works of art, with millions of unique traits all determined by the amazing symphony of genes inside us. But sometimes, a note in this symphony can change. These tiny changes are what scientists call ‘genetic polymorphisms’.143Albert PR. What is a functional genetic polymorphism? Defining classes of functionality. J Psychiatry Neurosci. 2011 Nov;36(6):363-5. doi: 10.1503/jpn.110137. PMID: 22011561; PMCID: PMC3201989.

Imagine you’re at a huge family gathering. Look around, and you’ll notice a sea of familiar faces, yet no two are exactly alike. That’s genetic polymorphism at play – tiny differences in our genes that make each of us unique. However, sometimes, these variations can have more serious implications than just determining the shape of our nose or the color of our eyes. Sometimes, they can affect our risk of developing diseases like coronary artery disease.144Sitinjak BDP, Murdaya N, Rachman TA, Zakiyah N, Barliana MI. The Potential of Single Nucleotide Polymorphisms (SNPs) as Biomarkers and Their Association with the Increased Risk of Coronary Heart Disease: A Systematic Review. Vasc Health Risk Manag. 2023 May 5;19:289-301. doi: 10.2147/VHRM.S405039. PMID: 37179817; PMCID: PMC10167955.

Let’s talk about a few of these:

APOE: There’s the Apolipoprotein E gene, for instance, which goes by the easier-to-pronounce nickname APOE. This gene comes in several flavors, or ‘polymorphisms’. Some versions of APOE are linked to a higher risk of developing coronary artery disease.145Marrzoq LF, Sharif FA, Abed AA. Relationship between ApoE gene polymorphism and coronary heart disease in Gaza Strip. J Cardiovasc Dis Res. 2011 Jan;2(1):29-35. doi: 10.4103/0975-3583.78584. PMID: 21716749; PMCID: PMC3120269.
MTHFR: Consider the MTHFR gene, another key player in our genetic symphony. This gene helps our bodies use a specific B vitamin called folate. However, certain polymorphisms of MTHFR can impact this process, indirectly influencing our heart health.146Zaghloul A, Iorgoveanu C, Desai A, Balakumaran K, Chen K. Methylenetetrahydrofolate Reductase Polymorphism and Premature Coronary Artery Disease. Cureus. 2019 Jun 27;11(6):e5014. doi: 10.7759/cureus.5014. PMID: 31497444; PMCID: PMC6716763.
PCSK9: Now, let’s not forget about the PCSK9 gene. This gene regulates cholesterol levels in our bodies. Polymorphisms in PCSK9 can lead to an increase in low-density lipoprotein cholesterol – the ‘bad’ cholesterol, increasing the risk for coronary artery disease.147Chaudhary R, Garg J, Shah N, Sumner A. PCSK9 inhibitors: A new era of lipid lowering therapy. World J Cardiol. 2017 Feb 26;9(2):76-91. doi: 10.4330/wjc.v9.i2.76. PMID: 28289523; PMCID: PMC5329749.
CETP: Consider the variant in the gene CETP, an abbreviation for the wordy cholesteryl ester transfer protein. This protein assists in the transport of cholesterol throughout your body. Now, one little difference in this gene can affect how effectively it carries out this task, leading to variations in your levels of high-density lipoprotein cholesterol (or the ‘good’ cholesterol as it’s often known). This, in turn, can influence your susceptibility to coronary artery disease.148Holmes MV, Smith GD. Dyslipidaemia: Revealing the effect of CETP inhibition in cardiovascular disease. Nat Rev Cardiol. 2017 Nov;14(11):635-636. doi: 10.1038/nrcardio.2017.156. Epub 2017 Oct 5. PMID: 28980665; PMCID: PMC5644574.
LPA: Also consider the LPA gene, which is responsible for the production of a protein called lipoprotein(a). Certain variants of this gene can result in higher levels of lipoprotein(a) in your blood, tipping the scales towards a higher risk of coronary artery disease.149Liu T, Yoon WS, Lee SR. Recent Updates of Lipoprotein(a) and Cardiovascular Disease. Chonnam Med J. 2021 Jan;57(1):36-43. doi: 10.4068/cmj.2021.57.1.36. Epub 2021 Jan 25. PMID: 33537217; PMCID: PMC7840349.150Šuran D, Blažun Vošner H, Završnik J, Kokol P, Sinkovič A, Kanič V, Kokol M, Naji F, Završnik T. Lipoprotein(a) in Cardiovascular Diseases: Insight From a Bibliometric Study. Front Public Health. 2022 Jul 5;10:923797. doi: 10.3389/fpubh.2022.923797. PMID: 35865239; PMCID: PMC9294325.

ALOX5AP: There’s also the ALOX5AP gene to consider. This gene contributes to the production of a protein involved in the inflammation and constriction of blood vessels. Specific variations in ALOX5AP could potentially exacerbate these processes, thereby increasing the likelihood of coronary artery disease development.151Alwan A, Youhanna SC, Platt DE, El-Sibai M, Yerezian JS, Deeb ME, Khazen G, Saadé S, Zreik TG, El Bayeh H, Maalouf A, Abchee A, Zalloua PA. ALOX5AP gene variants show differential association with coronary artery disease in different populations. J Community Genet. 2010 Sep;1(3):107-15. doi: 10.1007/s12687-010-0015-z. Epub 2010 Aug 18. PMID: 22460243; PMCID: PMC3185993.

AGT: A short stroll away, we encounter the AGT gene. It contributes to the production of a protein called angiotensinogen, one of the major actors in the drama of your blood pressure control. If AGT’s performance is off due to certain genetic variations, it can result in a dramatic plot twist—raising your blood pressure and putting added stress on your heart.152Kunz R, Kreutz R, Beige J, Distler A, Sharma AM. Association between the angiotensinogen 235T-variant and essential hypertension in whites: a systematic review and methodological appraisal. Hypertension. 1997 Dec;30(6):1331-7. doi: 10.1161/01.hyp.30.6.1331. PMID: 9403549.

IL6: And then, there’s the entire neighborhood of genes involved in inflammation—like the IL6 gene that codes for interleukin-6, a significant character in your body’s inflammatory response. Some genetic versions of IL6 might turn up the volume on this response, setting the stage for a persistent state of low-grade inflammation, a silent threat that may contribute to the development of coronary artery disease.153Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014 Sep 4;6(10):a016295. doi: 10.1101/cshperspect.a016295. PMID: 25190079; PMCID: PMC4176007.

CYP: As we delve deeper into this cityscape, the CYP genes come into view. These genes code for enzymes that metabolize drugs, toxins, and endogenous compounds. They’re like the sanitation department, working tirelessly to keep the city clean. Certain variations in these genes, however, can make this cleanup less effective, leading to the buildup of harmful substances and increased inflammation and oxidative stress – conditions that set the stage for CAD.154Zhao M, Ma J, Li M, Zhang Y, Jiang B, Zhao X, Huai C, Shen L, Zhang N, He L, Qin S. Cytochrome P450 Enzymes and Drug Metabolism in Humans. Int J Mol Sci. 2021 Nov 26;22(23):12808. doi: 10.3390/ijms222312808. PMID: 34884615; PMCID: PMC8657965.

9p21: In your DNA’s city, there’s another crucial actor playing a role, the gene titled 9p21. This particular gene doesn’t code for a protein, but it’s known for being a “non-coding RNA.” Let’s think of this non-coding RNA as the city’s news broadcaster. It doesn’t build anything physical in the city, but it certainly influences what happens.  Imagine if your news broadcaster began to share exaggerated stories or false news – this could lead to all sorts of chaos. That’s precisely what happens when there are variations, or polymorphisms, in this 9p21 gene. If you’re one of the unlucky ones to carry these variants (remember, we’re talking about an important yet potentially disruptive news broadcaster), research indicates that you may have an increased risk of heart disease, including coronary artery disease.155Roberts R. Genetics of coronary artery disease: an update. Methodist Debakey Cardiovasc J. 2014 Jan-Mar;10(1):7-12. doi: 10.14797/mdcj-10-1-7. PMID: 24932356; PMCID: PMC4051327. The 9p21 gene variants, it seems, influence the walls of your arteries.156Samani, N. J., & Schunkert, H. (2008). Chromosome 9p21 and cardiovascular disease. Circulation: Cardiovascular Genetics, 1(2), 81–84. https://doi.org/10.1161/circgenetics.108.832527 To paint a clearer picture, let’s liken your artery walls to the city’s fortifications. A well-functioning city needs robust, secure walls to protect it from external threats. In a similar vein, our bodies rely on the smooth and flexible walls of our arteries to ensure blood flows freely, delivering vital nutrients and oxygen to our organs and tissues.

However, when the city walls start to crumble or become rigid, invaders can easily breach the city, leading to chaos and destruction. That’s akin to what happens in our bodies when our artery walls become stiff and thick, a condition medically known as arteriosclerosis. The 9p21 gene variants, in this case, are like the misguided architects giving poor advice on how to build and maintain the city walls.157Patel RS, Asselbergs FW, Quyyumi AA, Palmer TM, Finan CI, Tragante V, Deanfield J, Hemingway H, Hingorani AD, Holmes MV. Genetic variants at chromosome 9p21 and risk of first versus subsequent coronary heart disease events: a systematic review and meta-analysis. J Am Coll Cardiol. 2014 Jun 3;63(21):2234-45. doi: 10.1016/j.jacc.2014.01.065. Epub 2014 Mar 7. PMID: 24607648; PMCID: PMC4035794.

PON1: You could think of the PON1 gene as the city’s sanitation department. In your body, the PON1 gene produces an enzyme that helps to clean up harmful substances from your blood, much like sanitation workers clean up waste in a city. One of the main jobs of PON1 is to break down oxidized low-density lipoprotein (LDL) cholesterol. In simpler terms, LDL is the ‘bad’ cholesterol, and when it gets oxidized, it’s like trash that’s been left out too long – it gets rotten and smells bad. And, just as the city’s sanitation department is responsible for cleaning up, PON1’s job is to clean up these ‘bad’ cholesterol particles before they can cause trouble.158Shunmoogam N, Naidoo P, Chilton R. Paraoxonase (PON)-1: a brief overview on genetics, structure, polymorphisms and clinical relevance. Vasc Health Risk Manag. 2018 Jun 18;14:137-143. doi: 10.2147/VHRM.S165173. PMID: 29950852; PMCID: PMC6014389.159Durrington PN, Bashir B, Soran H. Paraoxonase 1 and atherosclerosis. Front Cardiovasc Med. 2023 Feb 16;10:1065967. doi: 10.3389/fcvm.2023.1065967. PMID: 36873390; PMCID: PMC9977831.

But what happens when the sanitation department isn’t functioning well? Trash piles up, and the city starts to stink. That’s the situation in your arteries when there are certain genetic variants of PON1. The enzyme isn’t as efficient at cleaning up the ‘bad’ cholesterol, and the buildup contributes to plaque formation in your arteries, a central feature of coronary artery disease.160Shih DM, Lusis AJ. The roles of PON1 and PON2 in cardiovascular disease and innate immunity. Curr Opin Lipidol. 2009 Aug;20(4):288-92. doi: 10.1097/MOL.0b013e32832ca1ee. PMID: 19474728; PMCID: PMC3869948.

ACE: Now, let’s introduce the ACE gene. You can think of ACE as the city’s water management department, controlling the pressure and flow of water through the city’s pipes. In your body, the ACE gene controls blood pressure and fluid balance. However, certain genetic variations in the ACE gene can lead to higher levels of the ACE enzyme in your body. This increase could be like having too much water pressure in the city’s pipes, which might lead to damage and leaks. In your arteries, higher ACE levels can contribute to higher blood pressure and artery damage, both risk factors for coronary artery disease.161Yapijakis C, Papakosta V, Vassiliou S. ACE Gene Variant Causing High Blood Pressure May Be Associated With Medication-related Jaw Osteonecrosis. In Vivo. 2019 Mar-Apr;33(2):559-562. doi: 10.21873/invivo.11510. PMID: 30804141; PMCID: PMC6506304.

LPA: Imagine LPA as the fire department in your genetic city. When things are running smoothly, they are there in the background, maintaining order. The LPA gene produces a unique lipoprotein (a type of fat and protein molecule) known as lipoprotein(a). Normally, this lipoprotein helps in wound healing, much like a fire department puts out small fires. However, if you happen to inherit certain variations of the LPA gene, it could be like having a fire department that’s too eager, setting off the sprinkler system for a minor kitchen flare-up. These variations can lead to higher levels of lipoprotein(a) in your blood, which can contribute to the development of fatty buildups in your arteries, potentially leading to coronary artery disease.162Enas EA, Varkey B, Dharmarajan TS, Pare G, Bahl VK. Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction. Indian Heart J. 2019 Mar-Apr;71(2):99-112. doi: 10.1016/j.ihj.2019.03.004. Epub 2019 Mar 20. PMID: 31280836; PMCID: PMC6620428.

LDLR: Think of the LDLR gene as the manager of your city’s waste disposal system. It provides the blueprint for making low-density lipoprotein receptors. These receptors are like waste management workers, working tirelessly to clean up ‘bad’ LDL cholesterol from your bloodstream. A healthy, functioning LDLR gene ensures a tidy city, free of cholesterol litter. However, just like a city can suffer from inefficient waste management, certain variations in the LDLR gene can result in fewer or ineffective LDL receptors. This can be likened to having a waste disposal team on strike, leading to a buildup of rubbish, or in the case of the body, a buildup of LDL cholesterol. Over time, this can lead to the formation of plaque in your arteries, increasing the risk of coronary artery disease.163Franceschini N, Muallem H, Rose KM, Boerwinkle E, Maeda N. Low density lipoprotein receptor polymorphisms and the risk of coronary heart disease: the Atherosclerosis Risk in Communities Study. J Thromb Haemost. 2009 Mar;7(3):496-8. doi: 10.1111/j.1538-7836.2008.03262.x. PMID: 19087220; PMCID: PMC2656439.

ADD1: Let’s move on to another important character, the ADD1 gene. Picture ADD1 as the city’s architect, designing the infrastructure that holds your city together. This gene influences the structure of your arteries, including their size, flexibility, and overall health. Yet, as it goes in the tale of your genetic city, certain variations of the ADD1 gene can interfere with the architect’s plans. These variations can contribute to thicker, less flexible artery walls – a feature that can make it easier for plaques to build up and potentially lead to coronary artery disease.164Morrison, A. C., Bray, M. S., Folsom, A. R., & Boerwinkle, E. (2002). 460W allele associated with cardiovascular disease in hypertensive individuals. Hypertension, 39(6), 1053–1057. https://doi.org/10.1161/01.hyp.0000019128.94483.3a

eNOS: The eNOS gene is like the city’s traffic officer. It helps regulate the flow of blood through your arteries. The eNOS gene provides instructions for making a protein called endothelial nitric oxide synthase. This protein triggers the production of nitric oxide, which acts as a traffic signal for your blood vessels, telling them when to relax and widen. This allows smooth passage of traffic – in this case, blood flow. However, certain variations of the eNOS gene could be likened to a traffic signal malfunction. In these cases, nitric oxide production may not go as planned, leading to stiffer, narrower arteries that hinder traffic flow. This creates a favorable environment for plaque build-up and eventually, may contribute to coronary artery disease.165Tran N, Garcia T, Aniqa M, Ali S, Ally A, Nauli SM. Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States. Am J Biomed Sci Res. 2022;15(2):153-177. Epub 2022 Jan 4. PMID: 35072089; PMCID: PMC8774925.

CYP: On the other hand, the CYP gene family is like a team of chemists, diligently working to process the substances that enter your city. Members of this gene family, such as CYP2C19, are involved in the metabolism of various substances including many medications like clopidogrel, a drug often prescribed to individuals with coronary artery disease to prevent blood clots. Genetic variations in the CYP2C19 gene can impact how effectively your body metabolizes clopidogrel. This could be compared to a chemistry experiment gone wrong. The usual transformation doesn’t take place and this can make the medication less effective in preventing clot formation in some individuals. CYP2C19 variations can impact clopidogrel effectiveness and CAD treatment outcomes.166Brown SA, Pereira N. Pharmacogenomic Impact of CYP2C19 Variation on Clopidogrel Therapy in Precision Cardiovascular Medicine. J Pers Med. 2018 Jan 30;8(1):8. doi: 10.3390/jpm8010008. PMID: 29385765; PMCID: PMC5872082.

P2Y12: The P2Y12 gene has the role of a ‘security guard’ in our city, playing a pivotal role in regulating the formation of blood clots. It codes for a protein that lives on the surface of our platelets – tiny cells that rush to the site of an injury to initiate a clot and prevent bleeding. When this protein gets a signal, it springs into action, causing the platelets to stick together and form a clot. However, some of us carry a variation in the P2Y12 gene. Think of it as a security guard that’s a little too eager, causing the platelets to stick together more than they should. This could lead to an increased risk of developing clots within the arteries, which may eventually result in coronary artery disease.167Thomas, C. D., Williams, A. K., Lee, C. R., & Cavallari, L. H. (2023). Pharmacogenetics of P2Y12 receptor inhibitors. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 43(2), 158–175. https://doi.org/10.1002/phar.2758

GPIIIa: Now, meet another player in our city, the GPIIIa gene. This gene provides instructions for a protein that exists on our platelets’ surface and acts like a sticky hand reaching out to catch other platelets and form a clot. But what happens when this sticky hand becomes too grabby due to a certain variation in the GPIIIa gene? Just like the P2Y12 gene, this could lead to increased clot formation, potentially heightening the risk of coronary artery disease.168Galasso G, Santulli G, Piscione F, De Rosa R, Trimarco V, Piccolo R, Cassese S, Iaccarino G, Trimarco B, Chiariello M. The GPIIIA PlA2 polymorphism is associated with an increased risk of cardiovascular adverse events. BMC Cardiovasc Disord. 2010 Sep 16;10:41. doi: 10.1186/1471-2261-10-41. PMID: 20846430; PMCID: PMC2954874. These tales of P2Y12 and GPIIIa underline the complex interplay between our genes and our health. It’s like a grand orchestra where every instrument has a unique part to play. Sometimes the music is harmonious, promoting health and well-being. At other times, it’s dissonant, increasing the risk of conditions like coronary artery disease.

Fibrinogen Gamma (FGG): Think of the Fibrinogen Gamma gene as the architect of the city’s structure. It crafts fibrinogen – a key protein that helps in the formation of clots to prevent excessive bleeding. Under normal circumstances, it’s our body’s way of keeping things in check, a sort of first responder that ensures minor injuries don’t turn into major issues. Yet, some of us carry a unique version of the FGG gene. It’s as if this architect gets a little too enthusiastic, building too much, too fast. Overproduction of fibrinogen can lead to the formation of unwanted clots within your blood vessels. This increases the chances of a blockage in the coronary arteries, leading to coronary artery disease.169Surma S, Banach M. Fibrinogen and Atherosclerotic Cardiovascular Diseases-Review of the Literature and Clinical Studies. Int J Mol Sci. 2021 Dec 24;23(1):193. doi: 10.3390/ijms23010193. PMID: 35008616; PMCID: PMC8745133.

PAI-1: So, step into your imaginary boots and imagine the PAI-1 gene as the traffic warden of your body. It’s responsible for maintaining a healthy balance between clotting and bleeding. The PAI-1 gene codes for a protein called plasminogen activator inhibitor-1 that restricts blood clot dissolving mechanisms in your body. Now, imagine if this traffic warden becomes over-enthusiastic, controlling the traffic so tightly that it begins to cause a jam. That’s what happens with specific variants of the PAI-1 gene, which leads to higher levels of the PAI-1 protein. As a result, the balance shifts towards clotting, increasing the risk of developing dangerous clots in arteries, a significant factor in coronary artery disease.170Jung RG, Motazedian P, Ramirez FD, Simard T, Di Santo P, Visintini S, Faraz MA, Labinaz A, Jung Y, Hibbert B. Association between plasminogen activator inhibitor-1 and cardiovascular events: a systematic review and meta-analysis. Thromb J. 2018 Jun 5;16:12. doi: 10.1186/s12959-018-0166-4. PMID: 29991926; PMCID: PMC5987541.

TNF-alpha: But what happens when our environmental health officer is hyperactive, sparking alarms even when there’s no substantial threat? Certain variants of the TNF-alpha gene can cause an overactive inflammatory response, leading to a state of chronic inflammation in the body. This continuous inflammation can contribute to the development of atherosclerosis – a significant player in the story of coronary artery disease.171Hernández-Díaz Y, Tovilla-Zárate CA, Juárez-Rojop I, López-Narváez ML, Álvarez-Cámara JF, González-Castro TB. Association between CRP and TNF-α genes Variants and Cardiovascular Heart Disease in a Mexican Population: Protocol for a Case-Control Study. Int J Environ Res Public Health. 2016 Jan 6;13(1):103. doi: 10.3390/ijerph13010103. PMID: 26751459; PMCID: PMC4730494.

MMP and Apelin: To continue on our exploratory voyage through the vast terrain of genetic polymorphisms, we’ll next focus our attention on two additional genetic landmarks of interest: the MMPs (Matrix Metalloproteinases) gene and the Apelin gene. Both of these genes play fundamental roles in our cardiovascular health, and specific variations can increase the risk of coronary artery disease. Our first stop is the MMPs gene neighborhood. MMPs, much like an urban landscaping crew, work diligently to remodel the body’s tissues. They clear out old, damaged structures, allowing new, healthy tissue to grow in its place. This process is particularly crucial for the health of our arteries, as it aids in repairing any damage to the arterial walls.

But what happens when the landscaping crew starts overdoing their job, damaging healthy structures instead of just removing the old and weak ones? That’s what happens with certain variants of the MMPs genes, especially MMP-2 and MMP-9, which can lead to overactive protein production, causing excessive remodeling and degradation of the arterial walls. This excess activity can contribute to the development of atherosclerosis and, subsequently, coronary artery disease.172Wang X, Khalil RA. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. Adv Pharmacol. 2018;81:241-330. doi: 10.1016/bs.apha.2017.08.002. Epub 2017 Sep 19. PMID: 29310800; PMCID: PMC5765875.

Next, we will head over to the Apelin gene district. Picture the Apelin gene as the city’s water management system. The Apelin gene is responsible for regulating blood pressure and fluid balance, crucial for keeping your circulatory system running smoothly. But imagine if the water management system were to malfunction, leading to an overflow or shortage of water. Similarly, variations in the Apelin gene can disrupt the fine balance of blood pressure and fluid in your body. This disruption can cause elevated blood pressure, a key risk factor for coronary artery disease.173Zhang Q, Shen Y, Niloy SI, O’Rourke ST, Sun C. Chronic Effects of Apelin on Cardiovascular Regulation and Angiotensin II-Induced Hypertension. Pharmaceuticals (Basel). 2023 Apr 17;16(4):600. doi: 10.3390/ph16040600. PMID: 37111357; PMCID: PMC10145143.

Leptin: First, let’s drop by the area governed by the Leptin gene. Leptin, much like the head of a city’s food supply committee, is primarily responsible for regulating your body’s energy balance. It signals when you’re full and should stop eating, playing a critical role in maintaining healthy body weight.

However, imagine if the head of the food committee started sending misleading signals, causing the city’s residents to consume more than needed. Similarly, certain variations in the Leptin gene can lead to an increase in leptin levels. The strange part is, instead of causing you to feel full, your body may become “resistant” to the high leptin levels, disregarding the stop eating signals. This can result in weight gain and obesity, key risk factors for coronary artery disease.174Gruzdeva O, Borodkina D, Uchasova E, Dyleva Y, Barbarash O. Leptin resistance: underlying mechanisms and diagnosis. Diabetes Metab Syndr Obes. 2019 Jan 25;12:191-198. doi: 10.2147/DMSO.S182406. PMID: 30774404; PMCID: PMC6354688.

ABCA1: Next, let’s head over to the district of the ABCA1 gene. Think of the ABCA1 gene as the head of a recycling initiative in a city, playing a critical role in reusing waste. Specifically, it helps to transport cholesterol from cells back to the liver, where it can be broken down and removed from the body. But what happens when the head of this initiative isn’t performing as expected? Certain variants in the ABCA1 gene can disrupt this crucial recycling process, causing cholesterol to build up in the bloodstream instead of being taken back to the liver. This buildup can lead to atherosclerosis, a primary cause of coronary artery disease.175Tavoosi Z, Moradi-Sardareh H, Saidijam M, Yadegarazari R, Borzuei S, Soltanian A, Goodarzi MT. Cholesterol Transporters ABCA1 and ABCG1 Gene Expression in Peripheral Blood Mononuclear Cells in Patients with Metabolic Syndrome. Cholesterol. 2015;2015:682904. doi: 10.1155/2015/682904. Epub 2015 Dec 15. PMID: 26788366; PMCID: PMC4692991.

SCARB1: We’ll begin with the SCARB1 gene. Imagine it as the head of a busy port in your body’s metropolis. Its primary job is to ensure the docking and unloading of high-density lipoprotein cholesterol (HDL-C), often hailed as the ‘good cholesterol.’ However, every so often, this port manager might not be as efficient due to certain genetic variants, hampering the smooth docking of these HDL-C ships. These variations in the SCARB1 gene could lead to lower HDL-C levels, contributing to the buildup of ‘bad’ low-density lipoprotein cholesterol (LDL-C), the villain of our coronary artery disease story.176Hu S, Hu D, Wei H, Li SY, Wang D, Li CZ, Jiang J, Wang D, Cui G, Wang D. Functional Deletion/Insertion Promoter Variants in SCARB1 Associated With Increased Susceptibility to Lipid Profile Abnormalities and Coronary Heart Disease. Front Cardiovasc Med. 2022 Jan 13;8:800873. doi: 10.3389/fcvm.2021.800873. PMID: 35097019; PMCID: PMC8793335.

To put it in simpler terms, less ‘good’ cholesterol could mean more ‘bad’ cholesterol, a scenario that could escalate the risk for heart disease. Recognizing this could help you and your healthcare provider develop a tailored approach to maintain a healthy cholesterol balance, focusing on diet, exercise, and potentially medication.

PDGFD: PDGFD plays a key role in cell growth and division, particularly in the smooth muscle cells of your blood vessels. Now, what would happen if the city planner started to make decisions that led to overcrowded areas? Certain genetic variants in the PDGFD gene may lead to an overgrowth of these muscle cells, resulting in thickened blood vessel walls, or atherosclerosis, a primary player in coronary artery disease.177Zhou J, Shao L, Yu J, Huang J, Feng Q. PDGF-BB promotes vascular smooth muscle cell migration by enhancing Pim-1 expression via inhibiting miR-214. Ann Transl Med. 2021 Dec;9(23):1728. doi: 10.21037/atm-21-5638. PMID: 35071422; PMCID: PMC8743727.

RAGE: Let’s take the example of the RAGE (Receptor for Advanced Glycation End products) gene. This gene works like a vigilant watchman, standing guard at the city’s central fort, which represents your body’s defense mechanism. But occasionally, the watchman’s efficiency can be hampered due to variations in the RAGE gene. These variants could heighten the inflammatory response, amplifying your body’s reaction to any perceived threat. Picture it like a watchman who is easily startled, raising the alarm and marshaling defenses at the slightest hint of trouble. Over time, this heightened response can become a problem, leading to atherosclerosis, an underlying cause of CAD.178Zhang X, Cheng M, Tong F, Su X. Association between RAGE variants and the susceptibility to atherosclerotic lesions in Chinese Han population. Exp Ther Med. 2019 Mar;17(3):2019-2030. doi: 10.3892/etm.2019.7163. Epub 2019 Jan 9. PMID: 30783474; PMCID: PMC6364181.

KIF6: Next up is the KIF6 (Kinesin Family Member 6) gene, an important part of your body’s transportation system. Picture it like a delivery driver, tasked with moving vital supplies around the city. However, certain genetic variations can lead to the driver taking longer routes or stopping for breaks more frequently. In your body, these KIF6 variants can increase your risk of CAD by affecting the way lipoproteins are transported and processed in your body, thereby influencing the way cholesterol is managed.179Allingham-Hawkins D, Lea A, Levine S. KIF6 p.Trp719Arg Testing to Assess Risk of Coronary Artery Disease and/or Statin Response. PLoS Curr. 2010 Oct 21;2:RRN1191. doi: 10.1371/currents.RRN1191. PMID: 20975779; PMCID: PMC2959200.

ITGB3: Consider the stall of the ITGB3 gene. Think of it like a vendor selling exquisite rugs, with intricate patterns weaved into the fabric, each thread crucial to the design. But if one thread is altered or out of place, it disrupts the whole pattern. Similarly, the ITGB3 gene has a critical role in the formation of platelets, which are like the threads of your body’s emergency repair system, rushing to a site of injury to create a clot and stop bleeding. Genetic variants in the ITGB3 gene can alter how these platelets function, possibly leading to a higher tendency for clots to form inside your arteries, a significant risk factor for CAD.180Sheikhvatan M, Boroumand MA, Behmanesh M, Ziaee S, Cheraghee S. Integrin Beta-3 Gene Polymorphism and Risk for Myocardial Infarction in Premature Coronary Disease. Iran J Biotechnol. 2019 Apr 20;17(2):e1921. doi: 10.21859/ijb.1921. PMID: 31457051; PMCID: PMC6697842.

SMAD3: Next, think about the SMAD3 gene as another vendor, this time selling a unique type of clay for molding pots. This clay is incredible – it can be shaped into any form and will hold its shape under high pressure. Just like this clay, the SMAD3 gene plays a crucial role in maintaining the flexibility and integrity of your blood vessels, ensuring they can withstand the pressure of blood flow. But suppose there’s a slight variation in the SMAD3 gene. In that case, it’s like the clay has become brittle – your blood vessels could lose their elasticity, a change that could contribute to atherosclerosis and, ultimately, CAD.181Iyer D, Zhao Q, Wirka R, Naravane A, Nguyen T, Liu B, Nagao M, Cheng P, Miller CL, Kim JB, Pjanic M, Quertermous T. Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk. PLoS Genet. 2018 Oct 11;14(10):e1007681. doi: 10.1371/journal.pgen.1007681. PMID: 30307970; PMCID: PMC6198989.

ADIPOQ: Now, let’s turn our attention to the ADIPOQ gene, which could be pictured as a spice vendor. This vendor’s spices are renowned for their ability to enhance any dish, making it more enjoyable. The ADIPOQ gene, like the spice vendor, has a special role in enhancing your body’s sensitivity to insulin, a hormone critical for managing blood sugar levels. However, polymorphisms in the ADIPOQ gene could affect this process, like using the wrong spice in a dish. This could lead to insulin resistance, a condition that has been linked to an increased risk of CAD.182Zhang, X., Cao, Y.J., Zhang, H.Y. et al. Associations between ADIPOQ polymorphisms and coronary artery disease: a meta-analysis. BMC Cardiovasc Disord 19, 63 (2019). https://doi.org/10.1186/s12872-019-1041-3

SIRT1: Imagine the SIRT1 gene as a humble vendor selling a rare, precious metal. The products are known to withstand the test of time, retaining their shine and strength year after year. Similarly, the SIRT1 gene plays a significant role in cellular longevity, stress resistance, and energy efficiency. However, just as an impurity can affect the quality of the metal, a slight variation in the SIRT1 gene can impact its role, potentially influencing metabolic disorders, including those related to heart disease.183Askin L, Tibilli H, Tanriverdi O, Turkmen S. The relationship between coronary artery disease and SIRT1 protein. North Clin Istanb. 2020 Oct 1;7(6):631-635. doi: 10.14744/nci.2020.31391. PMID: 33381707; PMCID: PMC7754863.

ALOX5: Next, let’s visit the ALOX5 gene stall, akin to an artist carving exquisite sculptures from wood. A change in the artist’s tool or method could affect the sculpture’s final form. The ALOX5 gene plays a pivotal role in the formation of leukotrienes, molecules that mediate inflammation. If there’s a variation in the ALOX5 gene, it’s akin to changing the artist’s tools, potentially leading to an exaggerated inflammatory response that promotes the progression of CAD.184Assimes TL, Knowles JW, Priest JR, Basu A, Volcik KA, Southwick A, Tabor HK, Hartiala J, Allayee H, Grove ML, Tabibiazar R, Sidney S, Fortmann SP, Go A, Hlatky M, Iribarren C, Boerwinkle E, Myers R, Risch N, Quertermous T. Common polymorphisms of ALOX5 and ALOX5AP and risk of coronary artery disease. Hum Genet. 2008 May;123(4):399-408. doi: 10.1007/s00439-008-0489-5. Epub 2008 Mar 28. PMID: 18369664; PMCID: PMC4023692.

GJA4: Finally, let’s stop by the GJA4 gene. Picture this vendor as a skilled weaver, crafting beautiful pieces of fabric with threads interlacing. The GJA4 gene, much like this weaver, helps create a network of communication between your heart cells. But if a single thread is misplaced, the whole pattern can be disrupted. Similarly, a small change in the GJA4 gene might affect this communication network, impacting the heart’s functioning and contributing to CAD’s pathogenesis.185Meens MJPMT, Pfenniger A, Kwak BR. Risky communication in atherosclerosis and thrombus formation. Swiss Med Wkly [Internet]. 2012 Mar. 25 [cited 2023 Jul. 26];142(1314):w13553.

CRP: Our first dancer, CRP (C-Reactive Protein gene), stands at the edge of the dance floor, its movements often overlooked due to the flashy performances of other genes. But CRP is essential. It is a key player in the body’s response to inflammation. The gene variations in CRP can result in an elevated systemic inflammatory response, contributing to the development of atherosclerosis and, in turn, increasing the risk of CAD.186Zhu M, Lin J, Wang C, Yang M, Lv H, Yang M, Xu B, Chen X, Jiang J. The relationship among angiotensinogen genes polymorphisms and hs-CRP and coronary artery disease. J Clin Lab Anal. 2019 Jun;33(5):e22881. doi: 10.1002/jcla.22881. Epub 2019 Mar 26. PMID: 30912862; PMCID: PMC6595333.

TGFB1: Next, we have our second dancer, the TGFB1 (Transforming Growth Factor Beta 1) gene, moving gracefully across the floor. This gene is involved in many cell processes, including cell growth, proliferation, and differentiation. When the steps of TGFB1 are out of sync (due to a genetic variant), it can lead to an imbalanced regulation of cell processes, enhancing the susceptibility to CAD.187Malinowski D, Bochniak O, Luterek-Puszyńska K, Puszyński M, Pawlik A. Genetic Risk Factors Related to Coronary Artery Disease and Role of Transforming Growth Factor Beta 1 Polymorphisms. Genes. 2023; 14(7):1425. https://doi.org/10.3390/genes14071425

TLR4: Now, we turn our attention to the captivating performance of the TLR4 (Toll-Like Receptor 4) gene. Like a dancer responding to changes in the rhythm, TLR4 is a part of the body’s first line of defense, playing a critical role in the innate immune response. But, if there are changes in the TLR4 gene, the rhythm is thrown off, potentially leading to an enhanced inflammatory response, a major factor in the development and progression of CAD.188Holloway JW, Yang IA, Ye S. Variation in the toll-like receptor 4 gene and susceptibility to myocardial infarction. Pharmacogenet Genomics. 2005 Jan;15(1):15-21. doi: 10.1097/01213011-200501000-00003. PMID: 15864121.

AGTR1: AGTR1 (Angiotensin II Type 1 Receptor) gene enters the dance floor. AGTR1’s movements are tied to blood pressure regulation and electrolyte balance. However, if the AGTR1’s steps are misstepped due to a genetic variant, it can contribute to hypertension, a risk factor for CAD.189Li X, Wu N, Ji H, Huang Y, Hu H, Li J, Mi S, Duan S, Chen X. A male-specific association between AGTR1 hypermethylation and coronary heart disease. Bosn J Basic Med Sci. 2020 Feb 5;20(1):31-36. doi: 10.17305/bjbms.2019.4321. PMID: 31538912; PMCID: PMC7029202.

CYP11B2: Next in line, we find the CYP11B2 gene, the soloist playing a vital role in our body’s blood pressure regulation. Variations in its performance could lead to alterations in blood pressure, a strong risk factor for CAD, thus, creating a cacophony that disrupts the harmonious symphony of our health.190Normaznah Y, Azizah MR, Kuak SH, Rosli MA. CYP11B2 gene polymorphism among coronary heart disease patients and blood donors in Malaysia. Malays J Pathol. 2015 Apr;37(1):45-7. PMID: 25890613.

ALDH2: The complement of genes playing in this concert of CAD susceptibility also includes the ALDH2 gene. This gene orchestrates the breakdown of aldehyde, a compound that forms in our body after consuming alcohol. Genetic variants in ALDH2 can lead to the accumulation of aldehyde, resulting in increased oxidative stress and inflammation, factors that could induce an off-beat rhythm in our CAD symphony.191Li YY, Wang H, Wu JJ, Kim HJ, Yang XX, Geng HY, Gong G. ALDH2 gene G487A polymorphism and coronary artery disease: a meta-analysis including 5644 participants. J Cell Mol Med. 2018 Mar;22(3):1666-1674. doi: 10.1111/jcmm.13443. Epub 2017 Dec 26. PMID: 29278292; PMCID: PMC5824379.

HMGCR: Our spotlight shines on the HMGCR gene, the conductor of cholesterol production in our body. While cholesterol is essential for our health, too much of it can start to form plaques in our arteries, leading to CAD. Variants of the HMGCR gene could increase the production of cholesterol, creating a crescendo in CAD risk.192Medina, M. W., Gao, F., Naidoo, D., Rudel, L. L., Temel, R. E., McDaniel, A. L., Marshall, S. M., & Krauss, R. M. (2011). Coordinately Regulated Alternative Splicing of Genes Involved in Cholesterol Biosynthesis and Uptake. PLOS ONE, 6(4), e19420. https://doi.org/10.1371/journal.pone.0019420

SLCO1B1: Our voyage into the CAD cosmos brings us next to the SLCO1B1 gene, a guiding star involved in the metabolism of certain drugs used to treat high cholesterol, a risk factor for CAD. Changes in this gene could alter how well these drugs work, creating disturbances in the CAD constellation.193Bharath, G., Vishnuprabu, D. P., Preethi, L., Nagappan, A. S., Dhianeshwaran Isravanya, R. T., Bhaskar, L. V., Swaminathan, N., & Munirajan, A. K. (2022). slco1b1 and abcb1 variants synergistically influence the atorvastatin treatment response in south Indian coronary artery disease patients. Pharmacogenomics, 23(12), 683–694. https://doi.org/10.2217/pgs-2022-0044

NPPA gene: Another celestial body in our CAD cosmos is the NPPA gene. This gene plays a crucial role in regulating our body’s salt and water balance, which affects our blood pressure. When variants of the NPPA gene alter this balance, they could cause blood pressure fluctuations, creating a ripple effect through the CAD constellation.194Song W, Wang H, Wu Q. Atrial natriuretic peptide in cardiovascular biology and disease (NPPA). Gene. 2015 Sep 10;569(1):1-6. doi: 10.1016/j.gene.2015.06.029. Epub 2015 Jun 12. PMID: 26074089; PMCID: PMC4496260.

COL3A1: Let’s gaze upon the COL3A1 gene, which is involved in the formation of collagen, a major component of our arterial walls. Changes in this gene could lead to weakened arterial walls, making them more prone to rupture and contributing to the progression of CAD.195Muckian C, Fitzgerald A, O’Neill A, O’Byrne A, Fitzgerald DJ, Shields DC. Genetic variability in the extracellular matrix as a determinant of cardiovascular risk: association of type III collagen COL3A1 polymorphisms with coronary artery disease. Blood. 2002 Aug 15;100(4):1220-3. doi: 10.1182/blood-2002-01-0283. PMID: 12149201.

CDKN2B-AS1: Let’s meet the flautist, the CDKN2B-AS1 gene. It doesn’t directly produce a protein, but rather, it is involved in regulating other genes in the 9p21 region, a notorious region associated with CAD. Studies suggest that certain variants in this gene can lead to increased CAD susceptibility, essentially playing a haunting solo that disrupts the harmony.196Huang K, Zhong J, Li Q, Zhang W, Chen Z, Zhou Y, Wu M, Zhong Z, Lu S, Zhang S. Effects of CDKN2B-AS1 polymorphisms on the susceptibility to coronary heart disease. Mol Genet Genomic Med. 2019 Nov;7(11):e955. doi: 10.1002/mgg3.955. Epub 2019 Sep 8. PMID: 31496134; PMCID: PMC6825846.

CXCL12: Our orchestra also includes the drummer, the CXCL12 gene. This gene is involved in stem cell migration, which contributes to the repair of damaged tissues, including our heart tissues. Changes in this gene could lead to ineffective tissue repair after heart injury, drumming up a beat of vulnerability in our genetic orchestra.197Döring Y, van der Vorst EPC, Duchene J, Jansen Y, Gencer S, Bidzhekov K, Atzler D, Santovito D, Rader DJ, Saleheen D, Weber C. CXCL12 Derived From Endothelial Cells Promotes Atherosclerosis to Drive Coronary Artery Disease. Circulation. 2019 Mar 5;139(10):1338-1340. doi: 10.1161/CIRCULATIONAHA.118.037953. PMID: 30865486; PMCID: PMC6417827.

GUCY1A3: Finally, the bassist, the GUCY1A3 gene, often unnoticed yet integral to the rhythm of our orchestra. This gene plays a role in blood vessel dilation. Variants in this gene may affect this function, leading to blood pressure abnormalities and adding a deep, discordant bass line to the melody of our genetic symphony.198Thorsten Kessler and others, Association of the coronary artery disease risk gene GUCY1A3 with ischaemic events after coronary intervention, Cardiovascular Research, Volume 115, Issue 10, 1 August 2019, Pages 1512–1518, https://doi.org/10.1093/cvr/cvz015199Kessler T, Wobst J, Wolf B, Eckhold J, Vilne B, Hollstein R, von Ameln S, Dang TA, Sager HB, Moritz Rumpf P, Aherrahrou R, Kastrati A, Björkegren JLM, Erdmann J, Lusis AJ, Civelek M, Kaiser FJ, Schunkert H. Functional Characterization of the GUCY1A3 Coronary Artery Disease Risk Locus. Circulation. 2017 Aug 1;136(5):476-489. doi: 10.1161/CIRCULATIONAHA.116.024152. Epub 2017 May 9. PMID: 28487391; PMCID: PMC5560301.

Environmental Factors Influencing the Development of Coronary Artery Disease (CAD)

Diet and Exercise

Imagine you’re standing at the edge of a verdant field, poised to embark on a journey. This isn’t a typical journey, though, but rather an exploration of your own health landscape, specifically the terrain that shapes coronary artery disease (CAD). Think of CAD as a storm, brewing and swirling, with numerous contributing elements. There are elements you can control, like the wind direction of your lifestyle choices, and others you can’t, like the atmospheric pressure of your genetics. Today, you’re stepping into two of the most powerful and controllable winds – diet and exercise.

Let’s start by taking a close look at your everyday food choices. Picture your diet as the soil that nourishes the plants in your field. A nutrient-rich, well-tended soil is the foundation of a healthy, vibrant field, just as a well-balanced diet is the foundation of your health. Imagine turning your plate into a colorful canvas, filled with fresh fruits, vegetables, whole grains, lean proteins, and healthy fats. Foods rich in omega-3 fatty acids, like fish and walnuts, and monounsaturated fats, found in olive oil and avocados, can help boost your HDL levels. Each of these foods contributes to the rich tapestry of your health, providing the essential nutrients that your heart needs to perform at its best. On the flip side, a diet high in processed foods, trans fats, sugar, and sodium can be likened to poor, depleted soil, unable to support the growth of healthy plants. When you consume food high in saturated and trans fats, your body’s ‘bad’ cholesterol level rises. This could eventually lead to an unwanted traffic jam in your body’s highway system, hindering the smooth flow of life-giving blood, and potentially leading to coronary artery disease. It leaves the field, your body, susceptible to the erosion of CAD.200Anand SS, Hawkes C, de Souza RJ, Mente A, Dehghan M, Nugent R, Zulyniak MA, Weis T, Bernstein AM, Krauss RM, Kromhout D, Jenkins DJA, Malik V, Martinez-Gonzalez MA, Mozaffarian D, Yusuf S, Willett WC, Popkin BM. Food Consumption and its Impact on Cardiovascular Disease: Importance of Solutions Focused on the Globalized Food System: A Report From the Workshop Convened by the World Heart Federation. J Am Coll Cardiol. 2015 Oct 6;66(14):1590-1614. doi: 10.1016/j.jacc.2015.07.050. PMID: 26429085; PMCID: PMC4597475.201Gholizadeh E, Ayremlou P, Nouri Saeidlou S. The association between dietary pattern and coronary artery disease: A case-control study. J Cardiovasc Thorac Res. 2020;12(4):294-302. doi: 10.34172/jcvtr.2020.48. Epub 2020 Nov 28. PMID: 33510878; PMCID: PMC7828759.

Consider the simple, everyday decisions you make: opting for a piece of fruit instead of a candy bar, or choosing water over a sugary soda. Every healthy choice helps to enrich your dietary soil, planting seeds that can flourish into a heart-healthy life. Exercise, too, is integral in this landscape. Think of it as the rain that hydrates the plants, the sunshine that supports their growth. Regular physical activity is like a gentle, nourishing rain that keeps your field, your body, vibrant and thriving.202Nystoriak MA, Bhatnagar A. Cardiovascular Effects and Benefits of Exercise. Front Cardiovasc Med. 2018 Sep 28;5:135. doi: 10.3389/fcvm.2018.00135. PMID: 30324108; PMCID: PMC6172294.203Tian D, Meng J. Exercise for Prevention and Relief of Cardiovascular Disease: Prognoses, Mechanisms, and Approaches. Oxid Med Cell Longev. 2019 Apr 9;2019:3756750. doi: 10.1155/2019/3756750. PMID: 31093312; PMCID: PMC6481017.

You might be wondering, “how much exercise is enough?” It’s a valid question. You don’t need a deluge; just a consistent, gentle rain. Even modest amounts of physical activity, like a brisk walk for thirty minutes a day, can make a significant difference.204Warburton DE, Nicol CW, Bredin SS. Health benefits of physical activity: the evidence. CMAJ. 2006 Mar 14;174(6):801-9. doi: 10.1503/cmaj.051351. PMID: 16534088; PMCID: PMC1402378. Regular physical activity is like music to your heart, a melody that can lower your blood pressure, reduce bad cholesterol levels, and increase good cholesterol.205Albarrati AM, Alghamdi MSM, Nazer RI, Alkorashy MM, Alshowier N, Gale N. Effectiveness of Low to Moderate Physical Exercise Training on the Level of Low-Density Lipoproteins: A Systematic Review. Biomed Res Int. 2018 Nov 1;2018:5982980. doi: 10.1155/2018/5982980. PMID: 30515408; PMCID: PMC6236809. But, there’s more to exercise than stress relief. Regular physical activity helps control weight, combats health conditions and diseases, and improves mood. Exercise acts like a tonic, capable of revitalizing the city, keeping the heart – the city’s pumping station – robust and efficient.206Basso JC, Suzuki WA. The Effects of Acute Exercise on Mood, Cognition, Neurophysiology, and Neurochemical Pathways: A Review. Brain Plast. 2017 Mar 28;2(2):127-152. doi: 10.3233/BPL-160040. PMID: 29765853; PMCID: PMC5928534.

Remember, exercise isn’t just about intensity; it’s about consistency and enjoyment. Find activities you love, and they won’t feel like a chore. Dancing, cycling, gardening, hiking – these can all be great forms of exercise, supporting your heart health as well as your overall well-being.

“But what if I don’t have the time?” or “What if I’m not in the best shape?” you may ask. These are valid concerns. But remember, it’s not about running a marathon on your first day, or bench pressing twice your weight. Exercise can start small and should be something you enjoy. It could be a walk in the park, a dance class, or a gentle yoga session. Gradually, as your strength and stamina improve, you can challenge yourself to do more.

It’s essential to remember that change doesn’t occur overnight. Cultivating a heart-healthy lifestyle is like growing a garden. It requires patience, perseverance, and time. Each seed you plant with a healthy meal, each drop of sweat from a workout, is an investment in your health, in your life.

Remember, everyone’s garden is unique, shaped by different factors like family history, age, and other health conditions. Some plants might need more attention, others less. The same applies to your body. Some might require more rigorous exercise, others less. Some might respond well to certain diets, others might not.

So, keep exploring, keep learning, and keep tuning into your body’s needs. Listen to your body as it speaks the language of discomfort or ease, exhaustion or exhilaration, illness or vitality. In doing so, you will become the best gardener of your health, cultivating a vibrant, heart-healthy life.

You have already taken the first, most crucial step in this journey. You’ve acknowledged the power that diet and exercise hold over your health. This knowledge alone sets you apart and arms you with the tools to create positive change.

Smoking and Alcohol

As you navigate through your day, you probably don’t think twice about the air you breathe, do you? But what if you knew that the air you inhale may influence the health of your heart – the very engine of your life? That’s right, whether you’re lighting up a cigarette or opening another bottle of alcohol, you’re inviting environmental factors that can wreak havoc on your heart.

Let’s first venture into the smoky haze of tobacco. Visualize your heart as the heart of a very active city, with highways (arteries) running in all directions. These highways are meticulously maintained for smooth traffic (blood flow), ensuring all parts of the city (your body) receive essential supplies on time.

Now, consider what happens when you puff on a cigarette. You might relish that short-lived stress relief, but here’s the less enjoyable news: the nicotine in that smoke is like construction work on the highways, causing traffic snarls (narrowing arteries).207Salehi N, Janjani P, Tadbiri H, Rozbahani M, Jalilian M. Effect of cigarette smoking on coronary arteries and pattern and severity of coronary artery disease: a review. J Int Med Res. 2021 Dec;49(12):3000605211059893. doi: 10.1177/03000605211059893. PMID: 34855538; PMCID: PMC8647272.

Your heart races, blood pressure spikes, and the essential oxygen-carbon dioxide exchange take a hit, straining your heart. It’s like placing a crushing weight on your city’s supply system – unsustainable and detrimental. In the long run, the chronic construction work (nicotine-induced arterial narrowing) makes the city prone to shutdowns (heart attacks).

Now, let’s stroll into the world of alcohol. Like a riveting football game, a drink or two can be enjoyable. It might even be good for your heart. But as with a football match, extending it into overtime again and again (binge drinking) will wear out the players (your heart). Excessive alcohol can lead to high blood pressure and even cause cardiomyopathy, a condition where the heart muscle weakens.208Tasnim S, Tang C, Wright JM. Effect of alcohol on blood pressure. Cochrane Database Syst Rev. 2017 Sep 1;2017(9):CD012787. doi: 10.1002/14651858.CD012787. PMCID: PMC6483609.

Consider the wear and tear on the city’s transport fleet (your heart) if they have to work non-stop. Trucks break down (heart cells die), and soon, the city’s supply chain (blood circulation) is compromised, leading to a potential city-wide crisis (heart failure). It’s important to understand the difference between moderate and heavy drinking. It’s the difference between enjoying a peaceful drive through the city and careening down the highway at breakneck speed – only one is sustainable in the long run.

At this point, you might wonder about the specifics – what counts as heavy drinking? How bad is secondhand smoke? As you continue exploring these issues, you’ll delve into these nuances and more, helping laypeople understand the intricacies of these environmental factors and their impacts on the heart. These are topics you’ll need to explore further and provide citations for in your work.

Secondhand smoke is like a stealthy thief in the night. It robs your city (heart) without you even realizing it. Even if you aren’t the one lighting up, just being in a smoke-filled environment can affect your heart’s health. The city still gets polluted with hazardous gases, disrupting its serene ecosystem. Here, it’s worth noting that secondhand smoke has nearly twice the nicotine and tar as the smoke inhaled by smokers and contains over 7000 chemicals, many of which are toxic and about 70 can cause cancer.209Wipfli H, Avila-Tang E, Navas-Acien A, Kim S, Onicescu G, Yuan J, Breysse P, Samet JM; Famri Homes Study Investigators. Secondhand smoke exposure among women and children: evidence from 31 countries. Am J Public Health. 2008 Apr;98(4):672-9. doi: 10.2105/AJPH.2007.126631. Epub 2008 Feb 28. PMID: 18309121; PMCID: PMC2376995.

Think of it as your city getting invaded even when it has done nothing to provoke such an assault. The unfortunate result? Your risk of developing coronary artery disease escalates by about 25-30%, even if you’ve never smoked in your life. 210Gallucci G, Tartarone A, Lerose R, Lalinga AV, Capobianco AM. Cardiovascular risk of smoking and benefits of smoking cessation. J Thorac Dis. 2020 Jul;12(7):3866-3876. doi: 10.21037/jtd.2020.02.47. PMID: 32802468; PMCID: PMC7399440.

Now, let’s turn our attention back to alcohol. You’re already aware of the general rule of thumb – moderation is key. But what does that mean, exactly? It’s essential to define ‘moderate drinking.’ For men, it’s up to two drinks per day, and for women, it’s one. It’s critical to understand that exceeding these limits regularly can lead to a host of health problems, coronary artery disease being one of them.

Think of it like the city’s water supply system. A moderate, steady flow keeps everything running smoothly, but a flood (excessive alcohol) can cause immense damage. Not only can heavy drinking lead to direct heart issues like cardiomyopathy and arrhythmias, but it can also contribute to obesity, high blood pressure, and high triglycerides – all indirect paths leading to heart disease.211Piano MR. Alcohol’s Effects on the Cardiovascular System. Alcohol Res. 2017;38(2):219-241. PMID: 28988575; PMCID: PMC5513687.212Hoek AG, van Oort S, Mukamal KJ, Beulens JWJ. Alcohol Consumption and Cardiovascular Disease Risk: Placing New Data in Context. Curr Atheroscler Rep. 2022 Jan;24(1):51-59. doi: 10.1007/s11883-022-00992-1. Epub 2022 Feb 7. PMID: 35129737; PMCID: PMC8924109.

But remember, this is your city, and you can safeguard it. Limiting alcohol and maintaining distance from tobacco smoke, whether first or secondhand, can be your defense against these invaders. As the one in charge, the choices you make significantly determine how well your city thrives, no matter the challenges. The decisions may not always be easy, but they’re vital for a healthy, vibrant city – your heart.

When smoking and alcohol take hold, they don’t just affect your physical health, but also your mental well-being. Stress, anxiety, depression – these are psychological adversaries your heart may have to face, particularly if smoking and drinking are in the picture. Imagine your heart city under the grip of a hostile power. The city becomes gloomy, people are unhappy, and the atmosphere is thick with despair.213Ferreira VR, Jardim TV, Sousa ALL, Rosa BMC, Jardim PCV. Smoking, alcohol consumption and mental health: Data from the Brazilian study of Cardiovascular Risks in Adolescents (ERICA). Addict Behav Rep. 2018 Nov 22;9:100147. doi: 10.1016/j.abrep.2018.100147. PMID: 31193769; PMCID: PMC6542299.

Why does this matter, you ask? Because negative emotional states can trigger inflammatory responses in the body, thereby increasing your heart’s vulnerability.214Liu YZ, Wang YX, Jiang CL. Inflammation: The Common Pathway of Stress-Related Diseases. Front Hum Neurosci. 2017 Jun 20;11:316. doi: 10.3389/fnhum.2017.00316. PMID: 28676747; PMCID: PMC5476783.

Let’s delve into the mechanics of this. When you’re stressed or depressed, your body releases adrenaline, a hormone that increases your heart rate and blood pressure. It’s like sending your city into overdrive without providing the necessary resources to handle it. Over time, this ‘overdrive’ state can cause wear and tear on your heart, leading to heart disease.

Simultaneously, these negative states can lead you to develop unhealthy coping mechanisms, like smoking more or consuming alcohol excessively. It becomes a vicious cycle, with each factor feeding the other. You must remember this interaction between mental and physical health, as it’s a crucial component of your in-depth understanding of coronary artery disease.

The connection between smoking, drinking, and mental health is another layer of complexity that you should keep in mind. Nicotine in cigarettes and alcohol can provide temporary relief from stress, anxiety, and depression. This relief can be likened to a false sense of security in your city, where the underlying issues remain unaddressed while the symptoms are temporarily alleviated.

This can lead to dependence, where the absence of these substances can lead to withdrawal symptoms and increased psychological distress. It’s like the city becoming so dependent on a faulty system that trying to change it leads to chaos and dysfunction.215De Hert M, Detraux J, Vancampfort D. The intriguing relationship between coronary heart disease and mental disorders. Dialogues Clin Neurosci. 2018 Mar;20(1):31-40. doi: 10.31887/DCNS.2018.20.1/mdehert. PMID: 29946209; PMCID: PMC6016051.

But there’s hope. Just as the darkness is deepest before dawn, understanding these risks is the first step to mitigate them. Effective stress management techniques, therapy, and support can go a long way in helping you quit smoking and limit alcohol while also addressing mental health issues. Your city can return to peace and prosperity with the right steps and timely intervention. Your heart, the very active city, thrives on balance – be it in diet, exercise, or consumption habits. It craves moderation, detests excess, and appreciates thoughtfulness. It’s you who can shield it from the threat of smoking and alcohol, two foes that lurk in the shadows, unseen but not unfelt.

Remember, it’s a tough battle, but not an impossible one. With awareness, support, and determination, you can protect your city, ensuring it continues to throb with vitality, undeterred by the challenges thrown its way.

Other Medical Conditions

Hypertension as a Cause of Coronary Artery Disease (CAD)

Stepping deeper into the world of coronary artery disease, let’s picture a scene. Picture your heart as a vibrant, active city, pulsing with life, rhythm, and power. Now, imagine that city is surrounded by towering mountains, and those mountains are pressing in on all sides. That’s what hypertension, also known as high blood pressure, does to your heart. When the blood pressure in your veins and arteries is higher than it should be, it’s like those mountains pressing down on your heart city. Just like the city structures would struggle under the pressure, so do your heart and blood vessels.216Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension. Heart. 2003 Sep;89(9):1104-9. doi: 10.1136/heart.89.9.1104. PMID: 12923045; PMCID: PMC1767863.

Hypertension means your heart has to work harder to pump blood, just as city services would have to work harder if under siege. Over time, this increased effort can cause parts of your heart to thicken and stiffen – a condition known as left ventricular hypertrophy. When this happens, your heart isn’t able to pump as effectively as it should. The health of your heart city begins to decline.217Aronow WS. Hypertension and left ventricular hypertrophy. Ann Transl Med. 2017 Aug;5(15):310. doi: 10.21037/atm.2017.06.14. PMID: 28856150; PMCID: PMC5555990.

This extra workload also demands more oxygen and nutrients than your coronary arteries can supply. This lack is like a city running low on supplies because the roads are under strain. When demands aren’t met, parts of your heart can become ischemic, meaning they’re not getting enough oxygen, and this can lead to angina or a heart attack.218Picariello C, Lazzeri C, Attanà P, Chiostri M, Gensini GF, Valente S. The impact of hypertension on patients with acute coronary syndromes. Int J Hypertens. 2011;2011:563657. doi: 10.4061/2011/563657. Epub 2011 Jun 22. PMID: 21747979; PMCID: PMC3124673.

Hypertension doesn’t just increase the workload on your heart; it also damages your blood vessels. This damage can lead to atherosclerosis, where plaques form in your arteries, narrowing them, and making it even harder for blood to flow. It’s like if the main routes in and out of your city were blocked, limiting essential supplies from getting in or out. This link between hypertension and atherosclerosis should be marked for citation.219Poznyak AV, Sadykhov NK, Kartuesov AG, Borisov EE, Melnichenko AA, Grechko AV, Orekhov AN. Hypertension as a risk factor for atherosclerosis: Cardiovascular risk assessment. Front Cardiovasc Med. 2022 Aug 22;9:959285. doi: 10.3389/fcvm.2022.959285. PMID: 36072873; PMCID: PMC9441708.

Despite the threat hypertension poses to your heart city, the tricky part is that it often doesn’t show noticeable symptoms until it’s already caused significant damage. It’s a silent enemy, creeping up on your city under the cover of darkness. That’s why it’s often called the “silent killer.”220Mensah GA. Commentary: Hypertension Phenotypes: The Many Faces of a Silent Killer. Ethn Dis. 2019 Oct 17;29(4):545-548. doi: 10.18865/ed.29.4.545. PMID: 31641321; PMCID: PMC6802171.

But it’s not all doom and gloom, remember that awareness and regular check-ups can help detect hypertension early. Picture it as sentinels on your city walls, keeping a vigilant watch for any signs of the encroaching enemy. Early detection and management can significantly reduce the risks and help keep your heart city safe from this silent threat.

Your heart city is resilient. With the right care, it can resist the pressure of hypertension and continue to beat the rhythm of life.

Diabetes Mellitus and Coronary Artery Disease (CAD)

Let’s take a stroll through another chapter in the story of coronary artery disease. This chapter takes us to the land of sugar and spice, and not everything is nice. We’re talking about diabetes mellitus, a condition that can be as sticky and tricky as the sugary substance it affects – glucose.

When you think about diabetes, you probably think of sugar levels, insulin, and maybe frequent trips to the bathroom. You might not immediately think about your heart. But there’s a connection, a sinister link between diabetes and heart disease. Like the spider weaving a web, diabetes creates a network of risks that could trap your heart.221Leon BM, Maddox TM. Diabetes and cardiovascular disease: Epidemiology, biological mechanisms, treatment recommendations and future research. World J Diabetes. 2015 Oct 10;6(13):1246-58. doi: 10.4239/wjd.v6.i13.1246. PMID: 26468341; PMCID: PMC4600176.

Here’s how the tale unfolds. Imagine your body is a car, your heart is the engine, and glucose is the fuel. Normally, insulin acts like a key, opening the doors to your cells so glucose can enter and provide energy. In diabetes, that key is missing or damaged. Glucose can’t enter the cells and starts building up in your bloodstream.222Rahman MS, Hossain KS, Das S, Kundu S, Adegoke EO, Rahman MA, Hannan MA, Uddin MJ, Pang MG. Role of Insulin in Health and Disease: An Update. Int J Mol Sci. 2021 Jun 15;22(12):6403. doi: 10.3390/ijms22126403. PMID: 34203830; PMCID: PMC8232639.

Just like a car engine can be damaged if the wrong type of fuel is used, so can your heart. High levels of glucose in your blood can damage your blood vessels and the nerves that control your heart. Now, consider this – if your heart is the engine of your body, what happens if that engine is damaged? The car won’t run efficiently, right? Similarly, heart damage can lead to problems like coronary artery disease.223Yagihashi S, Mizukami H, Sugimoto K. Mechanism of diabetic neuropathy: Where are we now and where to go? J Diabetes Investig. 2011 Jan 24;2(1):18-32. doi: 10.1111/j.2040-1124.2010.00070.x. PMID: 24843457; PMCID: PMC4008011.

What makes this connection even more troublesome is that diabetes comes along with a band of troublemakers. We’re talking about conditions like high blood pressure and high levels of certain types of fat in your blood – elements that also contribute to coronary artery disease.224Petrie JR, Guzik TJ, Touyz RM. Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms. Can J Cardiol. 2018 May;34(5):575-584. doi: 10.1016/j.cjca.2017.12.005. Epub 2017 Dec 11. PMID: 29459239; PMCID: PMC5953551.

Moreover, remember those narrow roads we mentioned when talking about coronary artery disease? Well, having high glucose levels can make those roads even narrower. This is because the excess sugar in your blood can lead to an increase in plaque buildup in your arteries. The narrow roads now become winding, treacherous paths that limit the flow of blood and oxygen to your heart. It’s like if a city’s major roads were narrowed down to single lanes.225Poznyak A, Grechko AV, Poggio P, Myasoedova VA, Alfieri V, Orekhov AN. The Diabetes Mellitus-Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation. Int J Mol Sci. 2020 Mar 6;21(5):1835. doi: 10.3390/ijms21051835. PMID: 32155866; PMCID: PMC7084712.

Yet, in the shadows of this tale, there is a glimmer of hope. You see, even though diabetes is a serious condition, it can be managed. It’s not easy, but with determination, a healthy lifestyle, and possibly medication, you can control your blood sugar levels and reduce the risk of heart disease.

Obesity and Coronary Artery Disease (CAD)

One of the key companions on this journey, and sadly not a friendly one, is obesity. So, let’s take a closer look at how this unwelcome partner plays its part. Picture a world where everyone treats their body like a temple, eating nutritious meals and staying active. In that world, coronary artery disease might not be so prevalent.

But let’s face reality. In our modern world, obesity is a widespread issue. Picture yourself carrying a heavy backpack all day, every day. Exhausting, right? That’s what obesity does to your heart. It burdens your heart, forcing it to work harder. This might lead to high blood pressure.226Shariq OA, McKenzie TJ. Obesity-related hypertension: a review of pathophysiology, management, and the role of metabolic surgery. Gland Surg. 2020 Feb;9(1):80-93. doi: 10.21037/gs.2019.12.03. PMID: 32206601; PMCID: PMC7082272.

This pressure, over time, is like a constant pounding on the walls of your arteries, causing wear and tear. Your body, in an attempt to patch things up, sends a sticky substance to the rescue. Picture it like a hasty patch-up job on a leaky pipe using sticky tape. Over time, this sticky tape attracts more debris, narrowing the pipe further. This is the plaque that builds up in your arteries.

What’s worse, when you’re obese, your body is often home to higher levels of LDL cholesterol, the so-called ‘bad’ cholesterol. This cholesterol gets drawn to the sticky plaster in your arteries, building up and causing further damage.227Klop B, Elte JW, Cabezas MC. Dyslipidemia in obesity: mechanisms and potential targets. Nutrients. 2013 Apr 12;5(4):1218-40. doi: 10.3390/nu5041218. PMID: 23584084; PMCID: PMC3705344.

Social Determinants and Inequities in Coronary Artery Disease (CAD)

Imagine you’re about to embark on a journey, one that unravels the often unseen factors influencing your health, particularly coronary artery disease. Pack your curiosity and empathy; we’re delving into the world of social determinants.

Picture yourself at the intersection of two streets. One is lined with upscale homes, plush parks, and well-stocked grocery stores. The other is dotted with rundown buildings, fast-food chains, and a noticeable lack of green spaces. Your health may depend on which street you call home.228Poelman M, Strak M, Schmitz O, Hoek G, Karssenberg D, Helbich M, Ntarladima AM, Bots M, Brunekreef B, Grobbee R, Dijst M, Vaartjes I. Relations between the residential fast-food environment and the individual risk of cardiovascular diseases in The Netherlands: A nationwide follow-up study. Eur J Prev Cardiol. 2018 Sep;25(13):1397-1405. doi: 10.1177/2047487318769458. Epub 2018 Apr 24. PMID: 29688759; PMCID: PMC6130123.

We often think of health in terms of individual choices – to smoke, to exercise, to eat a balanced diet. But what if these choices aren’t entirely yours? What if they’re dictated by external forces? Forces like your income, education, or even employment conditions.

Now, let’s step into the shoes of a single parent, juggling multiple jobs just to make ends meet. Nutritious food and a gym membership might be unaffordable luxuries. You’re always on the go, stressed, and worn out. Chronic stress, we know, can be a harsh foe to the heart. The links between socioeconomic status, stress, and coronary artery disease form another important claim to remember.229Phillips JE, Klein WM. Socioeconomic Status and Coronary Heart Disease Risk: The Role of Social Cognitive Factors. Soc Personal Psychol Compass. 2010 Sep;4(9):704-727. doi: 10.1111/j.1751-9004.2010.00295.x. PMID: 21785652; PMCID: PMC3140045.

Consider also the barriers to healthcare access, be they financial, geographical, or cultural. Maybe there’s a scarcity of healthcare providers in your area, or perhaps your working hours clash with clinic timings. Or maybe, just maybe, you’re a victim of bias in healthcare delivery. So, when chest pain strikes, help might not be within easy reach.230Graham G. Disparities in cardiovascular disease risk in the United States. Curr Cardiol Rev. 2015;11(3):238-45. doi: 10.2174/1573403×11666141122220003. PMID: 25418513; PMCID: PMC4558355.

The journey is tough, isn’t it? It’s the harsh reality many face every day. However, in understanding these social determinants, we arm ourselves with the knowledge to tackle them. We’re not just discussing coronary artery disease in isolation; we’re looking at the bigger picture. We’re considering how society and systems impact heart health.

Transportation, often an overlooked factor, plays a significant role too. Imagine living miles away from the nearest healthcare facility with no reliable means of transportation. This hurdle could mean late diagnoses, missed appointments, and poor disease management. So, the seemingly unrelated aspect of transportation can become a key player in your coronary artery disease narrative.

Let’s also consider your workplace environment. Is it supportive and stress-free, or does it leave you drained, physically and mentally? Long hours, high demands, job insecurity, or hostile work environments can wreak havoc on your heart health over time.231Sara JD, Prasad M, Eleid MF, Zhang M, Widmer RJ, Lerman A. Association Between Work-Related Stress and Coronary Heart Disease: A Review of Prospective Studies Through the Job Strain, Effort-Reward Balance, and Organizational Justice Models. J Am Heart Assoc. 2018 Apr 27;7(9):e008073. doi: 10.1161/JAHA.117.008073. PMID: 29703810; PMCID: PMC6015274.

Bear in mind that these social determinants don’t operate in isolation; they intertwine and amplify each other, adding layers of complexity to the coronary artery disease story. But don’t lose heart! Each layer of complexity is an opportunity for intervention and improvement.

The Clinical Presentation and Diagnosis of Coronary Artery Disease (CAD)

Clinical Manifestations

Angina: Imagine feeling a pressure in your chest, like an elephant is sitting on you. It’s called angina. This is the heart’s cry for help when its blood supply is hindered. A noteworthy point to remember here is that angina is a common symptom of coronary artery disease. But here’s the tricky part: coronary artery disease can be a master of disguise. Sometimes, you may feel the discomfort not in your chest, but in your neck, jaw, shoulder, back, or even arm. Yes, your heart can signal its distress to seemingly unrelated parts of your body.

Heart Attack: Now, consider the storm unleashing its full power: a heart attack. It happens when a part of the heart is starved of blood and oxygen. Your body might signal this through severe chest pain, shortness of breath, sweating, nausea, or faintness. But remember, not all heart attacks announce their arrival. Some are silent, especially in people with diabetes. Here’s a crucial claim to underline: heart attacks can be both symptomatic and silent in coronary artery disease.

Fatigue: In some cases, coronary artery disease might make its presence known not through pain but through fatigue. Think about those days when you feel unusually tired, when even simple activities seem to drain you. This fatigue is your heart telling you that it’s working harder than it should.232Gecaite-Stonciene J, Hughes BM, Burkauskas J, Bunevicius A, Kazukauskiene N, van Houtum L, Brozaitiene J, Neverauskas J, Mickuviene N. Fatigue Is Associated With Diminished Cardiovascular Response to Anticipatory Stress in Patients With Coronary Artery Disease. Front Physiol. 2021 Aug 17;12:692098. doi: 10.3389/fphys.2021.692098. PMID: 34483954; PMCID: PMC8416171.

Dizziness: Feeling lightheaded or dizzy? This might be your heart’s call for attention too. Reduced blood flow to the heart can lower your blood pressure, making you feel faint. It’s another way your body might signal underlying coronary artery disease.

Shortness of Breath: You might also face shortness of breath. Imagine trying to fill your lungs with air, but no matter how hard you try, it just doesn’t feel enough. This breathlessness can be your heart telling you that it’s not getting enough oxygen-rich blood.233Barnett LA, Prior JA, Kadam UT, Jordan KP. Chest pain and shortness of breath in cardiovascular disease: a prospective cohort study in UK primary care. BMJ Open. 2017 May 25;7(5):e015857. doi: 10.1136/bmjopen-2017-015857. PMID: 28550024; PMCID: PMC5726088.

Edema: The symptoms of coronary artery disease might show up in unexpected ways. For instance, you could experience swelling in your legs, ankles, feet, or abdomen. This swelling, known as edema, is your body’s response to your heart not pumping blood effectively, and it’s something you should remember.

Sleep disturbances: Let’s not forget about sleep disturbances. If you find yourself waking up suddenly at night, feeling short of breath, it might be more than just a bad dream. This could be a symptom of coronary artery disease.

Diaphoresis: Also, you might notice excessive sweating without a clear reason like heat or physical exertion. That’s your body trying to cool itself down as your heart works overtime to pump blood. An important point to note here is that unexplained sweating can be a sign of coronary artery disease.

Anxiety: A symptom often overlooked is anxiety. The body and the mind are interconnected in ways we don’t fully understand yet. Hence, feeling anxious or restless without an apparent reason might be your heart signaling that something is amiss.

Nausea or Lack of Appetite: Do not forget the symptom of nausea or lack of appetite. You might not link these with your heart, but they can indeed be signals of coronary artery disease.

Heart Palpitations: Next on our list is rapid heartbeat or heart palpitations. It feels as if your heart is racing or fluttering in your chest, sometimes even skipping beats. This can happen because CAD disrupts the heart’s normal rhythm due to inadequate blood supply.

Memory Issues or Confusion: Furthermore, cognitive issues like memory loss or confusion can also be a result of CAD. When your brain doesn’t get enough blood, it can impact your cognitive function.

Weak Immune System: Next, you may notice that you get sick more often or take longer to recover from illnesses. This is because CAD can affect your immune system’s functioning.

Depression: Another aspect to consider is your mental health. Depression is commonly seen in people with CAD. It’s not just the emotional burden of dealing with a chronic disease; depression might also be a direct result of changes in your brain caused by decreased blood flow.

Decrease Exercise Tolerance: Another indirect effect of CAD is a decrease in exercise tolerance. If you find yourself struggling to complete workouts you could easily handle before, it could be a sign that your heart isn’t effectively pumping blood.

Loss of Appetite / Unintended Weight Loss: One symptom that you might not immediately connect with CAD is a loss of appetite or unintended weight loss. It could be a side effect of other symptoms, like nausea or constant fatigue.

White or Pink Mucus: Another interesting symptom is a persistent cough that produces white or pink mucus. While a cough can have many causes, it’s important not to overlook CAD, particularly when this symptom is coupled with others.

Not Feeling Right: Next, a symptom that may seem vague but can have significant implications is a general feeling of being unwell or not feeling “right.” The reason behind it might be CAD affecting the body’s overall functioning.

Erectile Dysfunction: A significant symptom that might not be initially associated with CAD is erectile dysfunction in men. This can happen due to impaired blood flow, which might also suggest issues with the coronary arteries.234Sai Ravi Shanker A, Phanikrishna B, Bhaktha Vatsala Reddy C. Association between erectile dysfunction and coronary artery disease and its severity. Indian Heart J. 2013 Mar-Apr;65(2):180-6. doi: 10.1016/j.ihj.2013.02.013. Epub 2013 Feb 24. PMID: 23647898; PMCID: PMC3861235.

Cyanosis: Another symptom worth noting is the onset of skin problems such as cyanosis, a bluish discoloration of the skin, nails, and mucous membranes due to insufficient oxygen in the blood. This could suggest that the heart is not pumping blood effectively because of CAD.

Tinnitus: Finally, CAD can lead to sudden onset of tinnitus (ringing in the ears) or hearing loss. This happens when the reduced blood flow affects the nerves in the ear. For citation: Sudden onset of tinnitus or hearing loss could suggest CAD.235Yüksel F, Karataş D, Türkdoğan FT, Yüksel Ö. Increased Atherosclerosis Correlates with Subjective Tinnitus Severity. Indian J Otolaryngol Head Neck Surg. 2018 Mar;70(1):119-124. doi: 10.1007/s12070-015-0845-4. Epub 2015 Apr 28. PMID: 29456955; PMCID: PMC5807274.

Indigestion, Heartburn, Stomach Pain: One of the less commonly discussed symptoms of CAD is digestive issues, such as nausea, indigestion, heartburn or stomach pain. This happens due to a phenomenon known as referred pain where the pain is perceived at a location other than the site of the painful stimulus.

Dark Urine: Lastly, individuals with CAD might notice that their urine has become darker and less frequent, indicating a decreased kidney function due to poor blood flow.236British Heart Foundation. (2021, May 3). The heart-kidney link. BHF. https://www.bhf.org.uk/informationsupport/heart-matters-magazine/medical/kidney-heart-link

Remember, these manifestations of CAD can be diverse and sometimes subtle. It’s crucial to seek professional medical advice if any new or unexplained symptoms occur.

Physical Examination

Medical and family health history as initial steps in physical examination for CAD.237Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/

The healthcare provider will then move on to checking your vital signs like heart rate, blood pressure, and temperature. Blood pressure is especially important because it can detect strain in the heart and arteries.

Listening to your heart through a stethoscope, the doctor will check for a heart murmur or other sounds indicating heart problems. A murmur could signify issues with your heart valves, which, if not working properly, might make it harder for the heart to pump blood, contributing to CAD.

Remember that little rubber hammer that your doctor might have used to tap on your knee? That’s another tool in their kit. The healthcare provider might check your pulses in your legs or feet to detect a diminished or absent pulse, a sign that your blood vessels could be narrowed or blocked.

Your doctor might also examine your skin for signs of cholesterol deposits, as high levels of cholesterol can lead to CAD. They may also look for signs of other conditions linked to CAD, such as diabetes, like skin changes or wounds that aren’t healing properly.

Your physician may recommend further tests. These could include an electrocardiogram, stress tests, or more advanced diagnostic procedures.

Diagnostic Modalities

Electrocardiogram

Imagine an electrocardiogram (EKG or ECG) as a high-speed snapshot of your heart in action. It records the electrical signals that trigger your heart’s pumps – the chambers – to contract and relax. Think of these signals as your heart’s drumbeat, setting the pace for how it moves blood to your body.238Sattar Y, Chhabra L. Electrocardiogram. [Updated 2023 Apr 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549803/

Why are these snapshots so important? The pattern of these signals can help your doctor detect several conditions linked to CAD. If the signals are irregular or follow a strange pattern, it could indicate issues like a heart attack or angina. In the context of CAD, these irregularities might mean that your heart isn’t getting the oxygen it needs, like a car trying to run on an empty gas tank.239Walker RW, Dewhurst M, Gray WK, Jusabani A, Aris E, Unwin N, Swai M, Adams PC, Mugusi F. Electrocardiographic assessment of coronary artery disease and stroke risk factors in rural and urban Tanzania: a case-control study. J Stroke Cerebrovasc Dis. 2014 Feb;23(2):315-20. doi: 10.1016/j.jstrokecerebrovasdis.2013.03.002. Epub 2013 Mar 30. PMID: 23545320; PMCID: PMC4185096.

Explain that EKG is non an invasive procedure. You may feel a bit exposed, but remember, your comfort and safety are the healthcare provider’s top priority. There’s no need to worry – these patches are completely safe and painless, and they’re how the EKG machine reads the electrical signals from your heart.240Sattar Y, Chhabra L. Electrocardiogram. [Updated 2023 Apr 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549803/

You should also know that an EKG is a quick procedure, typically taking just a few minutes. While you rest, the machine does its work, capturing each beat of your heart and recording it as a wave line on a graph. It’s these lines that your doctor will examine later to look for any irregularities.

Keep in mind that while EKGs are useful tools, they don’t catch everything. The EKG will catch any abnormality that occurs at the time of the test. It can also catch some past abnormalities like an old infarct.241Warner MJ, Tivakaran VS. Inferior Myocardial Infarction. [Updated 2023 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470572/ Even if you didn’t experience classic heart attack symptoms or were unaware it happened, an EKG might catch this historical event.

But that’s not all. EKG can also show if the heart is enlarged or overworked, both of which can happen in CAD. If the heart’s walls are too thick, it might mean that your heart has been working harder than usual to pump blood due to the narrowed arteries in CAD. An enlarged heart or changes in the heart’s structure can significantly affect the EKG readings.242de Hartog-Keyzer JML, El Messaoudi S, Harskamp R, Vart P, Ringoir L, Pop V, Nijveldt R. Electrocardiography for the detection of left ventricular hypertrophy in an elderly population with long-standing hypertension in primary care: a secondary analysis of the CHELLO cohort study. BMJ Open. 2020 Aug 20;10(8):e038824. doi: 10.1136/bmjopen-2020-038824. PMID: 32819998; PMCID: PMC7443300.

What’s even more amazing is that EKG might even give your doctor information about which arteries are blocked or narrowed. Different leads on an EKG correspond to different areas of the heart, and changes in these areas can suggest which specific coronary artery might be having trouble. This could be invaluable information for planning treatment or further diagnostic tests.243Mahmoodzadeh S, Moazenzadeh M, Rashidinejad H, Sheikhvatan M. Diagnostic performance of electrocardiography in the assessment of significant coronary artery disease and its anatomical size in comparison with coronary angiography. J Res Med Sci. 2011 Jun;16(6):750-5. PMID: 22091303; PMCID: PMC3214392.

With all these insights, an EKG isn’t just a snapshot; it’s an unfolding story of your heart’s health. It provides your healthcare team with critical chapters in your unique heart story, helping them navigate the best path for your health journey.

Stress Test 

This is all done to understand how your heart reacts to physical stress and to spot any potential signs of CAD during exertion. It’s like shining a spotlight on your heart’s performance to see if there are any shadows of concern.244Ananthasubramaniam G, Ananthasubramaniam K. Stress electrocardiography testing in coronary artery disease: Is it time for its swan song or to redefine its role in the modern era? Indian Heart J. 2022 Mar-Apr;74(2):81-85. doi: 10.1016/j.ihj.2022.02.003. Epub 2022 Feb 12. PMID: 35167825; PMCID: PMC9039687.

The main reason for this assessment is that sometimes, CAD symptoms might not manifest when you’re at rest, but they could become evident during physical activity. So, by observing your heart while you exercise, the healthcare team gains a more comprehensive understanding of its functionality and the potential challenges it might face.245Ananthasubramaniam G, Ananthasubramaniam K. Stress electrocardiography testing in coronary artery disease: Is it time for its swan song or to redefine its role in the modern era ? Indian Heart J. 2022 Mar-Apr;74(2):81-85. doi: 10.1016/j.ihj.2022.02.003. Epub 2022 Feb 12. PMID: 35167825; PMCID: PMC9039687.

As you walk or jog on the treadmill, the EKG continuously records your heart’s electrical signals. Any unusual patterns or irregularities on the EKG could be red flags for CAD. It’s like an intricate dance, where your heart’s rhythm tells a story that the healthcare team interprets with great care and attention to detail. They want to be sure that your heart is staying in tune and maintaining its steady beat during the test.246Rafie N, Kashou AH, Noseworthy PA. ECG Interpretation: Clinical Relevance, Challenges, and Advances. Hearts. 2021; 2(4):505-513. https://doi.org/10.3390/hearts2040039

After the stress test, your healthcare provider will thoroughly review the results and discuss them with you. They’ll explain what they observed during the test and whether any further investigations or treatments are needed. Communication is vital here, as they want to ensure you have a clear understanding of your heart’s health and any potential risks or interventions.247Vermeir P, Vandijck D, Degroote S, Peleman R, Verhaeghe R, Mortier E, Hallaert G, Van Daele S, Buylaert W, Vogelaers D. Communication in healthcare: a narrative review of the literature and practical recommendations. Int J Clin Pract. 2015 Nov;69(11):1257-67. doi: 10.1111/ijcp.12686. Epub 2015 Jul 6. PMID: 26147310; PMCID: PMC4758389.

Overall, the stress test is an essential tool in the diagnosis and management of CAD. It allows your healthcare team to tailor a personalized care plan, helping you navigate any challenges your heart might face with confidence and empowerment. Your heart’s health is their priority, and they’re here to support you on this journey toward a healthier heart.

Cardiac Catheterization

Cardiac Catheterization is like your heart’s personal detective, seeking out any trouble in those crucial arteries. It helps doctors measure pressure within the heart. By recording this, they gain an inside look at how your heart is functioning. If there are areas of concern – perhaps your heart is pumping harder than it should – it’ll show up here.248Chokkalingam Mani B, Chaudhari SS. Right Heart Cardiac Catheterization. [Updated 2023 Apr 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557404/ Furthermore, the procedure can also measure oxygen levels in different parts of your heart. This is crucial. Just like you might struggle in a room with low oxygen, so does your heart. This data provides another piece of the puzzle to help doctors fully understand what’s happening inside your heart.249Ralston BH, Waberski AT, Kanter JP, Schick JW, Downing TE. Measured Oxygen Consumption During Pediatric Cardiac Catheterization is More Accurate than Assumed Oxygen Consumption. Pediatr Cardiol. 2023 May 27. doi: 10.1007/s00246-023-03186-x. Epub ahead of print. PMID: 37243747.

Now, this test isn’t the first go-to for doctors. They usually reserve it for when other tests don’t provide clear answers or when you’re showing serious heart disease symptoms.250Manda YR, Baradhi KM. Cardiac Catheterization Risks and Complications. [Updated 2023 Jan 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK531461/251Kosova E, Ricciardi M. Cardiac Catheterization. JAMA. 2017;317(22):2344. doi:10.1001/jama.2017.0708

Let’s break down how this detective works. A doctor will gently insert a thin, flexible tube (the catheter) into a blood vessel, either in your arm or groin. With utmost care, they guide this tube up into your heart. Think of it as the probe NASA sends to Mars. Only in this case, the mission is to understand your heart’s inner workings.252Chokkalingam Mani B, Chaudhari SS. Right Heart Cardiac Catheterization. [Updated 2023 Apr 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557404/

Through this procedure, the doctors are looking to spot any blockages or narrowed areas in your coronary arteries. It’s quite fascinating! They inject a special dye through the catheter, which makes its way to your heart. This dye shows up on an X-ray monitor, revealing any trouble spots.253NHS. (2022, October 4). Cardiac catheterisation and coronary angiography. NHS choices. https://www.nhs.uk/conditions/coronary-angiography/

In the fight against CAD, Cardiac Catheterization is a game-changer. It’s an invaluable tool in our arsenal, not just for diagnosis, but also to assess the disease’s severity and help doctors chart the best path forward.

Cardiac Catheterization can also be used for angioplasty, a procedure that widens narrowed or blocked arteries. A tiny balloon attached to the catheter is inflated once it’s at the site of the blockage, pushing plaque to the sides and creating a more open passage for blood flow. Sometimes, a small wire mesh tube called a stent is left behind to keep the artery open.254Chhabra L, Zain MA, Siddiqui WJ. Angioplasty. [Updated 2023 Jan 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499894/

In cases where heart surgery is needed, Cardiac Catheterization provides invaluable information that guides surgeons. They can identify the exact location and extent of the problems, allowing them to plan the most effective surgical strategy.255Hemmerling, Thomas M.; Cyr, Shantale; Terrasini, Nora. Epidural catheterization in cardiac surgery: The 2012 risk assessment. Annals of Cardiac Anaesthesia 16(3):p 169-177, July–September 2013. | DOI: 10.4103/0971-9784.114237

Cardiac Catheterization can be used to take a biopsy, a sample of heart tissue, for examination under a microscope. This can help identify various heart diseases or gauge the health of a transplanted heart.256Kiamanesh O, Toma M. The State of the Heart Biopsy: A Clinical Review. CJC Open. 2020 Dec 1;3(4):524-531. doi: 10.1016/j.cjco.2020.11.017. PMID: 34027357; PMCID: PMC8129478.

Once CAD is diagnosed, you might be curious about the next steps. Your doctor might mention medical therapy or lifestyle modifications, but how do they know what will work best for you? That’s where Cardiac Catheterization can help. By assessing the severity of your CAD, it aids doctors in choosing the most effective treatment.

Think of it as a roadmap. It doesn’t just reveal where the roadblocks (or blockages) are but also indicates how serious they are. Is it a small detour, or is the highway completely blocked off? Understanding this can influence whether you would benefit more from medications and lifestyle changes or if you need interventions like angioplasty or bypass surgery.257Shah SM, Pfau SE. Coronary Physiology in the Cardiac Catheterization Laboratory. J Clin Med. 2019 Feb 18;8(2):255. doi: 10.3390/jcm8020255. PMID: 30781631; PMCID: PMC6406799.

Also, Cardiac Catheterization isn’t a one-time deal. After initial treatments, it can be used again to check on the status of CAD. Has the condition improved with the treatment? Are there new blockages? Is there a need to tweak the treatment plan? These are all questions that Cardiac Catheterization can help answer.

Sometimes, CAD can lead to heart damage, like a heart attack. In such scenarios, Cardiac Catheterization serves as an emergency diagnostic tool. It quickly reveals where the blockage causing the heart attack is located, allowing for immediate treatment. Time is muscle, as they say, and this test helps save valuable time.258Darshan Doshi, M. (2020, May 21). Are there benefits of cardiac catheterization for stable coronary artery disease?. Harvard Health. https://www.health.harvard.edu/blog/are-there-benefits-of-cardiac-catheterization-for-stable-coronary-artery-disease-2020052119817

It’s crucial to remember, Cardiac Catheterization is a procedure aimed at helping you take back control of your heart health when dealing with CAD. It’s like a scout on the battlefield, providing necessary information to strategize and fight effectively. With it, you’re not fighting blind. You’re informed, prepared, and capable, ready to face CAD head-on.

Coronary Computed Tomography Angiography (CCTA)

A non-invasive procedure, Coronary Computed Tomography Angiography helps us detect, measure, and understand CAD better. So, let’s together shed some light on this fascinating process.

You might already know that your heart, a little powerhouse, relies on a network of arteries to get the oxygen-rich blood it needs to function well. But CAD throws a wrench into this smooth process. This disease narrows and hardens these arteries, obstructing the blood flow. That’s where CCTA steps up to the plate.

CCTA acts like a highly detailed, sophisticated camera. This camera takes multiple images of your heart from different angles. It uses a combination of X-rays and computer technology to capture these images, creating cross-sectional views of your heart and its arteries.259Serruys PW, Hara H, Garg S, Kawashima H, Nørgaard BL, Dweck MR, Bax JJ, Knuuti J, Nieman K, Leipsic JA, Mushtaq S, Andreini D, Onuma Y. Coronary Computed Tomographic Angiography for Complete Assessment of Coronary Artery Disease: JACC State-of-the-Art Review. J Am Coll Cardiol. 2021 Aug 17;78(7):713-736. doi: 10.1016/j.jacc.2021.06.019. PMID: 34384554.

This technology is so advanced that it can visualize both the arteries and the blood within them. By injecting a harmless dye into your vein before the procedure, the CCTA can highlight your coronary arteries. This gives doctors a clearer look at any blockages or narrow areas that could be signs of CAD.260Sun Z. Coronary CT angiography: Beyond morphological stenosis analysis. World J Cardiol. 2013 Dec 26;5(12):444-52. doi: 10.4330/wjc.v5.i12.444. PMID: 24392188; PMCID: PMC3879698.

At this point, you might wonder how this feels, having such detailed images taken of your heart. It’s quite simple and straightforward. During a CCTA, you lie on a table that slides into a large, donut-shaped machine. This machine then takes images as the table moves. You might feel a warm flush when the dye is injected, but that’s it. It’s non-invasive and usually quick, often completed within 15 minutes.261Ramjattan NA, Lala V, Kousa O, et al. Coronary CT Angiography. [Updated 2023 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470279/

But why all this effort? Why do doctors want these detailed images? Well, the answer is simple and crucial. The CCTA offers a wealth of information to doctors. It helps them understand the extent of CAD, locate the blockages, and gauge their severity. This data is incredibly important when it comes to choosing the most suitable treatment approach for you.262Ramjattan NA, Lala V, Kousa O, et al. Coronary CT Angiography. [Updated 2023 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470279/

CCTA also shines in situations where other tests fall short. For instance, if your stress test results are inconclusive or inconsistent with your symptoms, CCTA can provide further clarity. By offering a direct visualization of your coronary arteries, it provides a more definitive assessment of CAD (Claim 25).

Plus, the benefits of CCTA aren’t limited to just diagnosing CAD. This incredible tool also has a say in how your treatment journey unfolds. By mapping out the anatomy of your heart and coronary arteries, it provides doctors with a blueprint. This detailed understanding helps in planning interventions like angioplasty or bypass surgery if needed.263Mueller J, Jeudy J, Poston R, White CS. Cardiac CT angiography after coronary bypass surgery: prevalence of incidental findings. AJR Am J Roentgenol. 2007 Aug;189(2):414-9. doi: 10.2214/AJR.06.0736. PMID: 17646469; PMCID: PMC4146433.

CCTA also serves as a sort of ‘health check’ for your heart. It allows doctors to monitor your heart’s health over time, especially if you’re undergoing treatment for CAD. With CCTA, they can evaluate how effective the treatment has been and make necessary adjustments to keep you on track.

But remember, while it’s a powerful tool, CCTA isn’t always the first choice for everyone. Depending on various factors like your age, overall health, and risk of CAD, doctors might opt for other diagnostic tests. It’s all about finding the best approach for you, the one that helps us understand your unique heart best.

So there you have it, the story of CCTA and its role in CAD. It’s like a superhero of the diagnostic world, revealing what’s often hidden, guiding treatment decisions, and keeping an eye on your heart’s well-being. With it, you’re armed with knowledge, ready to face CAD with strength and courage. After all, every beat counts in this journey towards heart health.

CCTA isn’t just a fancy camera capturing heart images; it’s a key player in assessing your risk of a heart attack. It helps visualize and measure calcifications or ‘plaques’ in the coronary arteries. This gives an insight into your overall ‘calcium score,’ a significant marker of heart attack risk.264Shreya D, Zamora DI, Patel GS, Grossmann I, Rodriguez K, Soni M, Joshi PK, Patel SC, Sange I. Coronary Artery Calcium Score – A Reliable Indicator of Coronary Artery Disease? Cureus. 2021 Dec 3;13(12):e20149. doi: 10.7759/cureus.20149. PMID: 35003981; PMCID: PMC8723785.

But remember, even though CCTA is a wonderful tool, it’s not standalone. It’s part of a bigger toolkit that your doctor uses to understand and manage your CAD. And while it’s natural to feel a little anxious about medical tests and procedures, remember that every step, every piece of knowledge, is a stride towards understanding and managing your heart health.

Biomarkers in Coronary Artery Disease (CAD)

Picture this: your body is like a busy city. It sends signals about its well-being, akin to how a city’s energy reflects its daily activities. And in the middle of this active city, biomarkers are like signposts. They provide valuable insights into the state of your heart health. They’re substances found in your blood that change in response to CAD, and their levels help doctors understand what’s going on inside your heart.

Troponin: Consider Troponin, for example. Troponin is released into the bloodstream when there is an injury to the heart muscle as a result of, say, myocardial infarction (heart attack). It’s like an SOS from your heart, letting doctors know that your heart is in distress.265Stark M, Kerndt CC, Sharma S. Troponin. [Updated 2023 Apr 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507805/

CRP: Another biomarker for coronary artery disease is C-reactive protein (CRP). CRP is released into your bloodstream when there’s inflammation somewhere in your body, and CAD is fundamentally an inflammatory process. So, elevated levels of CRP may indicate that CAD is present and causing inflammation in your heart arteries.266Emerging Risk Factors Collaboration; Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, Collins R, Danesh J. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet. 2010 Jan 9;375(9709):132-40. doi: 10.1016/S0140-6736(09)61717-7. Epub 2009 Dec 22. PMID: 20031199; PMCID: PMC3162187.

In addition to helping diagnose CAD, biomarkers like Troponin and CRP also help gauge the severity of your disease. Higher levels generally indicate more severe disease. They also guide treatment decisions. If your Troponin levels remain high over time, for instance, it suggests ongoing damage to your heart, signaling to your doctor that more aggressive treatment may be necessary.267Gherasim L. Troponins in Heart Failure – a Perpetual Challenge. Maedica (Bucur). 2019 Dec;14(4):371-377. doi: 10.26574/maedica.2019.14.4.371. PMID: 32153668; PMCID: PMC7035435.

Myeloperoxidase and Lipoprotein-associated phospholipase A2: Now, the world of biomarkers isn’t static – it’s always evolving, just like our understanding of CAD. Newer biomarkers, like Myeloperoxidase and Lipoprotein-associated phospholipase A2, are being studied for their potential role in predicting CAD risk. The hope is to catch CAD even before it becomes apparent, providing a head start in the race against this disease.268Chaikijurajai T, Tang WHW. Myeloperoxidase: a potential therapeutic target for coronary artery disease. Expert Opin Ther Targets. 2020 Jul;24(7):695-705. doi: 10.1080/14728222.2020.1762177. Epub 2020 May 7. PMID: 32336171; PMCID: PMC7387188.269Sofogianni A, Alkagiet S, Tziomalos K. Lipoprotein-associated Phospholipase A2 and Coronary Heart Disease. Curr Pharm Des. 2018;24(3):291-296. doi: 10.2174/1381612824666180111110550. PMID: 29332572.

B-type natriuretic peptide (BNP) and N-terminal pro b-type natriuretic peptide (NT-proBNP): Consider B-type natriuretic peptide (BNP) and N-terminal pro b-type natriuretic peptide (NT-proBNP) for starters. You’d commonly hear about these when discussing heart failure, but their story doesn’t end there. Elevated levels of BNP and NT-proBNP can also signal acute coronary syndromes, providing extra clues for the CAD detective in your doctor.270Goyal BM, Sharma SM, Walia M. B-type natriuretic peptide levels predict extent and severity of coronary artery disease in non-ST elevation acute coronary syndrome and normal left ventricular function. Indian Heart J. 2014 Mar-Apr;66(2):183-7. doi: 10.1016/j.ihj.2013.12.015. Epub 2013 Dec 26. PMID: 24814112; PMCID: PMC4017577.271Weber M, Mitrovic V, Hamm C. B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide – Diagnostic role in stable coronary artery disease. Exp Clin Cardiol. 2006 Summer;11(2):99-101. PMID: 18651043; PMCID: PMC2274852.

HDL: Then there’s High-density lipoprotein (HDL) cholesterol. Known as the ‘good’ cholesterol, it acts like a friendly neighborhood watch for your heart. Higher HDL levels are usually associated with lower CAD risk. Although not exclusive to CAD, shifts in HDL can give you a sense of your overall heart health.272Toth, P. P. (2004). High-density lipoprotein and cardiovascular risk. Circulation, 109(15), 1809–1812. https://doi.org/10.1161/01.cir.0000126889.97626.b8

Homocysteine: Let’s not forget Homocysteine, an amino acid in your blood. When its levels are high, it’s been linked to an increased risk of CAD. But its precise role and value as a CAD biomarker are still topics of scientific debate.273Ganguly P, Alam SF. Role of homocysteine in the development of cardiovascular disease. Nutr J. 2015 Jan 10;14:6. doi: 10.1186/1475-2891-14-6. PMID: 25577237; PMCID: PMC4326479.

Fibrinogen: Fibrinogen is another intriguing character. This protein has a crucial role in blood clot formation. If its levels rise, it might suggest an increased risk of CAD because of a greater tendency for blood clots to form within your heart arteries.274Shi Y, Wu Y, Bian C, Zhang W, Yang J, Xu G. Predictive value of plasma fibrinogen levels in patients admitted for acute coronary syndrome. Tex Heart Inst J. 2010;37(2):178-83. PMID: 20401290; PMCID: PMC2851424.

Lipoprotein: Meet Lipoprotein(a), or Lp(a), a unique lipoprotein that shuttles cholesterol around in your blood. High Lp(a) levels are considered a potential risk factor for CAD. However, researchers are still unraveling the mystery of Lp(a)’s role in diagnosing and managing CAD.275Mellwig KP, Horstkotte D, van Buuren F. Lipoprotein (a) and coronary heart disease – is there an efficient secondary prevention? Clin Res Cardiol Suppl. 2017 Mar;12(Suppl 1):18-21. doi: 10.1007/s11789-017-0088-x. PMID: 28233270; PMCID: PMC5352755.

LDL: You might think of LDL cholesterol as the arch-villain of coronary artery disease. It’s the ‘bad’ cholesterol, the one that, when levels rise, encourages the formation of artery-clogging plaques, triggering a cascade of events leading to CAD (Claim 46). It’s like a character in a movie who seems harmless at first but slowly reveals their true, destructive nature.

Triglycerides: Then we have triglycerides, fats in your blood that, if unchecked, can contribute to the drama. When these levels escalate in the company of high LDL or low HDL cholesterol, they act as a partner-in-crime, aiding in the development of atherosclerosis, that fatty buildup on artery walls and a major culprit behind CAD.276Miller, M., Stone, N. J., Ballantyne, C., Bittner, V., Criqui, M. H., Ginsberg, H. N., Goldberg, A. C., Howard, W. J., Jacobson, M. S., Kris-Etherton, P. M., Lennie, T. A., Levi, M., Mazzone, T., & Pennathur, S. (2011). Triglycerides and cardiovascular disease. Circulation, 123(20), 2292–2333. https://doi.org/10.1161/cir.0b013e3182160726 Think of triglycerides as an accomplice, an enabler, making the bad situation worse.

Lipoprotein-Associated Phospholipase A2: Next in our story is an enzyme called Lipoprotein-Associated Phospholipase A2 (Lp-PLA2). This character plays a role in inflammation and atherosclerosis. It’s a bit of a wildcard. Studies suggest it could be a useful marker for cardiovascular risk, but scientists are still deciphering its true role in the plot.277Madjid M, Ali M, Willerson JT. Lipoprotein-associated phospholipase A2 as a novel risk marker for cardiovascular disease: a systematic review of the literature. Tex Heart Inst J. 2010;37(1):25-39. PMID: 20200624; PMCID: PMC2829807.

Interleukin-6: Let’s also talk about Interleukin-6 (IL-6), a tiny but mighty protein. As a pro-inflammatory cytokine, it acts like a cellular gossip, spreading the word about inflammation, a process implicated in CAD. When IL-6 levels rise, it could be a sign that your heart’s tale is taking a dramatic turn.278Su JH, Luo MY, Liang N, Gong SX, Chen W, Huang WQ, Tian Y, Wang AP. Interleukin-6: A Novel Target for Cardio-Cerebrovascular Diseases. Front Pharmacol. 2021 Aug 24;12:745061. doi: 10.3389/fphar.2021.745061. PMID: 34504432; PMCID: PMC8421530.

Matrix Metalloproteinases: Next is Matrix Metalloproteinases (MMPs), the behind-the-scenes workers involved in tissue remodeling and disease processes. They might not be front and center, but they’re key to the plot, especially when it comes to the changes in your heart after a cardiac event.279Mittal B, Mishra A, Srivastava A, Kumar S, Garg N. Matrix metalloproteinases in coronary artery disease. Adv Clin Chem. 2014;64:1-72. doi: 10.1016/b978-0-12-800263-6.00001-x. PMID: 24938016.

Soluble ST2 (sST2): Imagine, if you will, the biomarker Soluble ST2 (sST2) as a silent observer, quietly watching the state of your body. This molecule is part of the interleukin 1 receptor family and springs into action when it senses tissue damage, becoming elevated. It’s like a watchman, sounding an alarm that something might be wrong in the context of CAD. Their presence might be more telling about the cardiovascular diseases prognosis than we thought.280Zhang J, Chen Z, Ma M, He Y. Soluble ST2 in coronary artery disease: Clinical biomarkers and treatment guidance. Front Cardiovasc Med. 2022 Sep 26;9:924461. doi: 10.3389/fcvm.2022.924461. PMID: 36225958; PMCID: PMC9548599.

Apolipoprotein B (ApoB): Next, we meet Apolipoprotein B (ApoB). This biomarker is like a master of disguise. It’s a major part of LDL cholesterol, and each LDL particle contains one ApoB molecule. The tricky part is that its levels might provide more insights into the total number of atherogenic (plaque-forming) particles, key players in the story of CAD.281Behbodikhah J, Ahmed S, Elyasi A, Kasselman LJ, De Leon J, Glass AD, Reiss AB. Apolipoprotein B and Cardiovascular Disease: Biomarker and Potential Therapeutic Target. Metabolites. 2021 Oct 8;11(10):690. doi: 10.3390/metabo11100690. PMID: 34677405; PMCID: PMC8540246.

Cystatin C: Cystatin C is another biomarker worth noting. This protein might seem nondescript at first, being produced at a constant rate by all human cells. But its real power lies in its ability to act as a mirror, reflecting how well the kidneys are clearing it from the bloodstream. It’s a quiet contender, and researchers think it might be a potential early warning sign for the risk of CAD, particularly in individuals with reduced kidney function.282van der Laan SW, Fall T, Soumaré A, Teumer A, Sedaghat S, Baumert J, Zabaneh D, van Setten J, Isgum I, Galesloot TE, Arpegård J, Amouyel P, Trompet S, Waldenberger M, Dörr M, Magnusson PK, Giedraitis V, Larsson A, Morris AP, Felix JF, Morrison AC, Franceschini N, Bis JC, Kavousi M, O’Donnell C, Drenos F, Tragante V, Munroe PB, Malik R, Dichgans M, Worrall BB, Erdmann J, Nelson CP, Samani NJ, Schunkert H, Marchini J, Patel RS, Hingorani AD, Lind L, Pedersen NL, de Graaf J, Kiemeney LA, Baumeister SE, Franco OH, Hofman A, Uitterlinden AG, Koenig W, Meisinger C, Peters A, Thorand B, Jukema JW, Eriksen BO, Toft I, Wilsgaard T, Onland-Moret NC, van der Schouw YT, Debette S, Kumari M, Svensson P, van der Harst P, Kivimaki M, Keating BJ, Sattar N, Dehghan A, Reiner AP, Ingelsson E, den Ruijter HM, de Bakker PI, Pasterkamp G, Ärnlöv J, Holmes MV, Asselbergs FW. Cystatin C and Cardiovascular Disease: A Mendelian Randomization Study. J Am Coll Cardiol. 2016 Aug 30;68(9):934-45. doi: 10.1016/j.jacc.2016.05.092. PMID: 27561768; PMCID: PMC5451109.

Galectin-3: Have you ever considered your body’s fibrosis processes? This is where Galectin-3 (Gal-3) enters the scene. As a biomarker, Gal-3 is like the director of a complex biological play. It’s known for its role in the formation of scar tissue (fibrosis) in the heart. When Gal-3 levels rise, it could signify more profound fibrotic activity in your body, potentially warning about the risk of CAD.283Gao Z, Liu Z, Wang R, Zheng Y, Li H, Yang L. Galectin-3 Is a Potential Mediator for Atherosclerosis. J Immunol Res. 2020 Feb 14;2020:5284728. doi: 10.1155/2020/5284728. PMID: 32149158; PMCID: PMC7042544.

Growth Differentiation Factor-15: Then, there’s Growth Differentiation Factor-15 (GDF-15). It’s the quiet member of the cast, a protein that’s normally present at low levels. However, when your body experiences stress, such as inflammation or injury, GDF-15 gets a starring role and its levels rise. This feature makes it an interesting character in the CAD story, potentially signaling the presence of cardiovascular stress.284Wollert KC, Kempf T, Wallentin L. Growth Differentiation Factor 15 as a Biomarker in Cardiovascular Disease. Clin Chem. 2017 Jan;63(1):140-151. doi: 10.1373/clinchem.2016.255174. Epub 2016 Oct 25. PMID: 28062617.

Heart-Type Fatty Acid-Binding Protein (H-FABP): Let’s bring on stage the Heart-Type Fatty Acid-Binding Protein (H-FABP). Despite its cumbersome name, H-FABP is a rather nimble player. It’s a small protein released from the heart soon after an injury to heart muscle cells – acting as an early alarm system of sorts. It might not be as famous as troponin, but it’s an important biomarker that can provide early evidence of a heart attack, adding a critical chapter to our CAD narrative.285Rezar R, Jirak P, Gschwandtner M, Derler R, Felder TK, Haslinger M, Kopp K, Seelmaier C, Granitz C, Hoppe UC, Lichtenauer M. Heart-Type Fatty Acid-Binding Protein (H-FABP) and its Role as a Biomarker in Heart Failure: What Do We Know So Far? J Clin Med. 2020 Jan 7;9(1):164. doi: 10.3390/jcm9010164. PMID: 31936148; PMCID: PMC7019786.

High-Sensitivity Cardiac Troponin (hs-cTn): Picture if you will, High-Sensitivity Cardiac Troponin (hs-cTn). A close cousin to the troponin you might be more familiar with, this biomarker serves as a kind of scout, venturing ahead and signaling trouble even earlier after heart muscle injury.286Eggers KM, Hammarsten O, Lindahl B. Differences between high-sensitivity cardiac troponin T and I in stable populations: underlying causes and clinical implications. Clin Chem Lab Med. 2022 Nov 28;61(3):380-387. doi: 10.1515/cclm-2022-0778. PMID: 36424851. While conventional troponin tests have been standard practice in diagnosing heart attacks, this high-sensitivity version could detect lower levels of troponin, potentially indicating minor heart damage that may precede a heart attack.

Endothelin-1 (ET-1): Now, imagine your body’s highways, with information zipping back and forth. Along these routes, a molecule named Endothelin-1 (ET-1) operates. ET-1 is a powerful vasoconstrictor; it’s like the traffic police of your blood vessels, controlling how tight or relaxed they should be. When ET-1 levels are high, they could signal potential troubles such as atherosclerosis, a pivotal event in the development of CAD.287Mayyas F, Al-Jarrah M, Ibrahim K, Mfady D, Van Wagoner DR. The significance of circulating endothelin-1 as a predictor of coronary artery disease status and clinical outcomes following coronary artery catheterization. Cardiovasc Pathol. 2015 Jan-Feb;24(1):19-25. doi: 10.1016/j.carpath.2014.08.004. Epub 2014 Aug 15. PMID: 25213716; PMCID: PMC5831113.

Oxidized LDL (oxLDL): oxLDL is a modified version of LDL cholesterol. Think of it as a rogue character that’s veered off the path. It contributes to the build-up of plaques, or atheromas, in the arteries – a central theme in the story of CAD. Elevated levels of oxLDL could hint at an ongoing atherosclerosis process and increased CAD risk.288Hong CG, Florida E, Li H, Parel PM, Mehta NN, Sorokin AV. Oxidized low-density lipoprotein associates with cardiovascular disease by a vicious cycle of atherosclerosis and inflammation: A systematic review and meta-analysis. Front Cardiovasc Med. 2023 Jan 16;9:1023651. doi: 10.3389/fcvm.2022.1023651. PMID: 36727024; PMCID: PMC9885196.

Ischemia-Modified Albumin (IMA): Next up, consider Ischemia-Modified Albumin (IMA). When your heart muscle isn’t getting enough oxygen – a state known as ischemia – it sends out a distress signal. One such call for help is the appearance of IMA. It’s like a flag waving from the ramparts, a potential early sign of ischemic heart disease, one of the dangerous faces of CAD.289Ismail Oran, Bulent Oran, “Ischemia-Modified Albumin as a Marker of Acute Coronary Syndrome: The Case for Revising the Concept of “N-Terminal Modification” to “Fatty Acid Occupation” of Albumin”, Disease Markers, vol. 2017, Article ID 5692583, 8 pages, 2017. https://doi.org/10.1155/2017/5692583

MicroRNA (miRNA): Let’s meet MicroRNA (miRNA), these tiny yet mighty molecules that control the activity of various genes. Some specific miRNAs have been found to be tell-tale signs of various diseases, including CAD. They might not be in the limelight often, but their role in predicting CAD makes them crucial to our story.290Melak T, Baynes HW. Circulating microRNAs as possible biomarkers for coronary artery disease: a narrative review. EJIFCC. 2019 Jun 24;30(2):179-194. PMID: 31263392; PMCID: PMC6599194.

HbA1c: Picture yourself in an unfamiliar city. Navigating through this place requires a map, some landmarks, and directions, right? Well, let’s imagine Glycated Hemoglobin (HbA1c) as one of these landmarks. HbA1c is a well-known biomarker used to monitor long-term blood sugar control in people with diabetes. But why is it important to our CAD story? You see, diabetes is a major risk factor for CAD. If HbA1c levels are high, it could mean that blood sugar hasn’t been well controlled over the past few months, and this could indirectly suggest a higher risk for CAD development.291Khan FR, Ali J, Ullah R, Hassan Z, Khattak S, Lakhta G, Gul N. Relationship Between High Glycated Hemoglobin and Severity of Coronary Artery Disease in Type II Diabetic Patients Hospitalized With Acute Coronary Syndrome. Cureus. 2021 Mar 6;13(3):e13734. doi: 10.7759/cureus.13734. PMID: 33842112; PMCID: PMC8021276.

Pregnancy-Associated Plasma Protein-A (PAPP-A): Now, let’s add another character to our story – the Pregnancy-Associated Plasma Protein-A (PAPP-A). Now, before you get puzzled by its name, PAPP-A isn’t only associated with pregnancy. Elevated levels of PAPP-A have been linked to the presence of vulnerable plaques in the arteries, a ticking time bomb that could lead to a heart attack, an end-stage event in CAD.292Pregnancy-Associated Plasma Protein-A (PAPP-A)

Circulating Endothelial Cells (CECs): Next is Circulating Endothelial Cells (CECs). As the name suggests, these are cells from the lining of your blood vessels, the endothelium, that have somehow ended up in the bloodstream. Increased numbers of CECs could indicate ongoing damage to the blood vessel walls, a crucial event in the early stages of atherosclerosis and CAD.293Farinacci M, Krahn T, Dinh W, Volk HD, Düngen HD, Wagner J, Konen T, von Ahsen O. Circulating endothelial cells as biomarker for cardiovascular diseases. Res Pract Thromb Haemost. 2018 Oct 26;3(1):49-58. doi: 10.1002/rth2.12158. PMID: 30656276; PMCID: PMC6332781.

Extracellular Vesicles (EVs): Did you ever consider that the body has its own internal postal system? Picture Vesicles, particularly Extracellular Vesicles (EVs), as the postmen of your body. These tiny structures carry important information in the form of proteins, lipids, and even genetic material from one cell to another. Emerging research suggests that the presence and content of these vesicles could provide invaluable information about the state of CAD.294Boulanger CM, Loyer X, Rautou PE, Amabile N. Extracellular vesicles in coronary artery disease. Nat Rev Cardiol. 2017 May;14(5):259-272. doi: 10.1038/nrcardio.2017.7. Epub 2017 Feb 2. PMID: 28150804.

CD40 Ligand (CD40L): Let’s meet CD40 Ligand (CD40L). This biomarker plays a key role in the body’s immune response. When triggered, CD40L sets off a cascade of events leading to inflammation – the body’s own fire alarm. Increased levels of CD40L have been linked to the progression of CAD, possibly by promoting inflammation and the formation of blood clots.295Angeli, Fabio, Verdecchia, Paolo, Savonitto, Stefano, Cavallini, Sara, Santucci, Andrea, Coiro, Stefano, Sclafani, Rocco, Riccini, Clara, De Servi, Stefano and Cavallini, Claudio. “Soluble CD40 ligand and outcome in patients with coronary artery disease undergoing percutaneous coronary intervention” Clinical Chemistry and Laboratory Medicine (CCLM), vol. 60, no. 1, 2022, pp. 118-126. https://doi.org/10.1515/cclm-2021-0817

Pentraxin 3 (PTX3): Pentraxin 3 (PTX3), an acute-phase protein like CRP but with a higher specificity to vascular inflammation, steps into the spotlight. It might not be a household name, but research is starting to acknowledge PTX3’s potential. It’s been found to be elevated in those with severe CAD, signaling a high level of inflammation and thus potential risk.296Chu Y, Teng J, Feng P, Liu H, Wang F, Li X. Pentraxin-3 in coronary artery disease: A meta-analysis. Cytokine. 2019 Jul;119:197-201. doi: 10.1016/j.cyto.2019.03.017. Epub 2019 Apr 4. PMID: 30954865.

Adiponectin: Adiponectin secreted by fat cells, is a friendly face in the crowd. As an insulin-sensitizing hormone, it generally plays a beneficial role. But in the CAD narrative, its presence signifies trouble. Lower adiponectin levels have been linked with the presence and severity of CAD, making it an intriguing player in our investigation.297Orlando A, Nava E, Giussani M, Genovesi S. Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents. Int J Mol Sci. 2019 Jun 30;20(13):3228. doi: 10.3390/ijms20133228. PMID: 31262082; PMCID: PMC6651242.

Albumin: While most biomarkers tend to speak up when things go wrong, Albumin does the opposite. The most abundant protein in your blood, Albumin levels dip when cardiovascular health is in jeopardy. This decrease is associated with poor prognosis in CAD, so keeping an eye on this silent biomarker is critical.298Orlando A, Nava E, Giussani M, Genovesi S. Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents. Int J Mol Sci. 2019 Jun 30;20(13):3228. doi: 10.3390/ijms20133228. PMID: 31262082; PMCID: PMC6651242.

Vitamin D: Vitamin D, a vital nutrient known for its role in bone health, also has a tale to tell in CAD. Emerging evidence suggests a link between Vitamin D deficiency and CAD. Low levels of Vitamin D may lead to an increased risk of CAD, and regular monitoring could be beneficial in CAD management.299Aggarwal R, Akhthar T, Jain SK. Coronary artery disease and its association with Vitamin D deficiency. J Midlife Health. 2016 Apr-Jun;7(2):56-60. doi: 10.4103/0976-7800.185334. PMID: 27499590; PMCID: PMC4960940.

Asymmetric dimethylarginine (ADMA): Asymmetric dimethylarginine (ADMA), a byproduct of protein processing in cells. This subtle compound can interfere with the production of nitric oxide, a molecule that helps keep your blood vessels flexible. An excess of ADMA could lead to impaired blood vessel relaxation, a precursor to CAD.300Ghayour-Mobarhan M, Ayati N, Sahebkar A, Moohebati M, Ayati N, Elyasi S, Mohammadpour AH. Evaluation of serum Asymmetric Dimethyl Arginine concentrations in coronary artery disease patients without traditional cardiovascular risk factors. Acta Biomed. 2018 Jun 7;89(2):203-208. doi: 10.23750/abm.v89i2.5335. PMID: 29957752; PMCID: PMC6179032.

Insulin-like growth factor-1 (IGF-1): The next biomarker is Insulin-like growth factor-1 (IGF-1). Research finds that a lower level of circulating IGF-1 can be linked with an increased risk of developing CAD. Like a double-edged sword, while it is essential for normal tissue maintenance, a deficiency could be harmful.301Larsson, S.C., Michaëlsson, K. & Burgess, S. IGF-1 and cardiometabolic diseases: a Mendelian randomisation study. Diabetologia 63, 1775–1782 (2020). https://doi.org/10.1007/s00125-020-05190-9

Resistin: Another biomarker to consider is Resistin, a hormone produced by adipose tissue. Researchers have found that higher levels of Resistin are associated with CAD, signifying its role in the disease’s inflammatory processes. Hence, monitoring Resistin levels might provide valuable insights into inflammation’s role in CAD progression.302Askin L, Abus S, Tanriverdi O. Resistin and Cardiovascular Disease: A Review of the Current Literature Regarding Clinical and Pathological Relationships. Curr Cardiol Rev. 2022;18(1):e290721195114. doi: 10.2174/1573403X17666210729101120. PMID: 34325643; PMCID: PMC9241124.

Uric Acid: Now, picture Uric Acid, a waste product that your body produces when it breaks down purines, substances found in certain foods. This seemingly innocent substance, when elevated, is associated with a higher risk of CAD. It serves as a reminder that even waste products have essential roles in our body’s storytelling.303Rahimi-Sakak, F., Maroofi, M., Rahmani, J. et al. Serum uric acid and risk of cardiovascular mortality: a systematic review and dose-response meta-analysis of cohort studies of over a million participants. BMC Cardiovasc Disord 19, 218 (2019). https://doi.org/10.1186/s12872-019-1215-z

Fibroblast growth factor 23 (FGF23): Let’s take a look at another biomarker, Fibroblast growth factor 23 (FGF23), a protein that helps regulate phosphate metabolism in your body. It’s been found that elevated levels of FGF23 are linked with an increased risk of CAD, emphasizing the need for proper mineral balance for heart health.304Batra J, Buttar RS, Kaur P, Kreimerman J, Melamed ML. FGF-23 and cardiovascular disease: review of literature. Curr Opin Endocrinol Diabetes Obes. 2016 Dec;23(6):423-429. doi: 10.1097/MED.0000000000000294. PMID: 27652999; PMCID: PMC6936216.

Endostatin: Now, introduce yourself to Endostatin, a protein that inhibits angiogenesis (the formation of new blood vessels). Researchers have found that higher Endostatin levels are associated with severe CAD, pointing to its influence on the body’s vascular network and thus on heart health.305El-Ashmawy HM, Roshdy HS, Saad Z, Ahmed AM. Serum endostatin level as a marker for coronary artery calcification in type 2 diabetic patients. J Saudi Heart Assoc. 2019 Jan;31(1):24-31. doi: 10.1016/j.jsha.2018.09.001. Epub 2018 Sep 20. PMID: 30364696; PMCID: PMC6197639.

E-selectin: And there’s also E-selectin, a cell adhesion molecule expressed only on endothelial cells activated by inflammation. The presence of E-selectin is indicative of an inflammatory response and has been linked to CAD, pointing towards the critical role inflammation plays in CAD progression.306Gorący J, Kaczmarczyk M, Ciechanowicz A, Safranow K, Gorący J, Jakubowska K, Chlubek D, Gorący I. E-selectin gene haplotypes are associated with the risk of myocardial infarction. Arch Med Sci. 2019 Sep;15(5):1223-1231. doi: 10.5114/aoms.2019.84413. Epub 2019 Apr 9. PMID: 31572467; PMCID: PMC6764297.

Plasminogen activator inhibitor-1: Plasminogen activator inhibitor-1 is also a CAD marker. If there’s too much PAI-1 in town, it might stir up trouble by forming clots that can’t easily be broken down, potentially raising the risk of heart disease.307Jung, R.G., Motazedian, P., Ramirez, F.D. et al. Association between plasminogen activator inhibitor-1 and cardiovascular events: a systematic review and meta-analysis. Thrombosis J 16, 12 (2018). https://doi.org/10.1186/s12959-018-0166-4

Apolipoprotein A-I (ApoA-I): Now let’s turn our attention to Apolipoprotein A-I (ApoA-I). It’s the main protein found in “good cholesterol” and helps with the housekeeping task of shuttling cholesterol away from where it’s not needed. But if there’s a shortage of ApoA-I, you could be at greater risk for heart disease.308Karjalainen MK, Holmes MV, Wang Q, Anufrieva O, Kähönen M, Lehtimäki T, Havulinna AS, Kristiansson K, Salomaa V, Perola M, Viikari JS, Raitakari OT, Järvelin MR, Ala-Korpela M, Kettunen J. Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study. Atherosclerosis. 2020 Apr;299:56-63. doi: 10.1016/j.atherosclerosis.2020.02.002. Epub 2020 Feb 14. PMID: 32113648.

Vascular cell adhesion molecule 1 (VCAM-1): Speaking of moving things around, meet Vascular cell adhesion molecule 1 (VCAM-1). This protein is like a sticky note that helps certain white blood cells adhere to blood vessel walls. If there’s too much VCAM-1, it might indicate inflammation and a higher risk of CAD.309Kaur, G., Sharma, D., Bisen, S. et al. Vascular cell-adhesion molecule 1 (VCAM-1) regulates JunB-mediated IL-8/CXCL1 expression and pathological neovascularization. Commun Biol 6, 516 (2023). https://doi.org/10.1038/s42003-023-04905-z

YKL-40: YKL-40, a glycoprotein often tied to inflammation and malfunctioning endothelial cells, has lately been turning heads as a potential CAD marker. It seems that people with CAD often have more YKL-40 than they should.310Rathcke, C.N., Vestergaard, H. YKL-40 – an emerging biomarker in cardiovascular disease and diabetes. Cardiovasc Diabetol 8, 61 (2009). https://doi.org/10.1186/1475-2840-8-61

Neopterin: Neopterin is another molecule to consider. This byproduct of cellular metabolism has been seen at higher levels in CAD patients, suggesting it could be an alarm bell for immune response and oxidative stress.311Pacileo M, Cirillo P, De Rosa S, Ucci G, Petrillo G, Musto D’Amore S, Sasso L, Maietta P, Spagnuolo R, Chiariello M. The role of neopterin in cardiovascular disease. Monaldi Arch Chest Dis. 2007 Jun;68(2):68-73. doi: 10.4081/monaldi.2007.454. PMID: 17886766.

Thrombospondin-1 (TSP-1): Thrombospondin-1 (TSP-1) comes into play. TSP-1 is like a social networker among cells. But in the context of CAD, this networker might be facilitating dangerous connections, as higher levels of TSP-1 have been associated with heart disease.312Zhang K, Li M, Yin L, Fu G, Liu Z. Role of thrombospondin‑1 and thrombospondin‑2 in cardiovascular diseases (Review). Int J Mol Med. 2020 May;45(5):1275-1293. doi: 10.3892/ijmm.2020.4507. Epub 2020 Feb 20. PMID: 32323748; PMCID: PMC7138268.

Chemokine ligand 5 (CCL5): Next is Chemokine ligand 5 (CCL5), also known as RANTES. Acting like a sort of chemical signal, CCL5 calls upon white blood cells, especially during inflammatory processes. High CCL5 is associated with increased CAD.313Herder C, Peeters W, Illig T, Baumert J, de Kleijn DP, Moll FL, Poschen U, Klopp N, Müller-Nurasyid M, Roden M, Preuss M; CARDIoGRAM Consortium; Karakas M, Meisinger C, Thorand B, Pasterkamp G, Koenig W, Assimes TL, Deloukas P, Erdmann J, Holm H, Kathiresan S, König IR, McPherson R, Reilly MP, Roberts R, Samani NJ, Schunkert H, Stewart AF. RANTES/CCL5 and risk for coronary events: results from the MONICA/KORA Augsburg case-cohort, Athero-Express and CARDIoGRAM studies. PLoS One. 2011;6(12):e25734. doi: 10.1371/journal.pone.0025734. Epub 2011 Dec 6. PMID: 22162987; PMCID: PMC3232218.

Fibronectin: Next, we have Fibronectin, a protein that acts as a sort of glue in the extracellular matrix and aids in wound healing. In CAD, elevated Fibronectin levels could indicate vascular damage, hence its potential role as a biomarker.314Zhang, X., Hu, C., Wu, Hm. et al. Fibronectin type III domain-containing 5 in cardiovascular and metabolic diseases: a promising biomarker and therapeutic target. Acta Pharmacol Sin 42, 1390–1400 (2021). https://doi.org/10.1038/s41401-020-00557-5

Heat shock proteins (HSP): Focusing on Heat shock proteins (HSPs), which are like the body’s emergency response team during times of cellular stress. Particularly, HSP60 and HSP70 have been noted in CAD, with research suggesting they may contribute to atherosclerosis.315Pockley AG, Frostegård J. Heat shock proteins in cardiovascular disease and the prognostic value of heat shock protein related measurements. Heart. 2005 Sep;91(9):1124-6. doi: 10.1136/hrt.2004.059220. PMID: 16103532; PMCID: PMC1769066.

Renin: Next is Renin, a hormone that plays a significant role in blood pressure regulation and fluid balance. Changes in renin levels have been linked with CAD, possibly due to their influence on blood pressure and vascular health.316Hammoud RA, Vaccari CS, Nagamia SH, Khan BV. Regulation of the renin-angiotensin system in coronary atherosclerosis: a review of the literature. Vasc Health Risk Manag. 2007;3(6):937-45. PMID: 18200812; PMCID: PMC2350139.

Cathepsin S: Then we have Cathepsin S, a protein-cleaving enzyme. Elevated levels of Cathepsin S have been found in people with CAD, suggesting it might play a role in atherosclerosis, potentially by promoting inflammation and plaque instability.317Jing Y, Shi J, Lu B, Zhang W, Yang Y, Wen J, Hu R, Yang Z, Wang X. Association of Circulating Cathepsin S and Cardiovascular Disease Among Patients With Type 2 Diabetes: A Cross-Sectional Community-Based Study. Front Endocrinol (Lausanne). 2021 Mar 5;12:615913. doi: 10.3389/fendo.2021.615913. PMID: 33746900; PMCID: PMC7973458.

Monocyte chemoattractant protein 1 (MCP-1): The protein Monocyte chemoattractant protein 1 (MCP-1) deserves attention as it’s involved in recruiting monocytes to the sites of inflammation. Increased MCP-1 levels have been found in CAD patients, highlighting its role in inflammation and atherosclerosis.318Ikeda U, Matsui K, Murakami Y, Shimada K. Monocyte chemoattractant protein-1 and coronary artery disease. Clin Cardiol. 2002 Apr;25(4):143-7. doi: 10.1002/clc.4960250403. PMID: 12000070; PMCID: PMC6654294.

Cadherins: Next, let’s delve into Cadherins, specifically, Vascular endothelial (VE)-Cadherin and N-Cadherin. These are proteins that mediate cell-to-cell adhesion. Altered levels of these Cadherins may signify endothelial cell dysfunction and increased risk of CAD.319Maria Philippova and others, T-cadherin is present on endothelial microparticles and is elevated in plasma in early atherosclerosis, European Heart Journal, Volume 32, Issue 6, March 2011, Pages 760–771, https://doi.org/10.1093/eurheartj/ehq206

Placental growth factor (PlGF): Our exploration would be incomplete without mentioning Placental growth factor (PlGF), a protein that promotes angiogenesis, or blood vessel formation. In the context of CAD, elevated PlGF levels could indicate ongoing angiogenesis, possibly as a compensatory mechanism for ischemic damage.320Matsui M, Uemura S, Takeda Y, Samejima K, Matsumoto T, Hasegawa A, Tsushima H, Hoshino E, Ueda T, Morimoto K, Okamoto K, Okada S, Onoue K, Okayama S, Kawata H, Kawakami R, Maruyama N, Akai Y, Iwano M, Shiiki H, Saito Y; NARA-CKD Investigators. Placental Growth Factor as a Predictor of Cardiovascular Events in Patients with CKD from the NARA-CKD Study. J Am Soc Nephrol. 2015 Nov;26(11):2871-81. doi: 10.1681/ASN.2014080772. Epub 2015 Mar 18. PMID: 25788536; PMCID: PMC4625670.

Soluble urokinase plasminogen activator receptor (suPAR): Further, Soluble urokinase plasminogen activator receptor (suPAR) is a protein associated with immune activation and inflammation. Higher levels of suPAR in CAD patients suggest that it might be a useful biomarker for indicating CAD severity.

Syndecans: a family of proteins that influence cell adhesion and migration – can’t be overlooked in CAD. Altered levels of Syndecans may point to a process of vascular remodeling and endothelial dysfunction in CAD.321Lunde IG, Herum KM, Carlson CC, Christensen G. Syndecans in heart fibrosis. Cell Tissue Res. 2016 Sep;365(3):539-52. doi: 10.1007/s00441-016-2454-2. Epub 2016 Jul 14. PMID: 27411689.

Osteopontin: Osteopontin is another resident of our city, a sticky character that helps cells stick to each other and move around. Just like how you’d find more glue in places where things are breaking down, we see more Osteopontin in parts of blood vessels affected by CAD, which could be a sign of increased repair activities due to atherosclerosis.322Cheong KI, Leu HB, Wu CC, Yin WH, Wang JH, Lin TH, Tseng WK, Chang KC, Chu SH, Yeh HI, Chen JW, Wu YW; National Taiwan Biosignature Research Investigators. The clinical significance of osteopontin on the cardiovascular outcomes in patients with stable coronary artery disease. J Formos Med Assoc. 2023 Apr;122(4):328-337. doi: 10.1016/j.jfma.2022.11.011. Epub 2022 Dec 7. PMID: 36494313.

Scavenger receptor class B type 1 (SR-B1): Switching gears to cholesterol regulation, picture Scavenger receptor class B type 1 (SR-B1) as the city’s waste management system. If SR-B1 isn’t working properly, it’s like the waste management team going on strike, potentially leading to a buildup of cholesterol and contributing to CAD.323Ma B, Jia J, Wang X, Zhang R, Niu S, Ni L, Di X, Liu C. Differential roles of Scavenger receptor class B type I: A protective molecule and a facilitator of atherosclerosis (Review). Mol Med Rep. 2020 Oct;22(4):2599-2604. doi: 10.3892/mmr.2020.11383. Epub 2020 Jul 28. PMID: 32945418; PMCID: PMC7453654.

Cyclin-dependent kinase inhibitor 2A (CDKN2A): Cyclin-dependent kinase inhibitor 2A (CDKN2A) can be likened to city planning regulations, controlling how the city grows and develops. Changes in CDKN2A might be akin to less strict regulations, possibly leading to ‘haphazard development’ and an increased risk of CAD.324Zhong J, Chen X, Ye H, Wu N, Chen X, Duan S. CDKN2A and CDKN2B methylation in coronary heart disease cases and controls. Exp Ther Med. 2017 Dec;14(6):6093-6098. doi: 10.3892/etm.2017.5310. Epub 2017 Oct 16. PMID: 29285163; PMCID: PMC5740815.

Sphingosine-1-phosphate (S1P): S1P is like a multipurpose tool. It helps our cells move around, multiply, and survive. There’s some evidence to suggest it might be a good guy in the story of artery-clogging plaque development, potentially helping to protect us against it.325Kurano M, Yatomi Y. Sphingosine 1-Phosphate and Atherosclerosis. J Atheroscler Thromb. 2018 Jan 1;25(1):16-26. doi: 10.5551/jat.RV17010. Epub 2017 Jul 20. PMID: 28724841; PMCID: PMC5770220.

Lipocalin-2 (LCN2): Also known by its alias, neutrophil gelatinase-associated lipocalin, LCN2 is produced by our fat cells and plays roles in inflammation, insulin resistance, and obesity. It’s like a siren, with its levels often sounding the alarm for more severe cases of CAD.326Ni J, Ma X, Zhou M, Pan X, Tang J, Hao Y, Lu Z, Gao M, Bao Y, Jia W. Serum lipocalin-2 levels positively correlate with coronary artery disease and metabolic syndrome. Cardiovasc Diabetol. 2013 Dec 21;12:176. doi: 10.1186/1475-2840-12-176. PMID: 24359145; PMCID: PMC3878105.

Fatty Acid Binding Protein 4 (FABP4): This protein is like a courier, released by fat cells into our bloodstream. High levels of FABP4 are linked to insulin resistance, diabetes, and artery plaque development, potentially warning us of future heart troubles.327von Jeinsen, B., Ritzen, L., Vietheer, J. et al. The adipokine fatty-acid binding protein 4 and cardiac remodeling. Cardiovasc Diabetol 19, 117 (2020). https://doi.org/10.1186/s12933-020-01080-x

Methylglyoxal (MG): MG is a byproduct from our sugar metabolism. Though it might seem insignificant, MG can create a storm of oxidative stress and inflammation when its levels get too high. This can be particularly troubling for people with diabetes, nudging them toward CAD.328Rabbani N, Godfrey L, Xue M, Shaheen F, Geoffrion M, Milne R, Thornalley PJ. Glycation of LDL by methylglyoxal increases arterial atherogenicity: a possible contributor to increased risk of cardiovascular disease in diabetes. Diabetes. 2011 Jul;60(7):1973-80. doi: 10.2337/db11-0085. Epub 2011 May 26. PMID: 21617182; PMCID: PMC3121424.

Leukotriene B4 (LTB4): LTB4 is a bit like a rally leader for immune cells, playing a part in their activation and movement. It’s linked to inflammation, and so, in the story of CAD, it might be one of the villains.329Satish M, Agrawal DK. Pro-resolving lipid mediators in the resolution of neointimal hyperplasia pathogenesis in atherosclerotic diseases. Expert Rev Cardiovasc Ther. 2019 Mar;17(3):177-184. doi: 10.1080/14779072.2019.1563483. Epub 2019 Jan 9. PMID: 30582389; PMCID: PMC6679914.

Chemerin: Produced by our fat cells, Chemerin has a hand in fat cell formation and sugar metabolism. If there’s too much chemerin in the system, particularly in people with metabolic syndrome, it could indicate CAD.330İnci S, Aksan G, Doğan P. Chemerin as an independent predictor of cardiovascular event risk. Ther Adv Endocrinol Metab. 2016 Apr;7(2):57-68. doi: 10.1177/2042018816629894. Epub 2016 Feb 8. PMID: 27092231; PMCID: PMC4820999.

MicroRNA-155 (miR-155): Think of miR-155 as a tiny, non-coding maestro directing the performance of our genes. If the maestro is too vigorous, it might whip up inflammatory processes, potentially playing a part in the development of CAD and artery-clogging plaque.331Cao RY, Li Q, Miao Y, Zhang Y, Yuan W, Fan L, Liu G, Mi Q, Yang J. The Emerging Role of MicroRNA-155 in Cardiovascular Diseases. Biomed Res Int. 2016;2016:9869208. doi: 10.1155/2016/9869208. Epub 2016 Nov 27. PMID: 28018919; PMCID: PMC5149600.

Hypoxia-Inducible Factor 1-alpha: Think of HIF-1α as a deep-sea diver, always responding to changes in oxygen levels. When oxygen is scarce – a condition known as hypoxia, common in atherosclerotic plaques – HIF-1α jumps into action. Research has shown that folks with CAD often have higher levels of our diver, HIF-1α, hinting at its importance in the disease’s landscape.332Semenza GL. Hypoxia-inducible factor 1 and cardiovascular disease. Annu Rev Physiol. 2014;76:39-56. doi: 10.1146/annurev-physiol-021113-170322. Epub 2013 Aug 21. PMID: 23988176; PMCID: PMC4696033.

Sortilin: Sortilin, a versatile player implicated in managing our body’s fats or lipids. However, when Sortilin gets thrown off its game, it can cause havoc in our body’s balance of lipids, potentially contributing to atherosclerosis and CAD. It’s like the manager of a team who struggles to keep things organized, affecting the overall game.333Møller PL, Rohde PD, Winther S, Breining P, Nissen L, Nykjaer A, Bøttcher M, Nyegaard M, Kjolby M. Sortilin as a Biomarker for Cardiovascular Disease Revisited. Front Cardiovasc Med. 2021 Apr 16;8:652584. doi: 10.3389/fcvm.2021.652584. PMID: 33937362; PMCID: PMC8085299.

Follistatin-like 1 (FSTL1): FSTL1 is the protective agent, exhibiting cardioprotective effects. Imagine it as the bodyguard of the heart. But when its levels drop, it could spell trouble, possibly associating with impaired heart function and worse outcomes in CAD patients.334Seki M, Powers JC, Maruyama S, Zuriaga MA, Wu CL, Kurishima C, Kim L, Johnson J, Poidomani A, Wang T, Muñoz E, Rajan S, Park JY, Walsh K, Recchia FA. Acute and Chronic Increases of Circulating FSTL1 Normalize Energy Substrate Metabolism in Pacing-Induced Heart Failure. Circ Heart Fail. 2018 Jan;11(1):e004486. doi: 10.1161/CIRCHEARTFAILURE.117.004486. PMID: 29317401; PMCID: PMC5765881.

Dipeptidyl peptidase-4: Next, meet Dipeptidyl peptidase-4, or DPP-4 for short. This worker bee in our body is super busy helping us metabolize glucose, our body’s primary source of energy. Some people use medicines called DPP-4 inhibitors to help them manage type 2 diabetes. Since diabetes and CAD are known to hang around together, any unusual activity of DPP-4 might hint that CAD is lurking around the corner.335Papagianni M, Tziomalos K. Cardiovascular effects of dipeptidyl peptidase-4 inhibitors. Hippokratia. 2015 Jul-Sep;19(3):195-9. PMID: 27418775; PMCID: PMC4938463.

Novel Diagnostic Techniques and Innovations in Coronary Artery Disease (CAD)

You’ve probably heard about CAD. It’s the usual suspect when we talk about heart diseases. And guess what, science has never been more prepared to tackle it head-on. The crux of the matter is that the earlier we catch CAD, the better the outcomes can be.336Regmi M, Siccardi MA. Coronary Artery Disease Prevention. [Updated 2023 Feb 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK547760/

One innovative technique is Coronary CT Angiography (CCTA), a type of scan that gives an ultra-detailed look at your heart and the vessels nourishing it. With this technology, doctors can see blockages with unprecedented clarity. It’s like giving them x-ray vision to see the earliest signs of CAD.

But CCTA is just the tip of the iceberg. Another innovation revolutionizing CAD diagnosis is Intravascular Ultrasound. Think of it as an insider’s tour of your arteries. It’s an ultrasound probe that doctors insert directly into the arteries to snap pictures from the inside. It’s like putting CAD under a microscope, offering a close-up view of any trouble lurking inside your arteries.337Xu J, Lo S. Fundamentals and role of intravascular ultrasound in percutaneous coronary intervention. Cardiovasc Diagn Ther. 2020 Oct;10(5):1358-1370. doi: 10.21037/cdt.2020.01.15. PMID: 33224762; PMCID: PMC7666933.

Then there’s something called Fractional Flow Reserve (FFR). Now, this isn’t about studying images; instead, it measures the pressure difference across a blockage in an artery. This way, doctors can understand how severe a blockage is, and whether it’s truly causing trouble. It’s like a weather vane for CAD, indicating when the winds of heart disease might be picking up.338Tebaldi M, Campo G, Biscaglia S. Fractional flow reserve: Current applications and overview of the available data. World J Clin Cases. 2015 Aug 16;3(8):678-81. doi: 10.12998/wjcc.v3.i8.678. PMID: 26301228; PMCID: PMC4539407.

However, the journey doesn’t stop at diagnosis. There are innovations in treatment that are changing the CAD game, too. For example, Bioresorbable Stents, which are like temporary scaffolds for weakened arteries. Unlike regular stents, these dissolve over time, reducing the risk of long-term complications. It’s almost like having a safety net that disappears once you’re back on your feet.339Zong J, He Q, Liu Y, Qiu M, Wu J, Hu B. Advances in the development of biodegradable coronary stents: A translational perspective. Mater Today Bio. 2022 Jul 19;16:100368. doi: 10.1016/j.mtbio.2022.100368. PMID: 35937578; PMCID: PMC9352968.

Consider this – the world of medicine is increasingly tapping into the power of genetics. Genomic medicine is becoming a powerful tool in our arsenal. Yes, you read that right! By studying your genes – the very essence of what makes you, you – doctors can now predict your risk of developing CAD. This goes beyond simply knowing your family history. Instead, it’s like looking into a crystal ball that can reveal what your DNA says about your CAD risk. This isn’t science fiction; it’s happening right here, right now.340Padmanabhan S, Hastie C, Prabhakaran D, Dominczak AF. Genomic approaches to coronary artery disease. Indian J Med Res. 2010 Nov;132(5):567-78. PMID: 21150009; PMCID: PMC3028944.

Genomic medicine’s wonder doesn’t end at risk prediction. It also opens up avenues for personalized treatment. In other words, your treatment plan could be as unique as you are, tailored to your genetic makeup. It’s like having a bespoke suit, but for your heart health!341Tada, H., Fujino, N., Nomura, A. et al. Personalized medicine for cardiovascular diseases. J Hum Genet 66, 67–74 (2021). https://doi.org/10.1038/s10038-020-0818-7

The innovations don’t stop at the human genome. We’re stepping into the fascinating world of nanomedicine. Nanoparticles, incredibly small particles that can carry drugs, are being explored as a method to deliver medication directly to the heart. Imagine having a fleet of tiny couriers, each carrying a small dose of medicine straight to your heart. It’s like precision-guided therapy that minimizes side effects and maximizes benefits.342Ambesh P, Campia U, Obiagwu C, Bansal R, Shetty V, Hollander G, Shani J. Nanomedicine in coronary artery disease. Indian Heart J. 2017 Mar-Apr;69(2):244-251. doi: 10.1016/j.ihj.2017.02.007. Epub 2017 Feb 24. PMID: 28460774; PMCID: PMC5414944.

But CAD management is not all about high-tech procedures and fancy drugs. It’s also about how we can improve our daily lives. There’s an explosion of mobile apps and wearable devices that can monitor your heart rate, blood pressure, and activity levels. It’s like having a personal trainer, nutritionist, and nurse all wrapped into one, right in your pocket or on your wrist! And the best part? They work 24/7, keeping a close watch on your heart health and helping you make heart-friendly lifestyle choices every day.343Dhingra LS, Aminorroaya A, Oikonomou EK, et al. Use of Wearable Devices in Individuals With or at Risk for Cardiovascular Disease in the US, 2019 to 2020. JAMA Netw Open. 2023;6(6):e2316634. doi:10.1001/jamanetworkopen.2023.16634

There’s also a surge in telemedicine. What if you could consult your doctor from the comfort of your home? Telemedicine makes that possible. It’s like a virtual bridge connecting you and your doctor, ensuring you get the care you need, no matter where you are. This means fewer trips to the hospital and more personalized, efficient care.

While we’re on the topic of promoting growth, let’s not forget stem cells. Scientists are researching ways to use stem cells regenerate heart tissue. That can potentially help us fight CAD. Imagine this: your body healing itself using its own resources. It’s like mobilizing an internal army to repair the damage caused by CAD.344Mahmud S, Alam S, Emon NU, Boby UH, Kamruzzaman, Ahmed F, Monjur-Al-Hossain ASM, Tahamina A, Rudra S, Ajrin M. Opportunities and challenges in stem cell therapy in cardiovascular diseases: Position standing in 2022. Saudi Pharm J. 2022 Sep;30(9):1360-1371. doi: 10.1016/j.jsps.2022.06.017. Epub 2022 Jun 22. PMID: 36249945; PMCID: PMC9563042.

We live in a digital age, and healthcare is no exception to this trend. We’ve already talked about mobile apps and wearable devices. But did you know there are now digital therapies available for CAD? That’s right – you can engage in guided programs designed to help you manage your heart health better. These therapies can support you in making healthier lifestyle choices, provide emotional support, and even help you navigate your treatment options. It’s like having a heart health coach on call, whenever you need it.345Li Y, Gong Y, Zheng B, Fan F, Yi T, Zheng Y, He P, Fang J, Jia J, Zhu Q, Jiang J, Huo Y. Effects on Adherence to a Mobile App-Based Self-management Digital Therapeutics Among Patients With Coronary Heart Disease: Pilot Randomized Controlled Trial. JMIR Mhealth Uhealth. 2022 Feb 15;10(2):e32251. doi: 10.2196/32251. PMID: 34906924; PMCID: PMC8889473.

When it comes to beating CAD, it’s also important to listen – literally! Acoustic detection is a new, non-invasive diagnostic technique that listens to the sounds of your coronary arteries. Like a stethoscope that listens to the sounds of your heart, this technique listens for any unusual sounds that might indicate CAD. It’s like having a heart whisperer who can interpret the rhythm of your life.346Semmlow J, Rahalkar K. Acoustic detection of coronary artery disease. Annu Rev Biomed Eng. 2007;9:449-69. doi: 10.1146/annurev.bioeng.9.060906.151840. PMID: 17425468.

Management and Treatment of Coronary Artery Disease (CAD)

Lifestyle Modifications

Navigating life with CAD might be tough, but remember, you hold the steering wheel when it comes to your heart health.

When we chat about heart health, diet probably pops into your mind first. And you’re right on the money! The choices you make in your meals can be game-changers in your fight against CAD. Picture your meals like a canvas, and you’re the artist. Paint it with the vibrant hues of fruits and vegetables. They’re packed with vital vitamins and fiber that can aid you in keeping CAD at a distance. But you’ll need to be on the lookout for trans and saturated fats, the notorious culprits in this saga. They can sneak their way into your meals, pump up your cholesterol levels, and set the groundwork for CAD. Now, that’s a plot twist you’d rather avoid! So, steer clear of processed foods, fried items, and high-fat dairy that could be their secret dens.347Du S, Kim H, Rebholz CM. Higher Ultra-Processed Food Consumption Is Associated with Increased Risk of Incident Coronary Artery Disease in the Atherosclerosis Risk in Communities Study. J Nutr. 2021 Dec 3;151(12):3746-3754. doi: 10.1093/jn/nxab285. PMID: 34494108; PMCID: PMC8643602.348Aune D, Giovannucci E, Boffetta P, Fadnes LT, Keum N, Norat T, Greenwood DC, Riboli E, Vatten LJ, Tonstad S. Fruit and vegetable intake and the risk of cardiovascular disease, total cancer and all-cause mortality-a systematic review and dose-response meta-analysis of prospective studies. Int J Epidemiol. 2017 Jun 1;46(3):1029-1056. doi: 10.1093/ije/dyw319. PMID: 28338764; PMCID: PMC5837313.

Now you may be pondering, “What’s the deal with meats and eggs?” Good news. Lean meats, fish abundant in omega-3 fatty acids, and eggs can be healthy additions to your plate. Picture them as the champions that can help keep your heart robust. But remember the mantra: everything in moderation. Overdoing anything doesn’t do any good.349Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017 Aug 30;16(1):53. doi: 10.1186/s12937-017-0271-4. PMID: 28854932; PMCID: PMC5577766.

Let’s hop onto another crucial element: physical activity. Picture your body as a machine, and exercise as the oil that keeps it purring smoothly. Regular physical activity can dial down your risk of CAD by bolstering your heart health and curbing factors like high blood pressure and cholesterol levels. Be it a brisk walk, a spin on your bike, or a dance session, find an exercise routine that sparks joy, and make it a daily habit. Remember, it’s not about pushing your limits; it’s about making steady, manageable lifestyle tweaks that help you lead a healthier life.350Barbiellini Amidei C, Trevisan C, Dotto M, et alAssociation of physical activity trajectories with major cardiovascular diseases in elderly peopleHeart 2022;108:360-366

We can’t wrap up this segment without mentioning something pivotal. Kicking the smoking habit is among the most impactful steps you can take in your tussle against CAD. Picture smoking as a rogue, subtly undermining your efforts to nurture a healthy heart. Each cigarette you don’t light up is a victory over CAD.351Gallucci G, Tartarone A, Lerose R, Lalinga AV, Capobianco AM. Cardiovascular risk of smoking and benefits of smoking cessation. J Thorac Dis. 2020 Jul;12(7):3866-3876. doi: 10.21037/jtd.2020.02.47. PMID: 32802468; PMCID: PMC7399440.

Excessive drinking is a slippery slope towards high blood pressure, heart failure, and even stroke. Now you’re wondering, how much is too much? Well, that varies, but as a general guide, no more than a drink a day for women and two for men. Every time you say no to alcohol, you protect your body from toxins.352Rehm J. The risks associated with alcohol use and alcoholism. Alcohol Res Health. 2011;34(2):135-43. PMID: 22330211; PMCID: PMC3307043.

Stress, the silent villain, is something we can’t overlook. Stress has a sneaky way of increasing heart disease risk, causing issues like high blood pressure and cholesterol levels. But don’t stress about being stressed! You’ve got tools to tackle it. Mindfulness and relaxation exercises, such as meditation, yoga, or just simple deep-breathing, can act as your personal shield against stress. Consider every moment of peace as a step back from CAD’s reach.353Assadi SN. What are the effects of psychological stress and physical work on blood lipid profiles? Medicine (Baltimore). 2017 May;96(18):e6816. doi: 10.1097/MD.0000000000006816. PMID: 28471984; PMCID: PMC5419930.

How about sleep? Sounds unimportant? Think again! A good night’s sleep is like a rejuvenating spa for your heart. Lack of sleep can usher in unwanted guests like obesity and type 2 diabetes, increasing your CAD risk. So, ensure that your body and mind get the rest they need. Think of every night of good sleep as a refreshing reboot for your heart.354Nagai M, Hoshide S, Kario K. Sleep duration as a risk factor for cardiovascular disease- a review of the recent literature. Curr Cardiol Rev. 2010 Feb;6(1):54-61. doi: 10.2174/157340310790231635. PMID: 21286279; PMCID: PMC2845795.

Let’s not forget weight management. Extra weight predisposes you to several health problems such as high blood pressure, high cholesterol, and diabetes, all leading to CAD. Each pound you shed is a step towards a heart that’s healthier and happier.355Manoharan MP, Raja R, Jamil A, Csendes D, Gutlapalli SD, Prakash K, Swarnakari KM, Bai M, Desai DM, Desai A, Penumetcha SS. Obesity and Coronary Artery Disease: An Updated Systematic Review 2022. Cureus. 2022 Sep 23;14(9):e29480. doi: 10.7759/cureus.29480. PMID: 36299943; PMCID: PMC9588166.

Ever considered what role your social connections might play in your heart health? It’s significant! Having a strong social network – family, friends, support groups – can be a secret weapon in your fight against CAD. Each moment spent with a loved one or a friend isn’t just enjoyable; it’s also a positive jolt to your heart health.

Now, let’s talk about your relationship with salt. Sure, it adds flavor to food, but too much of it can strain your heart by increasing blood pressure. The next time you reach for that salt shaker, think twice. Experiment with spices, herbs, and other heart-friendly flavor boosters. Each low-sodium meal you enjoy is like a “thank you” note to your heart.356Wang YJ, Yeh TL, Shih MC, Tu YK, Chien KL. Dietary Sodium Intake and Risk of Cardiovascular Disease: A Systematic Review and Dose-Response Meta-Analysis. Nutrients. 2020 Sep 25;12(10):2934. doi: 10.3390/nu12102934. PMID: 32992705; PMCID: PMC7601012.

We cannot stress enough the importance of regular health check-ups. These appointments aren’t just calendar reminders; they’re opportunities for you and your healthcare provider to stay ahead of CAD. You can monitor your blood pressure, cholesterol, and blood sugar levels, ensuring they are within healthy limits. Remember, early detection and management can be game-changers in your CAD journey.

Have you given thought to the role of mental health in managing CAD? Conditions like depression and anxiety can increase the risk of heart disease. Acknowledging and addressing these issues is a step forward in nurturing your heart health. Speak to mental health professionals, join support groups, or practice mindfulness techniques. Every step you take towards mental well-being is a leap towards a healthier heart.357De Hert M, Detraux J, Vancampfort D. The intriguing relationship between coronary heart disease and mental disorders. Dialogues Clin Neurosci. 2018 Mar;20(1):31-40. doi: 10.31887/DCNS.2018.20.1/mdehert. PMID: 29946209; PMCID: PMC6016051.

That’s the end of this segment of our heart-to-heart about lifestyle strategies to combat CAD. Remember, every day, you’re making choices that directly influence your heart health. You’re not just surviving CAD; you’re thriving in spite of it.

Pharmacological Management

Antiplatelet Agents

So what’s the scoop on these antiplatelet agents? Simply put, they help keep your blood flowing smoothly. Imagine your blood vessels like highways and the platelets like cars. When there’s an injury, these platelets come together, forming a clot to prevent excessive bleeding – a helpful action. However, in the case of CAD, these platelets might form a clot inside your arteries, a blockage – like an unexpected traffic jam – that can lead to a heart attack. Antiplatelet agents essentially guide these platelets, discouraging them from clumping together and forming these harmful clots.358Thachil J. Antiplatelet therapy – a summary for the general physicians. Clin Med (Lond). 2016 Apr;16(2):152-60. doi: 10.7861/clinmedicine.16-2-152. PMID: 27037385; PMCID: PMC4952969.

Low-dose aspirin is often recommended for people who’ve already had a heart attack or stroke to prevent a second one. It works by making the platelets less sticky and, therefore, less likely to clot.359Ornelas A, Zacharias-Millward N, Menter DG, Davis JS, Lichtenberger L, Hawke D, Hawk E, Vilar E, Bhattacharya P, Millward S. Beyond COX-1: the effects of aspirin on platelet biology and potential mechanisms of chemoprevention. Cancer Metastasis Rev. 2017 Jun;36(2):289-303. doi: 10.1007/s10555-017-9675-z. PMID: 28762014; PMCID: PMC5557878.

ASPIRIN: Now, when there’s an injury, like a cut, your body sends out a special group of workers called platelets, similar to traffic cops. Their job is to form a clot and stop the bleeding. Sometimes, however, these platelets can be overzealous and form clots where they’re not needed, potentially causing problems like a heart attack. Here’s where aspirin steps in. Aspirin acts like a soothing voice over the radio, calming these enthusiastic traffic cops. It specifically inhibits an enzyme called cyclooxygenase, which is involved in the production of thromboxane, a substance that encourages platelet aggregation. By doing this, aspirin reduces the risk of inappropriate clot formation, helping to maintain smooth traffic flow in your blood vessels.

P2Y12 INHIBITORS: P2Y12 inhibitors include medications like clopidogrel, prasugrel, and ticagrelor. Think of them as specialized traffic cops for your blood cells, ensuring they don’t cluster together and form a blockage in your arteries. Think of P2Y12 inhibitors as the master key that fits into a lock that’s specifically shaped to receive signals for clot formation. In our body’s busy thoroughfare, platelets — the tiny traffic cops — need specific signals to start clumping together and form a clot. One such signal comes from a substance called ADP, which fits into the P2Y12 receptor on the platelets like a key in a lock, signaling the platelets to spring into action. P2Y12 inhibitors work by fitting into these locks themselves, blocking ADP from attaching and sending that signal. With the signal interrupted, the platelets are less likely to form a clot, keeping the blood flowing smoothly and reducing the chance of blockages that can lead to heart problems.360Damman P, Woudstra P, Kuijt WJ, de Winter RJ, James SK. P2Y12 platelet inhibition in clinical practice. J Thromb Thrombolysis. 2012 Feb;33(2):143-53. doi: 10.1007/s11239-011-0667-5. PMID: 22183178; PMCID: PMC3269569.

But remember, these agents are not magic bullets. While they play a significant role in managing CAD, they also carry their risks, like the possibility of excessive bleeding. It’s a delicate balancing act that healthcare professionals strive to achieve – maintaining blood flow without risking unnecessary bleeding.361Shoeb M, Fang MC. Assessing bleeding risk in patients taking anticoagulants. J Thromb Thrombolysis. 2013 Apr;35(3):312-9. doi: 10.1007/s11239-013-0899-7. PMID: 23479259; PMCID: PMC3888359.

Of course, how long you need to stick with Dual Antiplatelet Therapy (DAPT) can vary. Picture this as a personalized game plan that your healthcare provider carefully tailors based on your unique needs. Depending on various factors, like the type of stent you’ve received and your overall health condition, your doctor might recommend DAPT for a few months to a year or even longer.362Bularga A, Meah MN, Doudesis D, Shah ASV, Mills NL, Newby DE, Lee KK. Duration of dual antiplatelet therapy and stability of coronary heart disease: a 60 000-patient meta-analysis of randomised controlled trials. Open Heart. 2021 Jul;8(2):e001707. doi: 10.1136/openhrt-2021-001707. PMID: 34341097; PMCID: PMC8330558.

Studies have shown that ticagrelor, when compared to clopidogrel, can lower the risk of heart attack and stroke in people with acute coronary syndrome (ACS). While clopidogrel is like a trusted, long-standing team player, ticagrelor is the new MVP stepping up the game in the fight against CAD.363Volney C, Collins A, Adams S. Ticagrelor versus clopidogrel in the management of acute myocardial infarction. J Community Hosp Intern Med Perspect. 2019 Sep 5;9(4):314-318. doi: 10.1080/20009666.2019.1644915. PMID: 31531213; PMCID: PMC6737723.

GPIIb/IIIa INHIBITORS: Also worth mentioning is a group of medications called GPIIb/IIIa inhibitors, including drugs like abciximab, eptifibatide, and tirofiban. These heavy hitters are typically used in hospitals during or after certain heart procedures to prevent clots. Think of them as your special task force, deployed during critical moments to keep your blood flowing smoothly.364Tummala R, Rai MP. Glycoprotein IIb/IIIa Inhibitors. [Updated 2022 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554376/

STATINS: 

Now, let’s shift our focus to another crucial teammate in the game against CAD – statins. Just as a goalkeeper shields the goal post, statins protect your heart by reducing the production of cholesterol in your liver. It’s like cutting off the supply to the enemy base in a strategy game, and in this case, the enemy is the high cholesterol that contributes to CAD.365Lim SY. Role of statins in coronary artery disease. Chonnam Med J. 2013 Apr;49(1):1-6. doi: 10.4068/cmj.2013.49.1.1. Epub 2013 Apr 25. PMID: 23678470; PMCID: PMC3651980.

Picture your bloodstream as a busy highway. Cholesterol, like cars, needs to be transported through this highway. Low-density lipoprotein (LDL) is often tagged as the ‘bad cholesterol’ because it carries cholesterol to your arteries, where it can form plaques and lead to heart disease. Statins come into play by lowering LDL levels, making the highway safer for travel.366Lim SY. Role of statins in coronary artery disease. Chonnam Med J. 2013 Apr;49(1):1-6. doi: 10.4068/cmj.2013.49.1.1. Epub 2013 Apr 25. PMID: 23678470; PMCID: PMC3651980.

A fascinating thing about statins is the ongoing research surrounding them. The medical community is like an enthusiastic detective, relentlessly seeking new clues. For instance, studies are being conducted to understand if statins can help reduce inflammation in the arteries, a player often overlooked in the game of CAD. If proven, it opens up an exciting new avenue in CAD managementp367Diamantis E, Kyriakos G, Quiles-Sanchez LV, Farmaki P, Troupis T. The Anti-Inflammatory Effects of Statins on Coronary Artery Disease: An Updated Review of the Literature. Curr Cardiol Rev. 2017;13(3):209-216. doi: 10.2174/1573403X13666170426104611. PMID: 28462692; PMCID: PMC5633715.

But how do statins manage to do this? Well, to produce cholesterol, your liver needs a key ingredient, a molecule called HMG-CoA. Statins work their magic by blocking the enzyme that helps convert HMG-CoA into cholesterol. In simpler terms, statins are the pest controller of your body, ensuring the cholesterol ‘pests’ don’t overrun your city.368Bansal AB, Cassagnol M. HMG-CoA Reductase Inhibitors. [Updated 2022 Jul 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542212/

What’s even more interesting is that when your liver can’t produce as much cholesterol, it turns to another source — your bloodstream. This prompts your liver to remove the ‘bad cholesterol,’ or LDL, from your blood, which further helps reduce the risk of CAD.369Young SG, Fong LG. Lowering plasma cholesterol by raising LDL receptors–revisited. N Engl J Med. 2012 Mar 22;366(12):1154-5. doi: 10.1056/NEJMe1202168. PMID: 22435375; PMCID: PMC5611813.

Imagine the process like this. You’re throwing a big party (your body) and you’ve stocked up on snacks (cholesterol). If you realize you have too many snacks and don’t want to waste them, what do you do? Right, you invite more people (LDL receptors) to your party to consume the snacks. Similarly, when statins reduce the production of cholesterol, your liver compensates by producing more LDL receptors to pull in the cholesterol from the blood.

But remember, while statins are truly remarkable in their function, they are not a magic bullet. They are one part of a team, working hand in hand with a healthy lifestyle to control CAD. Statins can’t replace good habits. Imagine a football team where only the goalkeeper is working hard while the other players slack off. They wouldn’t win many matches, would they? The same principle applies to your body. The effectiveness of statins is significantly increased when combined with a heart-healthy lifestyle.

Statins, those amazing tiny molecules, have a structure similar to HMG-CoA, the substance this particular enzyme works on. So, when you take a statin, it competes with HMG-CoA to bind with the enzyme. The statin, being a master of disguise, is picked up by the enzyme, who mistakes it for the real deal. This results in the enzyme binding with the statin instead of the HMG-CoA. This process inhibits or slows down the enzyme’s ability to produce cholesterol, hence reducing the overall level of cholesterol in your body.370Jiang, SY., Li, H., Tang, JJ. et al. Discovery of a potent HMG-CoA reductase degrader that eliminates statin-induced reductase accumulation and lowers cholesterol. Nat Commun 9, 5138 (2018). https://doi.org/10.1038/s41467-018-07590-3

One of the most commonly reported side effects of statins is muscle pain. Picture your muscles like a car engine. When everything is running smoothly, the car moves effortlessly. But sometimes, issues might cause the engine to stutter, and this is how muscle pain or weakness might feel in your body. It can range from a mild discomfort to a severe pain that can interfere with daily activities.371Suliman I, Batarfi A, Almohammadi H, Aljeraisi H, Alnaserallah H, Alghamdi A. Prevalence of Self-Reported Muscle Pain Among Statin Users From National Guard Hospital, Riyadh. Cureus. 2022 Mar 24;14(3):e23463. doi: 10.7759/cureus.23463. PMID: 35481326; PMCID: PMC9034880.

In addition to muscle pain, some people may also experience digestive problems. Think of your digestive system as a well-organized assembly line. When statins enter the scene, they can sometimes disrupt this line, causing nausea, gas, diarrhea, or constipation.372Fernandes R, Shaikh I, Wegstapel H. Possible association between statin use and bowel dysmotility. BMJ Case Rep. 2012 Feb 25;2012:bcr1020114918. doi: 10.1136/bcr.10.2011.4918. PMID: 22665551; PMCID: PMC3291011.373Cheng T, Li C, Shen L, Wang S, Li X, Fu C, Li T, Liu B, Gu Y, Wang W, Feng B. The Intestinal Effect of Atorvastatin: Akkermansia muciniphila and Barrier Function. Front Microbiol. 2022 Feb 2;12:797062. doi: 10.3389/fmicb.2021.797062. PMID: 35185821; PMCID: PMC8847773.

Moreover, statins may increase your blood sugar levels. Imagine sugar as workers in a factory. Normally, the body ensures the right number of workers are on the floor. But with statins, there might be more workers than needed, and this could increase the risk of developing type 2 diabetes. (Claim 84)

Another rare but serious side effect is liver damage. Picture your liver as a waste treatment plant, filtering out the waste products from your blood. When statins are introduced, for some people, it’s like adding extra work to this plant. It could lead to an increase in liver enzymes, which might indicate liver damage. However, your doctor will monitor this closely, and adjustments can be made if necessary.374Averbukh LD, Turshudzhyan A, Wu DC, Wu GY. Statin-induced Liver Injury Patterns: A Clinical Review. J Clin Transl Hepatol. 2022 Jun 28;10(3):543-552. doi: 10.14218/JCTH.2021.00271. Epub 2022 Jan 10. PMID: 35836753; PMCID: PMC9240239.

While the thought of side effects can be daunting, remember that statins are usually well-tolerated, and the benefits often outweigh the risks, particularly for those battling CAD. They’re part of the toolbox that helps manage the disease and safeguard your heart. And just like a surfer navigates the waves, being aware of the potential bumps in your journey with statins can empower you to make informed decisions about your health.

Angiotensin-Converting Enzyme Inhibitors

ACE inhibitors work by blocking the production of a hormone called angiotensin II. Angiotensin II is like that pesky traffic officer who narrows the highway, causing the blood vessels to constrict and ordering the release of another hormone that increases the volume of traffic by retaining water. With less of this hormone around thanks to ACE inhibitors, your blood vessels can relax and widen, and there’s less water retained. This means the blood traffic flows more freely, reducing the pressure and making it easier for your heart to pump blood around the body.375Fyhrquist F, Metsärinne K, Tikkanen I. Role of angiotensin II in blood pressure regulation and in the pathophysiology of cardiovascular disorders. J Hum Hypertens. 1995 Nov;9 Suppl 5:S19-24. PMID: 8583476.

But, like any medication, ACE inhibitors are not without potential side effects. They might cause a persistent, dry cough, a drop in blood pressure when you stand up, or a high potassium level in your blood. Sometimes, you might feel dizzy or have headaches or changes in your sense of taste. There’s also a risk, though rare, of swelling in your skin and mucous membranes, a condition known as angioedema.376Haymore BR, Yoon J, Mikita CP, Klote MM, DeZee KJ. Risk of angioedema with angiotensin receptor blockers in patients with prior angioedema associated with angiotensin-converting enzyme inhibitors: a meta-analysis. Ann Allergy Asthma Immunol. 2008 Nov;101(5):495-9. doi: 10.1016/S1081-1206(10)60288-8. PMID: 19055203.

Now, don’t let these side effects intimidate you. Always remember, the goal here is to manage your coronary artery disease effectively. While it’s essential to be aware of these potential side effects, also remember that not everyone experiences them, and many people have found ACE inhibitors to be their trusty shield in their battle against coronary artery disease.377Oemrawsingh, R. M., Akkerhuis, K. M., Van Vark, L. C., Redekop, W. K., Rudez, G., Remme, W. J., Bertrand, M. E., Fox, K. M., Ferrari, R., Danser, A. H. J., de Maat, M., Simoons, M. L., Brugts, J. J., & Boersma, E. (2016). Individualized angiotensin‐converting enzyme (ace)‐inhibitor therapy in stable coronary artery disease based on clinical and pharmacogenetic determinants: The Perindopril Genetic (PERGENE) risk model. Journal of the American Heart Association, 5(3). https://doi.org/10.1161/jaha.115.002688

One such player is Lisinopril, a stalwart who’s always ready to do its job with consistency. Then there’s Ramipril, a tenacious one that never backs down from the task at hand. Enalapril also joins this lineup, bringing its strong defense against the enemy, coronary artery disease. And let’s not forget Quinapril, another potent force on this team. Each one, with their unique strengths and skills, plays a crucial part in the match to manage your coronary artery disease.

But remember, starting on ACE inhibitors isn’t like buying a ticket to a football match. It’s a commitment, like becoming a season ticket holder. For ACE inhibitors to work effectively, they need to be taken consistently as directed by your healthcare provider. It’s also not a one-size-fits-all scenario – the right ACE inhibitor and the correct dosage for you will depend on your individual health circumstances.

Importantly, ACE inhibitors are usually well tolerated, but they may not be suitable for everyone. They should be used with caution if you have certain conditions, such as kidney disease, and are generally avoided during pregnancy. Remember, your healthcare provider is your coach in this game against coronary artery disease. They know the players, they understand the game plan, and they can guide you through the journey, making adjustments as necessary to help you succeed.

Beta-Blockers

Beta-blockers play an essential role in the management of coronary artery disease (CAD) by blocking the beta-adrenergic receptors in the body. This blockade leads to a decreased heart rate, reduced force of heart contraction, and lowered blood pressure, collectively reducing the heart’s workload and its demand for oxygen.378Boyette LC, Manna B. Physiology, Myocardial Oxygen Demand. [Updated 2022 Jul 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499897/

They are particularly effective in CAD, where the arteries supplying blood to the heart are narrowed or obstructed. Beta-blockers alleviate the angina or chest pain associated with this disease and are routinely recommended following a heart attack to prevent future events.379Wu T, Chen X, Deng L. Beta‐blockers for unstable angina. Cochrane Database Syst Rev. 2017 Nov 24;2017(11):CD007050. doi: 10.1002/14651858.CD007050.pub2. PMCID: PMC6486012.

There are multiple types of beta-blockers, including non-selective ones like Propranolol, which block both beta-1 and beta-2 receptors. This non-selectivity can lead to side effects such as cold extremities or fatigue. More selective beta-blockers, such as Metoprolol and Atenolol, target only beta-1 receptors, minimizing these side effects.380Shahrokhi M, Gupta V. Propranolol. [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557801/381Rehman B, Sanchez DP, Shah S. Atenolol. [Updated 2022 Oct 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539844/

One important consideration with beta-blockers is the risk of a ‘rebound’ effect when the medication is discontinued abruptly. This can lead to an excessive increase in heart activity, escalating the risk of heart issues. Therefore, any discontinuation or modification of the dosage should be under a healthcare provider’s supervision.382Anık A. Beta-blocker Rebound Phenomenon in an Adolescent with Graves’ Disease. J Clin Res Pediatr Endocrinol. 2022 Dec 1;14(4):490-491. doi: 10.4274/jcrpe.galenos.2022.2022-6-2. Epub 2022 Jul 21. PMID: 35859995; PMCID: PMC9724061.

While beta-blockers don’t cure CAD, they are instrumental in symptom management and improving the quality of life for patients. Their use is typically part of a larger treatment plan that also involves lifestyle modifications and potentially other medications. Adverse effects of beta-blockers can include fatigue, bradycardia (slow heart rate), and hypotension (low blood pressure).383Anık A. Beta-blocker Rebound Phenomenon in an Adolescent with Graves’ Disease. J Clin Res Pediatr Endocrinol. 2022 Dec 1;14(4):490-491. doi: 10.4274/jcrpe.galenos.2022.2022-6-2. Epub 2022 Jul 21. PMID: 35859995; PMCID: PMC9724061.

In summary, beta-blockers are a critical tool in the management of CAD, helping reduce the heart’s workload, and consequently its oxygen demand, relieving symptoms, and reducing the risk of future heart attacks. As with any medication, understanding its action, side effects, and proper usage is vital to achieve the best possible outcome in CAD management.

Invasive Management of Coronary Artery Disease (CAD)

Percutaneous Coronary Intervention

When medications are not enough, a procedure known as Percutaneous Coronary Intervention, often just called PCI, comes into play.384Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/

Imagine having a blocked pipe at home. You can’t just push the obstruction further along; you need to remove or bypass it to get the water flowing smoothly again. That’s what PCI does for your heart. It’s like calling a plumber, but in this case, your doctor plays the role of the plumber, and the pipe is your coronary artery.385Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/

Now, you might be wondering how exactly this PCI works. Your doctor threads a thin tube through your blood vessels, all the way to the blocked artery in your heart. A tiny balloon at the end of the tube is inflated, pushing the plaque to the sides and opening up the artery. Often, a small metal mesh tube, known as a stent, is left in place to keep the artery open.386Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/

Imagine this procedure like an expedition into the heart’s network of blood vessels, much like navigating a busy, winding highway. The journey begins with the insertion of a thin, flexible tube called a catheter into a large blood vessel, usually in your arm or groin. A small amount of contrast dye is then injected through this catheter, providing the ‘map’ for your doctors on a screen using X-rays (a process known as angiography). This will guide them in their journey towards the coronary arteries.387Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/

The primary objective of the PCI is to unblock the bottlenecked regions of your heart’s highways – the coronary arteries. These bottlenecks, composed of plaques or fatty build-ups, can disrupt the flow of blood. If left unchecked, they might cause a traffic jam, cutting off vital oxygen and nutrients from portions of your heart muscle. It’s at this critical juncture that the PCI enters the scene, restoring the smooth flow of traffic or, in this case, the blood flow.388Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/

Post-procedure, the balloon is deflated and removed, leaving the stent (if used) in place. With the blockade now cleared, blood can freely circulate, delivering the much-needed oxygen and nutrients to your heart muscle. This process can be repeated for any additional blockages, ensuring all critical routes to your heart are free-flowing.389Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/

Isn’t it interesting to think of this procedure as a sort of repair job on the essential highways of your heart? But instead of constructing something brand new, the aim is more about restoration and preservation – keeping your heart’s blood flow in its best possible condition. Yet, just like any restoration project, some potential hitches could occur.

At times, you might experience some minor inconveniences following the procedure. Potential side effects might range from some bruising at the point of catheter insertion to instances of irregular heartbeats, which are medically termed as arrhythmias. But it’s equally crucial to be aware that there exists a marginal risk of more intense complications such as heart attacks, strokes, issues with your kidneys, or, in extremely uncommon circumstances, death.390Doll, J. A., Hira, R. S., Kearney, K. E., Kandzari, D. E., Riley, R. F., Marso, S. P., Grantham, J. A., Thompson, C. A., McCabe, J. M., Karmpaliotis, D., Kirtane, A. J., & Lombardi, W. (2020). Management of percutaneous coronary intervention complications. Circulation: Cardiovascular Interventions, 13(6). https://doi.org/10.1161/circinterventions.120.008962 Furthermore, your arteries could potentially become narrow again, a scenario referred to as restenosis, particularly if a stent wasn’t part of your procedure.

This risk factor brings us to another important aspect of PCI – aftercare. Once your arteries have been cleared, it doesn’t mean you can return to old habits that might have contributed to the blockages in the first place. Post-PCI, it becomes crucial to embrace lifestyle modifications such as a balanced diet, regular exercise, cessation of smoking, and stress management. Moreover, your healthcare provider might prescribe medications, such as antiplatelet drugs, to help prevent the formation of blood clots in the stents and to further reduce the risk of future heart attacks.

These drugs are particularly crucial if you’ve had a stent placed during the procedure. Blood clots forming on the stent could be a potential cause of another blockage, leading to a situation known as stent thrombosis. Thus, these medications serve as an essential part of the safety measures, ensuring the smooth and uninterrupted flow of traffic in your heart’s highways.391Angiolillo DJ, Galli M, Collet JP, Kastrati A, O’Donoghue ML. Antiplatelet therapy after percutaneous coronary intervention. EuroIntervention. 2022 Apr 1;17(17):e1371-e1396. doi: 10.4244/EIJ-D-21-00904. PMID: 35354550; PMCID: PMC9896394.

As you journey towards recovery post-PCI, regular follow-ups with your healthcare provider become integral pitstops. These check-ins allow your doctor to monitor your progress, address any concerns you might have, and adjust your treatment plan as needed. Your healing journey might have bumps along the way, and it’s essential to navigate through them under expert guidance.

While the idea of a construction project unfolding within your heart might appear intimidating, it’s essential to keep in mind that PCI is a well-established method, underpinned by an enormous amount of scientific investigation and clinical expertise. In fact, PCI has played a pivotal role in both preserving countless lives and enhancing the quality of life for those dealing with coronary artery disease.392Blankenship JC, Marshall JJ, Pinto DS, Lange RA, Bates ER, Holper EM, Grines CL, Chambers CE; Society for Cardiovascular Angiography and Interventions. Effect of percutaneous coronary intervention on quality of life: a consensus statement from the Society for Cardiovascular Angiography and Interventions. Catheter Cardiovasc Interv. 2013 Feb;81(2):243-59. doi: 10.1002/ccd.24376. Epub 2012 Apr 27. PMID: 22431260.

It’s more than just a technical maneuver to clear blockages; it’s about offering you an opportunity to reclaim your life, participate in the activities you enjoy, and treasure the moments spent with your loved ones. Despite potential hurdles and complications, the ultimate aim is to guide you towards a journey of heart health and an enriched life.

In closing, the story of PCI is a story of restoration and maintenance. It’s about ensuring the vital highways in your heart are free-flowing and the life-nourishing blood can reach every part of your heart muscle. This narrative underscores the marvels of medical advancements and the astounding ability of the body to recover, provided it receives appropriate conditions and attention.

Throughout this process, it’s vital to recall that you’re not traversing this path alone. Your healthcare team, your family and friends, and innumerable others who’ve embarked on this journey stand by your side. Together, you can navigate the twists and turns of coronary artery disease, leveraging the power of procedures like PCI, and continue to drive towards a future of health and vitality.

Coronary Artery Bypass Grafting (CABG)

To visualize the procedure, think of a city choked with traffic due to a major road closure. In such a case, the solution often lies in creating a bypass or an alternate route to alleviate congestion. CABG accomplishes something very similar within your heart.

When the coronary arteries—your heart’s major blood highways—are blocked due to plaque buildup, CABG works by creating an alternate pathway for blood to reach the heart. This ‘detour’ circumvents the blocked artery, allowing life-sustaining blood to flow freely to your heart muscle.393Bachar BJ, Manna B. Coronary Artery Bypass Graft. [Updated 2023 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507836/

CABG is performed using a blood vessel graft—often taken from your chest, leg, or arm—that acts as this alternate route for blood flow. Your surgeon attaches one end of the graft above the blocked artery and the other end below the blockage. And voila, you have a new route for blood to reach your heart!394Diodato M, Chedrawy EG. Coronary artery bypass graft surgery: the past, present, and future of myocardial revascularisation. Surg Res Pract. 2014;2014:726158. doi: 10.1155/2014/726158. Epub 2014 Jan 2. PMID: 25374960; PMCID: PMC4208586.

The decision to undergo CABG isn’t taken lightly. It’s usually recommended when other less invasive treatments, such as medications or angioplasty, aren’t sufficient to manage your condition. You might be a candidate for CABG if you have severe blockages in your large coronary arteries, especially if your heart’s pumping action has already been weakened.395Bachar BJ, Manna B. Coronary Artery Bypass Graft. [Updated 2023 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507836/

Despite being a major surgery, CABG has a proven track record of success. Numerous individuals living with coronary artery disease have had their lives drastically improved and extended thanks to this procedure.396Bachar BJ, Manna B. Coronary Artery Bypass Graft. [Updated 2023 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507836/

Potential risks of CABG include infection, bleeding, and reactions to anesthesia.

The recovery period following CABG is a journey in itself, often involving several months of rehabilitation. Regular follow-ups with your healthcare provider, a gradual return to daily activities, and adopting heart-healthy lifestyle modifications are key components of this recovery process.

While CABG represents a significant undertaking, for many individuals living with coronary artery disease, it offers a life-enhancing solution. It’s a major leap on the journey towards a healthier heart, providing a new lease on life for you to continue building precious memories with your loved ones.

Rehabilitation

Rehabilitation is not a switch that flips overnight. It’s a gradual process, tailored to your unique needs and progress rate. Following treatment for coronary artery disease, whether it be medications, PCI, CABG, or a combination thereof, your body has experienced significant changes. It’s important to understand that easing back into the rhythms of your daily life requires patience and dedication.397Taylor RS, Dalal HM, McDonagh STJ. The role of cardiac rehabilitation in improving cardiovascular outcomes. Nat Rev Cardiol. 2022 Mar;19(3):180-194. doi: 10.1038/s41569-021-00611-7. Epub 2021 Sep 16. PMID: 34531576; PMCID: PMC8445013.

The heart of your rehabilitation process will likely be a structured program known as cardiac rehabilitation. This scientifically-backed regimen is designed to improve your cardiovascular health post-treatment. It’s a balanced blend of monitored exercises, nutritional counseling, emotional support, and education about the lifestyle modifications that can slow or even reverse the progression of coronary artery disease.398Tessler J, Bordoni B. Cardiac Rehabilitation. 2023 May 22. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 30725881.

Don’t underestimate the power of that morning walk or the 20 minutes spent on a stationary bike. These seemingly small steps of physical activity are the building blocks of your new, heart-healthy life. Regular, monitored physical activity can significantly improve both your cardiovascular fitness and overall quality of life, reducing symptoms such as chest pain and fatigue.

Beyond physical activity, rehab is a time to explore the fuel that powers your body—your diet. During rehabilitation, you’ll learn to make heart-friendly dietary choices, swapping out saturated fats for heart-healthy omega-3s and saying hello to whole grains, fruits, and vegetables. Remember, every meal is an opportunity to nourish your body and strengthen your heart.

Your healthcare team, your loved ones, and countless others who’ve embarked on similar journeys stand beside you. Together, you can negotiate the journey of coronary artery disease rehabilitation, harnessing the power of these techniques to stride towards a future of health and vitality.

After treatment, you might find it harder to sleep due to anxiety, discomfort, or as a side effect of certain medications. Yet, quality sleep is vital for your body to heal and rejuvenate.

Your healthcare team is also likely to address risk factor modification during your rehabilitation. This includes controlling high blood pressure, high cholesterol, diabetes, smoking, and being overweight. Regular monitoring and appropriate management of these risk factors is a crucial part of your rehabilitation and long-term heart health.

Education is another key pillar of the rehabilitation process. Understanding your disease, its causes, and how your lifestyle impacts your heart health can empower you to make meaningful changes. Your rehab team will provide you with valuable resources and learning sessions to make you an active participant in your health journey, rather than just a passive recipient of care.

Also, don’t forget the impact of social support during your rehabilitation. Connecting with others who are on similar journeys can provide a sense of community and understanding that friends and family might not be able to offer. Many cardiac rehab programs include group sessions or can refer you to support groups for this reason.

Epidemiology of Coronary Artery Disease (CAD)

Prevalence and Incidence of Coronary Artery Disease (CAD)

The curtain rises on a grim but very real global health issue, coronary artery disease (CAD). This isn’t some rare, unknown condition; it’s a ubiquitous silent enemy that impacts lives in every corner of our world. Its grip is so tight that it’s considered a leading cause of death globally, accounting for millions of deaths each year. That’s millions of lives abruptly changed or prematurely ended by this ruthless condition.399Brown JC, Gerhardt TE, Kwon E. Risk Factors for Coronary Artery Disease. 2023 Jan 23. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 32119297.

Now, let’s dive into the depth of the words ‘prevalence’ and ‘incidence’. Imagine you’re looking at a photograph of a vast, crowded scene. Prevalence in the context of diseases like CAD is quite like that photograph. It’s a snapshot that captures the total number of people, both old and new cases, who are living with CAD at any given moment. It gives us a sweeping view of how far and wide CAD has spread its ominous shadow. And let’s just say, for CAD, the snapshot is akin to a dense, crowded scene at the peak of rush hour. It tells us that CAD is an immense health problem we are battling against globally.400Ralapanawa U, Sivakanesan R. Epidemiology and the Magnitude of Coronary Artery Disease and Acute Coronary Syndrome: A Narrative Review. J Epidemiol Glob Health. 2021 Jun;11(2):169-177. doi: 10.2991/jegh.k.201217.001. Epub 2021 Jan 7. PMID: 33605111; PMCID: PMC8242111.

Incidence, on the other hand, is like watching a video of a busy city street, focusing on how many new people enter the scene every second. It’s the count of new cases that arise in a specific period. It’s about watching that unfortunate moment when someone, previously healthy, steps into the arena of CAD. Once again, in the case of CAD, this is like witnessing a relentless flow of people onto an already crowded street. The incidence of CAD remains high, with millions of people joining the CAD club every year.401Ferreira-González, I. (2014a, February 1). The epidemiology of coronary heart disease: Revista Española de Cardiología. Revista Española de Cardiología (English Edition). https://www.revespcardiol.org/en-the-epidemiology-coronary-heart-disease-articulo-S1885585713003381

The sad reality is that CAD is not a respecter of borders, cultures, or economic status. Whether you’re in the United States, a tranquil town in Europe, the heart of Africa, or anywhere in Asia, CAD is an unwelcome guest that can knock on anyone’s door. It’s a global battle that we’re all a part of, knowingly or unknowingly.

However, the silver lining in this seemingly gloomy scenario is the immense work that is being done in the field of CAD research and treatment. There’s a whole army of doctors, researchers, and healthcare professionals worldwide who are continually striving to understand this complex disease better and find effective ways to treat and manage it. Their aim? To turn the tide of this global health crisis, so that one day, the picture of CAD prevalence and incidence would look much less crowded and ominous than it does today.

This narrative around CAD is not just about numbers and facts; it’s about real people, real lives. It’s about the unyielding human spirit that continues to fight against this health monster, armed with the weapons of knowledge, medical advancement, and preventive strategies. So, while we’re talking about prevalence and incidence, let’s not forget the faces behind these numbers. They are the reason why fighting CAD matters. It’s for them we need to keep pushing the boundaries of our understanding and treatment of CAD402Kandaswamy E, Zuo L. Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology. Int J Mol Sci. 2018 Jan 31;19(2):424. doi: 10.3390/ijms19020424. PMID: 29385089; PMCID: PMC5855646.

Geographic and Demographic Disparities in Coronary Artery Disease (CAD)

Imagine your feet touching different corners of a world map. As you hop from one place to another, the face of CAD changes. The Western world, known for its fast-paced lifestyle, bears a significant burden of this disease. Higher rates of CAD echo through the bustling cities of America and the calm countrysides of Europe. Many argue that a diet high in fast food and a sedentary lifestyle play a key role here. However, don’t let that be your only takeaway. Socioeconomic factors and access to healthcare facilities are also major players.403Graham G. Disparities in cardiovascular disease risk in the United States. Curr Cardiol Rev. 2015;11(3):238-45. doi: 10.2174/1573403×11666141122220003. PMID: 25418513; PMCID: PMC4558355. Rapid urbanization and adoption of Western lifestyle habits are pushing CAD numbers higher.

But CAD doesn’t just differ from place to place. Take a look at how it affects different age groups and genders. You may think that CAD only threatens older men, but it’s spreading its reach to younger people and women too. So, age and gender stereotypes don’t apply when it comes to CAD. It’s a global issue affecting diverse groups of people.404Aggarwal A, Srivastava S, Velmurugan M. Newer perspectives of coronary artery disease in young. World J Cardiol. 2016 Dec 26;8(12):728-734. doi: 10.4330/wjc.v8.i12.728. PMID: 28070240; PMCID: PMC5183972.

Let’s consider race and ethnicity. From the outside, it might seem that CAD should affect all races and ethnicities equally. But in reality, certain racial and ethnic groups bear a heavier burden of CAD. The reasons behind this disparity are complex, spanning genetic predisposition, cultural practices, and, yes, systemic healthcare inequities 405Mochari-Greenberger H, Mosca L. Differential Outcomes by Race and Ethnicity in Patients with Coronary Heart Disease: A Contemporary Review. Curr Cardiovasc Risk Rep. 2015 May;9(5):20. doi: 10.1007/s12170-015-0447-4. PMID: 25914758; PMCID: PMC4405256. For instance, South Asians living in the U.S have a higher risk of developing CAD than their Caucasian counterparts. It’s a sobering reminder that when it comes to CAD, our differences matter, and understanding these differences is crucial to creating tailored, effective solutions.

Another crucial element is the urban-rural divide. Think about it: the hustle and bustle of city life versus the tranquillity of the countryside. Urban areas, with their fast-paced lifestyles and easy access to unhealthy food options, can inadvertently foster CAD.406Kumar R, Singh MC, Singh MC, Ahlawat SK, Thakur JS, Srivastava A, Sharma MK, Malhotra P, Bali HK, Kumari S. Urbanization and coronary heart disease: a study of urban-rural differences in northern India. Indian Heart J. 2006 Mar-Apr;58(2):126-30. PMID: 18989056. However, rural areas, often lacking adequate healthcare facilities and health awareness, are no safe havens either. People living in rural areas might struggle with timely diagnosis and treatment, worsening the CAD outcomes.407American Heart Association. (2020, April 22). Health disparities in rural us: Higher coronary artery disease death in women under 65 and people with heart failure. Health disparities in rural US: Higher coronary artery disease death in women under 65 and people with heart failure. https://newsroom.heart.org/news/health-disparities-in-rural-us-higher-coronary-artery-disease-death-in-women-under-65-and-people-with-heart-failure

The role of education cannot be underestimated. An individual’s educational level can influence their understanding of CAD, its risks, and the steps needed to prevent it. Lower levels of education often correlate with a higher risk of CAD, highlighting the power of knowledge in combating this disease.408Kelli HM, Mehta A, Tahhan AS, Liu C, Kim JH, Dong TA, Dhindsa DS, Ghazzal B, Choudhary MK, Sandesara PB, Hayek SS, Topel ML, Alkhoder AA, Martini MA, Sidoti A, Ko YA, Lewis TT, Vaccarino V, Sperling LS, Quyyumi AA. Low Educational Attainment is a Predictor of Adverse Outcomes in Patients With Coronary Artery Disease. J Am Heart Assoc. 2019 Sep 3;8(17):e013165. doi: 10.1161/JAHA.119.013165. Epub 2019 Sep 2. PMID: 31476920; PMCID: PMC6755831.

Impact of Socioeconomic Status

Imagine you’re walking down the streets of a busy city, passing people from all walks of life. Among the sea of faces, a hidden thread runs through them, binding some more tightly than others. This invisible thread is Coronary Artery Disease (CAD), and it doesn’t weave the same pattern for everyone. The pattern it does weave, though, is often influenced by something you may not readily consider – socioeconomic status.

Let’s journey through the complex world of CAD, taking a close look at how socioeconomic status shapes its landscape. You might assume that wealth acts as a shield, protecting those with higher income from CAD. After all, more money should mean better access to nutritious food, good healthcare, and opportunities for exercise, right? However, the reality isn’t quite so black-and-white. In fact, research shows that individuals of higher socioeconomic status can experience elevated stress levels, a known risk factor for CAD.409Fioranelli M, Bottaccioli AG, Bottaccioli F, Bianchi M, Rovesti M, Roccia MG. Stress and Inflammation in Coronary Artery Disease: A Review Psychoneuroendocrineimmunology-Based. Front Immunol. 2018 Sep 6;9:2031. doi: 10.3389/fimmu.2018.02031. PMID: 30237802; PMCID: PMC6135895.

On the flip side, people on the lower end of the economic scale face their own challenges. Less money can mean less access to healthy food options and a higher likelihood of living in what’s known as a “food desert” where fresh, affordable food is hard to find. Limited resources also mean less access to quality healthcare, leading to potential delays in diagnosis and treatment of CAD.

Now, envision the workplace, a place where we spend a significant chunk of our lives. Here, socioeconomic status continues to play a crucial role in CAD risk. Lower-wage jobs often come with more physical stress, fewer opportunities for exercise, and longer hours—all factors contributing to higher CAD risks.

Reading this, you might feel a weight in your chest that isn’t physical but emotional. It’s a sobering reality that CAD, like many other diseases, doesn’t affect everyone equally. But your journey to understand CAD isn’t a cause for despair. Instead, let it fuel your determination to make a difference.

Prevention Strategies and Public Health Interventions in Coronary Artery Disease (CAD)

Primary Prevention

Picture yourself driving on a road trip. To keep your journey smooth and safe, you fill up the fuel, check the tire pressure, and make sure the engine is in top shape, right? This is akin to primary prevention for coronary artery disease – it’s about taking proactive steps to keep your ‘heart motor’ running smoothly.

Think about it this way. Your heart, that vital engine keeping you alive, also needs preventative maintenance. It’s not enough to only respond when things go wrong, like when you face a ‘heart roadblock’. You want to prevent those roadblocks from happening in the first place.

Foods high in salt, saturated fats, and sugar can contribute to the buildup of fatty plaques in your arteries, leading to coronary artery disease. Swapping those for heart-healthy options like fruits, vegetables, whole grains, and lean proteins is like choosing a clean, traffic-free highway for your heart.

Imagine it as the fuel that keeps your heart engine running efficiently. Regular exercise is a game-changer when it comes to preventing coronary artery disease. It’s as if your heart is saying, “Hey, let’s keep this journey interesting and energized!”

Moreover, smoking is a big no-no. It’s like throwing huge rocks in the path of your heart’s journey. Smoking accelerates the development of fatty deposits in your arteries and is a significant risk factor for coronary artery disease. When you say no to smoking, it’s like clearing the roadway for a smoother, safer drive.

Let’s not forget about stress, the hidden monster. Chronic stress might not physically clutter your heart’s road, but it can lead to behaviors that do, like overeating or smoking. So, learning to manage stress effectively is like learning how to navigate through difficult driving conditions. It keeps your heart’s journey safer and more controlled.

In the end, remember, prevention is like a protective shield for your heart. It’s a lifelong commitment, just like maintaining a car for those long, adventure-filled road trips. It involves making choices every day that keep the road clear, keep the engine humming, and make the journey pleasant.

It’s a responsibility, yes. But it’s also an empowering journey of self-care. One where you’re in the driver’s seat, steering your health towards a heart-friendly destination. So, let’s buckle up and embark on this journey of primary prevention against coronary artery disease. After all, every heartbeat counts, and the journey of heart health is a journey worth taking.

Having a glass or two of your favorite beverage won’t derail your heart’s health. But if you turn this into a frequent habit, or if you often find yourself losing count of the glasses, then it’s like placing unnecessary hurdles on your heart’s path. Cutting back on alcohol is a kind, caring gesture you can make for your heart.

Now, consider regular health check-ups as heart-to-heart chats. It’s you, sitting down with your body, asking, “Hey, how’s everything going? Anything I should know about?” Regular check-ups help you catch potential heart risk factors early, even when they’re whispering rather than shouting. It’s like getting a heads-up about a road closure or traffic jam on your journey, allowing you to navigate around it smoothly.

Being overweight is like forcing your heart to carry heavy suitcases day in, day out. It’s exhausting, right? When you work towards maintaining a healthy weight, it’s as if you’re helping your heart to unload those heavy suitcases. Your heart becomes lighter, happier, and more efficient.

Lastly, imagine being lost in a new city without a map or GPS. Confusing, isn’t it? Now, think about all the complex roads and highways in the city of heart health. Without proper knowledge and awareness, it’s easy to get lost or miss essential signs. But when you take time to learn about heart health, it’s like you’re giving yourself a reliable map and a well-functioning GPS. You become better equipped to navigate your way to a healthier heart.

Keep in mind that heart health is a continuous journey, not a one-time event. It’s about making daily choices that favor your heart. Every step, every decision, every act of self-care brings you closer to a healthier heart. It’s like reaching new milestones on a road trip, where the journey itself is the real destination. Here’s to embracing the ride, one heartbeat at a time.

 Secondary Prevention

Medications in this scenario are like your helmet, knee pads, or sturdy hiking boots – they’re there to protect you and prevent another fall. These medications, which can range from those managing your blood pressure to those preventing clot formation, serve as your body’s defense mechanism. But remember, just as a helmet alone won’t prevent a fall, medications alone are not enough. They are one piece of the puzzle in the protection of your heart.

Continuing with our analogy, just as you’d learn to balance better on your bike or watch your step more carefully on the trail, lifestyle modifications are key in this journey of secondary prevention. This includes the nutrition your body takes in, which is like the quality of fuel you’d put in your bike or the supplies you’d carry on your hike. Your commitment to physical activity is like practicing your bike skills or conditioning for the trail – it keeps your heart strong and prepared.

Importantly, your emotional well-being during this journey is as critical as your physical health. Imagine having a friend by your side when you’re learning to ride a bike or during that challenging hike. That friend is like the support groups and counseling services available to you after a coronary event.

Remember, just as each fall teaches you something new about how to balance or where to step, experiencing a coronary event teaches you more about your heart and your health. It’s a hard teacher, but the lessons are invaluable. The journey to secondary prevention isn’t about bouncing back to where you were, but growing stronger and wiser, armed with the lessons learned from the stumble.

And remember, every little improvement counts. Every healthier meal, every completed workout, every shared feeling in a support group – they’re all steps forward in your journey.

So, as you navigate this path of secondary prevention, remember, it’s not about the speed, but the direction.

It’s important to consider a program of cardiac rehabilitation as part of your healing journey. Imagine it as a specialized training course you can join after an unfortunate mishap while driving. It helps you regain confidence, improve your driving skills, and familiarize yourself with new safety norms. In the context of your heart, cardiac rehabilitation is a program designed specifically for people who have had a heart event. It often includes physical training, nutritional counseling, emotional support, and education about the lifestyle changes you can make to prevent further issues.

Stress management also plays a crucial role in secondary prevention. In our driving analogy, stress is akin to driving in heavy traffic or harsh weather conditions. It demands more of your attention, drains your energy, and increases the risk of accidents. Similarly, chronic stress puts extra pressure on your heart and can worsen heart disease. Hence, adopting stress management techniques such as deep breathing, meditation, or yoga can help you navigate through the heavy traffic of life with more ease and less harm to your heart.

Moreover, secondary prevention is a lifelong commitment. It’s not about doing a quick fix or a temporary change, but about embracing a new lifestyle that prioritizes your heart health. To go back to our driving analogy, it’s like deciding to always follow traffic rules, keep your vehicle well-maintained, and be vigilant about road safety, long after recovering from the mishap. It becomes part of your driving routine, just as secondary prevention needs to be part of your everyday life.

Lastly, remember that open and regular communication with your healthcare team is vital for successful secondary prevention. It’s like keeping in touch with traffic updates, road conditions, and vehicle status during a long journey. It helps you make well-informed decisions, anticipate potential challenges, and make timely interventions if needed.

In the end, secondary prevention of coronary artery disease is about empowering yourself with knowledge, tools, and habits that help you take the best care of your heart. It’s about driving with more caution and care, knowing that you’ve faced a bump on the road before, and are now better prepared to continue your journey safely and confidently.

Tertiary Prevention

Imagine your journey with CAD like being on a ship at sea. The primary prevention was your pre-voyage prep – maintaining a sturdy ship, learning navigational skills, and avoiding stormy weather. The secondary prevention was your response after surviving a storm – repairing the ship, improving your sailing skills, and being extra cautious. Now, tertiary prevention is about managing in the aftermath of a storm so severe it’s left lasting damage. It’s about learning how to sail despite the damage, making your ship resilient, and ensuring your safety in the uncertain seas of the future.

In your body’s context, tertiary prevention comes into play when CAD has advanced to a point where it’s caused substantial heart damage, like after a major heart attack or progression of heart failure. Your goal at this point? To manage the condition, reduce symptoms, and improve quality of life.

A key part of this management plan is adhering to your medication regimen. These medicines are now like the essential tools and equipment you need to keep your damaged ship afloat. They’ll help manage symptoms, slow down disease progression, and prevent complications.

Another critical aspect of tertiary prevention is careful monitoring and regular check-ups with your healthcare provider. Think of this like frequent inspections of your ship for any new or worsening damage, and meeting with experienced sailors to learn from their knowledge. Regular cardiac evaluations help keep track of your heart’s condition and adjust treatment plans as needed.

Remember, just because your ship is damaged doesn’t mean you abandon your sailing skills or let go of caution. Maintaining a heart-healthy lifestyle is still crucial. In fact, with the added challenge of sailing a damaged ship, these habits become even more important.

Lastly, there’s a component often overlooked when talking about tertiary prevention – managing the emotional and psychological impact of living with advanced heart disease. It’s like dealing with the fear and uncertainty that comes with sailing a damaged ship. Therapy, support groups, and stress management techniques can be immensely helpful here.

Tertiary prevention of CAD is challenging but remember, you’re not alone on this voyage. With your healthcare team as your guiding lighthouse, and your inner resilience as your compass, you can navigate these tough waters. It’s a journey of courage, of endurance, and above all, hope. And every single day you sail forward, despite the odds, is a testament to your strength. Remember, the beauty of sailing lies not in calm seas but in navigating the stormy ones.

Imagine a narrow, congested road is causing traffic. What if you could just push the sides and make the road wider? That’s essentially what PCI does. A balloon-tipped catheter is inserted into the blocked artery and then inflated to widen the artery, improving blood flow. Sometimes, a small wire-mesh tube called a stent is left in the artery to keep it open. This procedure can be life-saving in the case of a heart attack and can also help manage chronic CAD symptoms.

In the face of advanced CAD, tertiary prevention is also about symptom management. Certain symptoms like angina (chest pain), breathlessness, and fatigue can significantly impact quality of life. Apart from medical and surgical interventions, personalized approaches like physiotherapy, guided exercise programs, dietary plans, and mental health counseling can help manage these symptoms and improve daily function.

In the end, tertiary prevention in CAD is about making the best out of a challenging situation. It’s about maximizing your health, function, and well-being, and reducing the risk of future heart events. Despite the turbulent seas, with effective tertiary prevention, you can continue sailing and embracing the journey of life.

References

  • 1
    National Library of Medicine – National Center for Biotechnology Information. (2023, February 9). Coronary artery disease – statpearls – NCBI bookshelf. Coronary Artery Disease. https://www.ncbi.nlm.nih.gov/books/NBK564304/
  • 2
    Gulati M, Levy P, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain. J Am Coll Cardiol. 2021 Nov, 78 (22) e187–e285.
  • 3
    U.S. Department of Health and Human Services. (2022, March 25). Causes and risk factors. National Heart Lung and Blood Institute. https://www.nhlbi.nih.gov/health/heart-attack/causes
  • 4
    Ojha N, Dhamoon AS. Myocardial Infarction. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537076/
  • 5
    Ambrose JA, Singh M. Pathophysiology of coronary artery disease leading to acute coronary syndromes. F1000Prime Rep. 2015 Jan 14;7:08. doi: 10.12703/P7-08. PMID: 25705391; PMCID: PMC4311268.
  • 6
    Said MA, van de Vegte YJ, Zafar MM, van der Ende MY, Raja GK, Verweij N, van der Harst P. Contributions of Interactions Between Lifestyle and Genetics on Coronary Artery Disease Risk. Curr Cardiol Rep. 2019 Jul 27;21(9):89. doi: 10.1007/s11886-019-1177-x. PMID: 31352625; PMCID: PMC6661028.
  • 7
    Khera AV, Emdin CA, Drake I, Natarajan P, Bick AG, Cook NR, Chasman DI, Baber U, Mehran R, Rader DJ, Fuster V, Boerwinkle E, Melander O, Orho-Melander M, Ridker PM, Kathiresan S. Genetic Risk, Adherence to a Healthy Lifestyle, and Coronary Disease. N Engl J Med. 2016 Dec 15;375(24):2349-2358. doi: 10.1056/NEJMoa1605086. Epub 2016 Nov 13. PMID: 27959714; PMCID: PMC5338864.
  • 8
    Yoriko Heianza , Lu Qi, Impact of Genes and Environment on Obesity and Cardiovascular Disease, Endocrinology, Volume 160, Issue 1, January 2019, Pages 81–100, https://doi.org/10.1210/en.2018-00591
  • 9
    American College of Cardiology. (2011, April 5). Earliest case of coronary artery disease found in Egyptian princess. Earliest Case Of Coronary Artery Disease Found In Egyptian Princess. https://www.acc.org/about-acc/press-releases/2011/04/05/16/22/mummies
  • 10
    Hajar R. Coronary Heart Disease: From Mummies to 21st Century. Heart Views. 2017 Apr-Jun;18(2):68-74. doi: 10.4103/HEARTVIEWS.HEARTVIEWS_57_17. PMID: 28706602; PMCID: PMC5501035.
  • 11
    Nabel, E. G., & Braunwald, E. (2012). A tale of coronary artery disease and myocardial infarction. New England Journal of Medicine, 366(1), 54–63. https://doi.org/10.1056/nejmra1112570
  • 12
    Mahmood SS, Levy D, Vasan RS, Wang TJ. The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective. Lancet. 2014 Mar 15;383(9921):999-1008. doi: 10.1016/S0140-6736(13)61752-3. Epub 2013 Sep 29. PMID: 24084292; PMCID: PMC4159698.
  • 13
    Gallestey, J. Bacallao (2016, April 22). Framingham Heart Study. Encyclopedia Britannica. https://www.britannica.com/event/Framingham-Heart-Studay
  • 14
    O’Donnell, C. J., & Elosua, R. (2008). Cardiovascular risk factors. insights from Framingham Heart Study. Revista Española de Cardiología (English Edition), 61(3), 299–310. https://doi.org/10.1016/s1885-5857(08)60118-8
  • 15
    Yngve A. A Historical Perspective of the Understanding of the Link between Diet and Coronary Heart Disease. Am J Lifestyle Med. 2009;3(1 Suppl.):35S-38S. doi: 10.1177/1559827609334887. PMID: 20046857; PMCID: PMC2790142.
  • 16
    Katherine D Pett, MS, MEd, RDN and others, The Seven Countries Study, European Heart Journal, Volume 38, Issue 42, 07 November 2017, Pages 3119–3121, https://doi.org/10.1093/eurheartj/ehx603
  • 17
    Brown JC, Gerhardt TE, Kwon E. Risk Factors for Coronary Artery Disease. 2023 Jan 23. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 32119297.
  • 18
    Brown JC, Gerhardt TE, Kwon E. Risk Factors for Coronary Artery Disease. [Updated 2023 Jan 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554410/
  • 19
    Amini, M., Zayeri, F. & Salehi, M. Trend analysis of cardiovascular disease mortality, incidence, and mortality-to-incidence ratio: results from global burden of disease study 2017. BMC Public Health 21, 401 (2021). https://doi.org/10.1186/s12889-021-10429-0
  • 20
    American College of Cardiology . (2019, March 7). Heart attacks increasingly common in young adults. Heart Attacks Increasingly Common in Young Adults. https://www.acc.org/about-acc/press-releases/2019/03/07/08/45/heart-attacks-increasingly-common-in-young-adults
  • 21
    Gaziano TA, Bitton A, Anand S, Abrahams-Gessel S, Murphy A. Growing epidemic of coronary heart disease in low- and middle-income countries. Curr Probl Cardiol. 2010 Feb;35(2):72-115. doi: 10.1016/j.cpcardiol.2009.10.002. PMID: 20109979; PMCID: PMC2864143.
  • 22
    Wurie HR, Cappuccio FP. Cardiovascular disease in low- and middle-income countries: an urgent priority. Ethn Health. 2012;17(6):543-50. doi: 10.1080/13557858.2012.778642. PMID: 23534502; PMCID: PMC7613448.
  • 23
    Garcia M, Mulvagh SL, Merz CN, Buring JE, Manson JE. Cardiovascular Disease in Women: Clinical Perspectives. Circ Res. 2016 Apr 15;118(8):1273-93. doi: 10.1161/CIRCRESAHA.116.307547. PMID: 27081110; PMCID: PMC4834856.
  • 24
    Heidenreich, P. (2011). Forecasting the future of cardiovascular disease in the United States: A policy statement from the American Heart Association. American Heart Association, 2011, 12–13. https://doi.org/10.1016/j.yane.2012.01.067
  • 25
    Powell-Wiley, T. M., Poirier, P., Burke, L. E., Després, J.-P., Gordon-Larsen, P., Lavie, C. J., Lear, S. A., Ndumele, C. E., Neeland, I. J., Sanders, P., & St-Onge, M.-P. (2021). Obesity and cardiovascular disease: A scientific statement from the American Heart Association. Circulation, 143(21). https://doi.org/10.1161/cir.0000000000000973
  • 26
    Cassar A, Holmes DR Jr, Rihal CS, Gersh BJ. Chronic coronary artery disease: diagnosis and management. Mayo Clin Proc. 2009 Dec;84(12):1130-46. doi: 10.4065/mcp.2009.0391. PMID: 19955250; PMCID: PMC2787400.
  • 27
    Kandaswamy E, Zuo L. Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology. Int J Mol Sci. 2018 Jan 31;19(2):424. doi: 10.3390/ijms19020424. PMID: 29385089; PMCID: PMC5855646.
  • 28
    Warren TY, Barry V, Hooker SP, Sui X, Church TS, Blair SN. Sedentary behaviors increase risk of cardiovascular disease mortality in men. Med Sci Sports Exerc. 2010 May;42(5):879-85. doi: 10.1249/MSS.0b013e3181c3aa7e. PMID: 19996993; PMCID: PMC2857522.
  • 29
    Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.
  • 30
    Roberts R. Genetics of coronary artery disease: an update. Methodist Debakey Cardiovasc J. 2014 Jan-Mar;10(1):7-12. doi: 10.14797/mdcj-10-1-7. PMID: 24932356; PMCID: PMC4051327.
  • 31
    van Rosendael AR, Bax AM, van den Hoogen IJ, Smit JM, Al’Aref SJ, Achenbach S, Al-Mallah MH, Andreini D, Berman DS, Budoff MJ, Cademartiri F, Callister TQ, Chang HJ, Chinnaiyan K, Chow BJW, Cury RC, DeLago A, Feuchtner G, Hadamitzky M, Hausleiter J, Kaufmann PA, Kim YJ, Leipsic JA, Maffei E, Marques H, de Araújo Gonçalves P, Pontone G, Raff GL, Rubinshtein R, Villines TC, Gransar H, Lu Y, Peña JM, Lin FY, Shaw LJ, Narula J, Min JK, Bax JJ. Associations between dyspnoea, coronary atherosclerosis, and cardiovascular outcomes: results from the long-term follow-up CONFIRM registry. Eur Heart J Cardiovasc Imaging. 2022 Jan 24;23(2):266-274. doi: 10.1093/ehjci/jeaa323. PMID: 33538308; PMCID: PMC8932389.
  • 32
    Celano CM, Daunis DJ, Lokko HN, Campbell KA, Huffman JC. Anxiety Disorders and Cardiovascular Disease. Curr Psychiatry Rep. 2016 Nov;18(11):101. doi: 10.1007/s11920-016-0739-5. PMID: 27671918; PMCID: PMC5149447.
  • 33
    Askin L, Uzel KE, Tanrıverdi O, Kavalcı V, Yavcin O, Turkmen S. The relationship between coronary artery disease and depression and anxiety scores. North Clin Istanb. 2020 Aug 5;7(5):523-526. doi: 10.14744/nci.2020.72602. PMID: 33163893; PMCID: PMC7603855.
  • 34
    Gaudel P, Neupane S, Koivisto AM, Kaunonen M, Rantanen A. Effects of intervention on lifestyle changes among coronary artery disease patients: A 6-month follow-up study. Nurs Open. 2022 Jul;9(4):2024-2036. doi: 10.1002/nop2.1212. Epub 2022 Apr 17. PMID: 35434911; PMCID: PMC9190674.
  • 35
    Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.
  • 36
    Bauersachs R, Zeymer U, Brière JB, Marre C, Bowrin K, Huelsebeck M. Burden of Coronary Artery Disease and Peripheral Artery Disease: A Literature Review. Cardiovasc Ther. 2019 Nov 26;2019:8295054. doi: 10.1155/2019/8295054. PMID: 32099582; PMCID: PMC7024142.
  • 37
    Ekinci G. Economic Impacts of Cardiovascular Diseases: An Econometric Evaluation in Turkey. Iran J Public Health. 2023 Jan;52(1):118-127. doi: 10.18502/ijph.v52i1.11673. PMID: 36824237; PMCID: PMC9941436.
  • 38
    Reid RD, McDonnell LA, Riley DL, Mark AE, Mosca L, Beaton L, Papadakis S, Blanchard CM, Mochari-Greenberger H, O’Farrell P, Wells GA, Slovinec D’Angelo ME, Pipe AL. Effect of an intervention to improve the cardiovascular health of family members of patients with coronary artery disease: a randomized trial. CMAJ. 2014 Jan 7;186(1):23-30. doi: 10.1503/cmaj.130550. Epub 2013 Nov 18. PMID: 24246588; PMCID: PMC3883820.
  • 39
    Kandaswamy E, Zuo L. Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology. Int J Mol Sci. 2018 Jan 31;19(2):424. doi: 10.3390/ijms19020424. PMID: 29385089; PMCID: PMC5855646.
  • 40
    Khatib R, Marshall K, Silcock J, Forrest C, Hall AS. Adherence to coronary artery disease secondary prevention medicines: exploring modifiable barriers. Open Heart. 2019 Jul 3;6(2):e000997. doi: 10.1136/openhrt-2018-000997. PMID: 31354954; PMCID: PMC6615814.
  • 41
    Coping with feelings. www.heart.org. (n.d.). https://www.heart.org/en/health-topics/cardiac-rehab/taking-care-of-yourself/coping-with-feelings
  • 42
    Gomes L, Liébana-Presa C, Araújo B, Marques F, Fernández-Martínez E. Heart Disease, Now What? Improving Quality of Life through Education. Int J Environ Res Public Health. 2021 Mar 17;18(6):3077. doi: 10.3390/ijerph18063077. PMID: 33802701; PMCID: PMC8002524.
  • 43
    Sharifi-Rad J, Rodrigues CF, Sharopov F, Docea AO, Can Karaca A, Sharifi-Rad M, Kahveci Karıncaoglu D, Gülseren G, Şenol E, Demircan E, Taheri Y, Suleria HAR, Özçelik B, Nur Kasapoğlu K, Gültekin-Özgüven M, Daşkaya-Dikmen C, Cho WC, Martins N, Calina D. Diet, Lifestyle and Cardiovascular Diseases: Linking Pathophysiology to Cardioprotective Effects of Natural Bioactive Compounds. Int J Environ Res Public Health. 2020 Mar 30;17(7):2326. doi: 10.3390/ijerph17072326. PMID: 32235611; PMCID: PMC7177934.
  • 44
    Chiuve, S. E., McCullough, M. L., Sacks, F. M., & Rimm, E. B. (2006). Healthy lifestyle factors in the primary prevention of coronary heart disease among men. Circulation, 114(2), 160–167. https://doi.org/10.1161/circulationaha.106.621417
  • 45
    Compare A, Zarbo C, Manzoni GM, Castelnuovo G, Baldassari E, Bonardi A, Callus E, Romagnoni C. Social support, depression, and heart disease: a ten year literature review. Front Psychol. 2013 Jul 1;4:384. doi: 10.3389/fpsyg.2013.00384. PMID: 23847561; PMCID: PMC3696881.
  • 46
    Wenn P, Meshoyrer D, Barber M, Ghaffar A, Razka M, Jose S, Zeltser R, Makaryus AN. Perceived Social Support and its Effects on Treatment Compliance and Quality of Life in Cardiac Patients. J Patient Exp. 2022 Feb 4;9:23743735221074170. doi: 10.1177/23743735221074170. PMID: 35141401; PMCID: PMC8819762.
  • 47
    Rakhshan M, Toufigh A, Dehghani-Firouzabadi A, Yektatalab S. Effect of Cardiac Rehabilitation on Hope Among Cardiac Patients After Coronary Artery Bypass Graft Surgery. Risk Manag Healthc Policy. 2020 Aug 25;13:1319-1326. doi: 10.2147/RMHP.S262656. PMID: 32922100; PMCID: PMC7457873.
  • 48
    Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/
  • 49
    Chaudhry R, Rahman S, Law MA. Anatomy, Thorax, Heart Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470522/
  • 50
    Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/
  • 51
    Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/
  • 52
    Chaudhry R, Rahman S, Law MA. Anatomy, Thorax, Heart Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470522/
  • 53
    Saxton A, Chaudhry R, Manna B. Anatomy, Thorax, Heart Right Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537357/
  • 54
    Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/
  • 55
    InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. Coronary artery disease: Overview. 2013 Feb 13 [Updated 2017 Jul 27]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK355313/
  • 56
    Goodwill AG, Dick GM, Kiel AM, Tune JD. Regulation of Coronary Blood Flow. Compr Physiol. 2017 Mar 16;7(2):321-382. doi: 10.1002/cphy.c160016. PMID: 28333376; PMCID: PMC5966026.
  • 57
    Pittman RN. Regulation of Tissue Oxygenation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Chapter 2, The Circulatory System and Oxygen Transport. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54112/
  • 58
    InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. How does the blood circulatory system work? 2010 Mar 12 [Updated 2019 Jan 31]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279250/
  • 59
    Sharma B, Chang A, Red-Horse K. Coronary Artery Development: Progenitor Cells and Differentiation Pathways. Annu Rev Physiol. 2017 Feb 10;79:1-19. doi: 10.1146/annurev-physiol-022516-033953. Epub 2016 Dec 9. PMID: 27959616; PMCID: PMC5513160.
  • 60
    Tucker WD, Arora Y, Mahajan K. Anatomy, Blood Vessels. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470401/
  • 61
    Pittman RN. Regulation of Tissue Oxygenation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Chapter 2, The Circulatory System and Oxygen Transport. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54112/
  • 62
    Falk, E., Shah, P. K., & Fuster, V. (1995). Coronary plaque disruption. Circulation, 92(3), 657–671. https://doi.org/10.1161/01.cir.92.3.657
  • 63
    Saleh M, Ambrose JA. Understanding myocardial infarction. F1000Res. 2018 Sep 3;7:F1000 Faculty Rev-1378. doi: 10.12688/f1000research.15096.1. PMID: 30228871; PMCID: PMC6124376.
  • 64
    Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.
  • 65
    Pittman RN. Regulation of Tissue Oxygenation. San Rafael (CA): Morgan & Claypool Life Sciences; 2011. Chapter 2, The Circulatory System and Oxygen Transport. Available from: https://www.ncbi.nlm.nih.gov/books/NBK54112/
  • 66
    InformedHealth.org [Internet]. Cologne, Germany: Institute for Quality and Efficiency in Health Care (IQWiG); 2006-. How does the blood circulatory system work? 2010 Mar 12 [Updated 2019 Jan 31]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK279250/
  • 67
    Chaudhry R, Miao JH, Rehman A. Physiology, Cardiovascular. [Updated 2022 Oct 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493197/
  • 68
    Joyner MJ, Casey DP. Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiol Rev. 2015 Apr;95(2):549-601. doi: 10.1152/physrev.00035.2013. PMID: 25834232; PMCID: PMC4551211.
  • 69
    Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/
  • 70
    Pimple P, Hammadah M, Wilmot K, Ramadan R, Al Mheid I, Levantsevych O, Sullivan S, Garcia EV, Nye J, Shah AJ, Ward L, Mehta P, Raggi P, Bremner JD, Quyyumi AA, Vaccarino V. Chest Pain and Mental Stress-Induced Myocardial Ischemia: Sex Differences. Am J Med. 2018 May;131(5):540-547.e1. doi: 10.1016/j.amjmed.2017.11.026. Epub 2017 Dec 7. PMID: 29224740; PMCID: PMC5910270.
  • 71
    Pinckard K, Baskin KK, Stanford KI. Effects of Exercise to Improve Cardiovascular Health. Front Cardiovasc Med. 2019 Jun 4;6:69. doi: 10.3389/fcvm.2019.00069. PMID: 31214598; PMCID: PMC6557987.
  • 72
    Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.
  • 73
    Holzapfel, G. A., Sommer, G., Gasser, C. T., & Regitnig, P. (2005). Determination of layer-specific mechanical properties of human coronary arteries with nonatherosclerotic intimal thickening and related constitutive modeling. American Journal of Physiology-Heart and Circulatory Physiology, 289(5). https://doi.org/10.1152/ajpheart.00934.2004
  • 74
    OpenStax, L. L. &. (n.d.). Anatomy and Physiology II. Structure and Function of Blood Vessels | Anatomy and Physiology II. https://courses.lumenlearning.com/suny-ap2/chapter/structure-and-function-of-blood-vessels/
  • 75
    Milutinović, A., Šuput, D. ., & Zorc-Pleskovič, R. (2020). Pathogenesis of atherosclerosis in the tunica intima, media, and adventitia of coronary arteries: An updated review. Biomolecules and Biomedicine, 20(1), 21–30. https://doi.org/10.17305/bjbms.2019.4320
  • 76
    Khalilgharibi N, Mao Y. To form and function: on the role of basement membrane mechanics in tissue development, homeostasis, and disease. Open Biol. 2021 Feb;11(2):200360. doi: 10.1098/rsob.200360. Epub 2021 Feb 17. PMID: 33593159; PMCID: PMC8061686.
  • 77
    Imo E. Hoefer and others, Biomechanical factors as triggers of vascular growth, Cardiovascular Research, Volume 99, Issue 2, 15 July 2013, Pages 276–283, https://doi.org/10.1093/cvr/cvt089
  • 78
    Vatner, S. F., Zhang, J., Vyzas, C., Mishra, K., Graham, R. M., & Vatner, D. E. (2021). Vascular stiffness in aging and disease. Frontiers in Physiology, 12. https://doi.org/10.3389/fphys.2021.762437
  • 79
    Majesky MW, Dong XR, Hoglund V, Mahoney WM Jr, Daum G. The adventitia: a dynamic interface containing resident progenitor cells. Arterioscler Thromb Vasc Biol. 2011 Jul;31(7):1530-9. doi: 10.1161/ATVBAHA.110.221549. PMID: 21677296; PMCID: PMC3382115.
  • 80
    Belhoul-Fakir, H., Wu, J., Yeow, Y. L., Musk, G. C., Kershaw, H., Ingley, E., Zhao, B. S., Reid, C. M., Lagat, C., Evans, B., Thompson, P. L., Brown, M. L., Hamzah, J., & Jansen, S. (2023). Injury to the Tunica Media Initiates Atherogenesis in the presence of Hyperlipidemia. Frontiers in Cardiovascular Medicine, 10. https://doi.org/10.3389/fcvm.2023.1152124
  • 81
    Chow MJ, Turcotte R, Lin CP, Zhang Y. Arterial extracellular matrix: a mechanobiological study of the contributions and interactions of elastin and collagen. Biophys J. 2014 Jun 17;106(12):2684-92. doi: 10.1016/j.bpj.2014.05.014. PMID: 24940786; PMCID: PMC4070071.
  • 82
    Majesky MW, Dong XR, Hoglund V, Mahoney WM Jr, Daum G. The adventitia: a dynamic interface containing resident progenitor cells. Arterioscler Thromb Vasc Biol. 2011 Jul;31(7):1530-9. doi: 10.1161/ATVBAHA.110.221549. PMID: 21677296; PMCID: PMC3382115.
  • 83
    Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/
  • 84
    Swirski FK, Nahrendorf M. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Science. 2013 Jan 11;339(6116):161-6. doi: 10.1126/science.1230719. PMID: 23307733; PMCID: PMC3891792.
  • 85
    Swirski FK, Nahrendorf M. Leukocyte behavior in atherosclerosis, myocardial infarction, and heart failure. Science. 2013 Jan 11;339(6116):161-6. doi: 10.1126/science.1230719. PMID: 23307733; PMCID: PMC3891792.
  • 86
    Javadifar A, Rastgoo S, Banach M, Jamialahmadi T, Johnston TP, Sahebkar A. Foam Cells as Therapeutic Targets in Atherosclerosis with a Focus on the Regulatory Roles of Non-Coding RNAs. Int J Mol Sci. 2021 Mar 3;22(5):2529. doi: 10.3390/ijms22052529. PMID: 33802600; PMCID: PMC7961492.
  • 87
    Dong J, Yang S, Zhuang Q, Sun J, Wei P, Zhao X, Chen Y, Chen X, Li M, Wei L, Chen C, Fan Y, Shen C. The Associations of Lipid Profiles With Cardiovascular Diseases and Death in a 10-Year Prospective Cohort Study. Front Cardiovasc Med. 2021 Nov 25;8:745539. doi: 10.3389/fcvm.2021.745539. PMID: 34901209; PMCID: PMC8655628.
  • 88
    Wilson PW. High-density lipoprotein, low-density lipoprotein and coronary artery disease. Am J Cardiol. 1990 Sep 4;66(6):7A-10A. doi: 10.1016/0002-9149(90)90562-f. PMID: 2203248.
  • 89
    Tall AR, Yvan-Charvet L. Cholesterol, inflammation and innate immunity. Nat Rev Immunol. 2015 Feb;15(2):104-16. doi: 10.1038/nri3793. PMID: 25614320; PMCID: PMC4669071.
  • 90
    Ilhan F, Kalkanli ST. Atherosclerosis and the role of immune cells. World J Clin Cases. 2015 Apr 16;3(4):345-52. doi: 10.12998/wjcc.v3.i4.345. PMID: 25879006; PMCID: PMC4391004.
  • 91
    Parthasarathy S, Raghavamenon A, Garelnabi MO, Santanam N. Oxidized low-density lipoprotein. Methods Mol Biol. 2010;610:403-17. doi: 10.1007/978-1-60327-029-8_24. PMID: 20013192; PMCID: PMC3315351.
  • 92
    Bjornstad P, Eckel RH. Pathogenesis of Lipid Disorders in Insulin Resistance: a Brief Review. Curr Diab Rep. 2018 Oct 17;18(12):127. doi: 10.1007/s11892-018-1101-6. PMID: 30328521; PMCID: PMC6428207.
  • 93
    Ference BA, Ginsberg HN, Graham I, Ray KK, Packard CJ, Bruckert E, Hegele RA, Krauss RM, Raal FJ, Schunkert H, Watts GF, Borén J, Fazio S, Horton JD, Masana L, Nicholls SJ, Nordestgaard BG, van de Sluis B, Taskinen MR, Tokgözoglu L, Landmesser U, Laufs U, Wiklund O, Stock JK, Chapman MJ, Catapano AL. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017 Aug 21;38(32):2459-2472. doi: 10.1093/eurheartj/ehx144. PMID: 28444290; PMCID: PMC5837225.
  • 94
    Mann S, Beedie C, Jimenez A. Differential effects of aerobic exercise, resistance training and combined exercise modalities on cholesterol and the lipid profile: review, synthesis, and recommendations. Sports Med. 2014 Feb;44(2):211-21. doi: 10.1007/s40279-013-0110-5. PMID: 24174305; PMCID: PMC3906547.
  • 95
    Sarwar, N., Danesh, J., Eiriksdottir, G., Sigurdsson, G., Wareham, N., Bingham, S., Boekholdt, S. M., Khaw, K.-T., & Gudnason, V. (2007). Triglycerides and the risk of coronary heart disease. Circulation, 115(4), 450–458. https://doi.org/10.1161/circulationaha.106.637793
  • 96
    Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/
  • 97
    Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/
  • 98
    Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/
  • 99
    Feingold KR. Introduction to Lipids and Lipoproteins. [Updated 2021 Jan 19]. In: Feingold KR, Anawalt B, Blackman MR, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK305896/
  • 100
    Holesh JE, Aslam S, Martin A. Physiology, Carbohydrates. [Updated 2023 May 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459280/
  • 101
    Ludwig D S, Hu F B, Tappy L, Brand-Miller J. Dietary carbohydrates: role of quality and quantity in chronic disease BMJ 2018; 361 :k2340 doi:10.1136/bmj.k2340
  • 102
    Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005 May;26(2):19-39. PMID: 16278749; PMCID: PMC1204764.
  • 103
    Chang, L., Chiang, SH. & Saltiel, A.R. Insulin Signaling and the Regulation of Glucose Transport. Mol Med 10, 65–71 (2004). https://doi.org/10.2119/2005-00029.Saltiel
  • 104
    Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005 May;26(2):19-39. PMID: 16278749; PMCID: PMC1204764.
  • 105
    Freeman AM, Pennings N. Insulin Resistance. [Updated 2022 Sep 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507839/
  • 106
    Ormazabal, V., Nair, S., Elfeky, O. et al. Association between insulin resistance and the development of cardiovascular disease. Cardiovasc Diabetol 17, 122 (2018). https://doi.org/10.1186/s12933-018-0762-4
  • 107
    Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/
  • 108
    Aronson D, Edelman ER. Coronary artery disease and diabetes mellitus. Cardiol Clin. 2014 Aug;32(3):439-55. doi: 10.1016/j.ccl.2014.04.001. Epub 2014 Jun 10. PMID: 25091969; PMCID: PMC4672945.
  • 109
    Undas A, Wiek I, Stêpien E, Zmudka K, Tracz W. Hyperglycemia is associated with enhanced thrombin formation, platelet activation, and fibrin clot resistance to lysis in patients with acute coronary syndrome. Diabetes Care. 2008 Aug;31(8):1590-5. doi: 10.2337/dc08-0282. Epub 2008 May 16. PMID: 18487475; PMCID: PMC2494657.
  • 110
    Liu X, Li T, Xu H, Wang C, Ma X, Huang H, Hu Y, Chu H. Hyperglycemia may increase deep vein thrombosis in trauma patients with lower limb fracture. Front Cardiovasc Med. 2022 Sep 8;9:944506. doi: 10.3389/fcvm.2022.944506. PMID: 36158801; PMCID: PMC9498976.
  • 111
    Chaudhry R, Rahman S, Law MA. Anatomy, Thorax, Heart Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470522/
  • 112
    Ogobuiro I, Wehrle CJ, Tuma F. Anatomy, Thorax, Heart Coronary Arteries. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK534790/
  • 113
    Rehman S, Khan A, Rehman A. Physiology, Coronary Circulation. [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482413/
  • 114
    Duncker DJ, Bache RJ. Regulation of coronary blood flow during exercise. Physiol Rev. 2008 Jul;88(3):1009-86. doi: 10.1152/physrev.00045.2006. PMID: 18626066.
  • 115
    Sandy N Shah, D. (2023, July 20). Coronary artery atherosclerosis. Practice Essentials, Background, Anatomy. https://emedicine.medscape.com/article/153647-overview?form=fpf
  • 116
    Fang J, Luncheon C, Ayala C, Odom E, Loustalot F. Awareness of Heart Attack Symptoms and Response Among Adults – United States, 2008, 2014, and 2017. MMWR Morb Mortal Wkly Rep. 2019 Feb 8;68(5):101-106. doi: 10.15585/mmwr.mm6805a2. PMID: 31851653; PMCID: PMC6366680.
  • 117
    Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. Int J Mol Sci. 2020 Oct 15;21(20):7609. doi: 10.3390/ijms21207609. PMID: 33076218; PMCID: PMC7589849.
  • 118
    Fang J, Luncheon C, Ayala C, Odom E, Loustalot F. Awareness of Heart Attack Symptoms and Response Among Adults – United States, 2008, 2014, and 2017. MMWR Morb Mortal Wkly Rep. 2019 Feb 8;68(5):101-106. doi: 10.15585/mmwr.mm6805a2. PMID: 31851653; PMCID: PMC6366680.
  • 119
    Punchard NA, Whelan CJ, Adcock I. The Journal of Inflammation. J Inflamm (Lond). 2004 Sep 27;1(1):1. doi: 10.1186/1476-9255-1-1. PMID: 15813979; PMCID: PMC1074343.
  • 120
    Pahwa R, Goyal A, Jialal I. Chronic Inflammation. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK493173/
  • 121
    Furman D, Campisi J, Verdin E, Carrera-Bastos P, Targ S, Franceschi C, Ferrucci L, Gilroy DW, Fasano A, Miller GW, Miller AH, Mantovani A, Weyand CM, Barzilai N, Goronzy JJ, Rando TA, Effros RB, Lucia A, Kleinstreuer N, Slavich GM. Chronic inflammation in the etiology of disease across the life span. Nat Med. 2019 Dec;25(12):1822-1832. doi: 10.1038/s41591-019-0675-0. Epub 2019 Dec 5. PMID: 31806905; PMCID: PMC7147972.
  • 122
    Rajendran P, Rengarajan T, Thangavel J, Nishigaki Y, Sakthisekaran D, Sethi G, Nishigaki I. The vascular endothelium and human diseases. Int J Biol Sci. 2013 Nov 9;9(10):1057-69. doi: 10.7150/ijbs.7502. PMID: 24250251; PMCID: PMC3831119.
  • 123
    Rajendran P, Rengarajan T, Thangavel J, Nishigaki Y, Sakthisekaran D, Sethi G, Nishigaki I. The vascular endothelium and human diseases. Int J Biol Sci. 2013 Nov 9;9(10):1057-69. doi: 10.7150/ijbs.7502. PMID: 24250251; PMCID: PMC3831119.
  • 124
    Sharma JN, Al-Omran A, Parvathy SS. Role of nitric oxide in inflammatory diseases. Inflammopharmacology. 2007 Dec;15(6):252-9. doi: 10.1007/s10787-007-0013-x. PMID: 18236016.
  • 125
    Iwata M, Inoue T, Asai Y, Hori K, Fujiwara M, Matsuo S, Tsuchida W, Suzuki S. The protective role of localized nitric oxide production during inflammation may be mediated by the heme oxygenase-1/carbon monoxide pathway. Biochem Biophys Rep. 2020 Jul 24;23:100790. doi: 10.1016/j.bbrep.2020.100790. PMID: 32760814; PMCID: PMC7390790.
  • 126
    Chiu JJ, Chien S. Effects of disturbed flow on vascular endothelium: pathophysiological basis and clinical perspectives. Physiol Rev. 2011 Jan;91(1):327-87. doi: 10.1152/physrev.00047.2009. PMID: 21248169; PMCID: PMC3844671.
  • 127
    Park KH, Park WJ. Endothelial Dysfunction: Clinical Implications in Cardiovascular Disease and Therapeutic Approaches. J Korean Med Sci. 2015 Sep;30(9):1213-25. doi: 10.3346/jkms.2015.30.9.1213. Epub 2015 Aug 13. PMID: 26339159; PMCID: PMC4553666.
  • 128
    Gimbrone MA Jr, García-Cardeña G. Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis. Circ Res. 2016 Feb 19;118(4):620-36. doi: 10.1161/CIRCRESAHA.115.306301. PMID: 26892962; PMCID: PMC4762052.
  • 129
    Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.
  • 130
    Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.
  • 131
    Semaev S, Shakhtshneider E. Genetic Risk Score for Coronary Heart Disease: Review. J Pers Med. 2020 Nov 20;10(4):239. doi: 10.3390/jpm10040239. PMID: 33233501; PMCID: PMC7712936.
  • 132
    Chow CK, Pell AC, Walker A, O’Dowd C, Dominiczak AF, Pell JP. Families of patients with premature coronary heart disease: an obvious but neglected target for primary prevention. BMJ. 2007 Sep 8;335(7618):481-5. doi: 10.1136/bmj.39253.577859.BE. PMID: 17823190; PMCID: PMC1971158.
  • 133
    Virolainen, S.J., VonHandorf, A., Viel, K.C.M.F. et al. Gene–environment interactions and their impact on human health. Genes Immun 24, 1–11 (2023). https://doi.org/10.1038/s41435-022-00192-6
  • 134
    Said, M.A., van de Vegte, Y.J., Zafar, M.M. et al. Contributions of Interactions Between Lifestyle and Genetics on Coronary Artery Disease Risk. Curr Cardiol Rep 21, 89 (2019). https://doi.org/10.1007/s11886-019-1177-x
  • 135
    Sahu M, Prasuna JG. Twin Studies: A Unique Epidemiological Tool. Indian J Community Med. 2016 Jul-Sep;41(3):177-82. doi: 10.4103/0970-0218.183593. PMID: 27385869; PMCID: PMC4919929.
  • 136
    Prescott CA, Kendler KS. Twin Study Design. Alcohol Health Res World. 1995;19(3):200-205. PMID: 31798103; PMCID: PMC6875762.
  • 137
    Smith MC, Baker JR, Gleaves E, Singh A, Kazimuddin M. Twinning: Coronary Artery Disease in Monozygotic Twins. Cureus. 2021 Jul 3;13(7):e16139. doi: 10.7759/cureus.16139. PMID: 34367763; PMCID: PMC8330499.
  • 138
    Drobni, Z. D., Kolossvary, M., Karady, J., Jermendy, A. L., Tarnoki, A. D., Tarnoki, D. L., Simon, J., Szilveszter, B., Littvay, L., Voros, S., Jermendy, G., Merkely, B., & Maurovich-Horvat, P. (2022). Heritability of coronary artery disease: Insights from a classical twin study. Circulation: Cardiovascular Imaging, 15(3). https://doi.org/10.1161/circimaging.121.013348
  • 139
    Khera AV, Kathiresan S. Genetics of coronary artery disease: discovery, biology and clinical translation. Nat Rev Genet. 2017 Jun;18(6):331-344. doi: 10.1038/nrg.2016.160. Epub 2017 Mar 13. PMID: 28286336; PMCID: PMC5935119.
  • 140
    Acheson LS, Wang C, Zyzanski SJ, Lynn A, Ruffin MT 4th, Gramling R, Rubinstein WS, O’Neill SM, Nease DE Jr; Family Healthware Impact Trial (FHITr) Group. Family history and perceptions about risk and prevention for chronic diseases in primary care: a report from the family healthware impact trial. Genet Med. 2010 Apr;12(4):212-8. doi: 10.1097/GIM.0b013e3181d56ae6. PMID: 20216073; PMCID: PMC4037165.
  • 141
    McPherson, R., & Tybjaerg-Hansen, A. (2016). Genetics of coronary artery disease. Circulation Research, 118(4), 564–578. https://doi.org/10.1161/circresaha.115.306566
  • 142
    McPherson, R., & Tybjaerg-Hansen, A. (2016). Genetics of coronary artery disease. Circulation Research, 118(4), 564–578. https://doi.org/10.1161/circresaha.115.306566
  • 143
    Albert PR. What is a functional genetic polymorphism? Defining classes of functionality. J Psychiatry Neurosci. 2011 Nov;36(6):363-5. doi: 10.1503/jpn.110137. PMID: 22011561; PMCID: PMC3201989.
  • 144
    Sitinjak BDP, Murdaya N, Rachman TA, Zakiyah N, Barliana MI. The Potential of Single Nucleotide Polymorphisms (SNPs) as Biomarkers and Their Association with the Increased Risk of Coronary Heart Disease: A Systematic Review. Vasc Health Risk Manag. 2023 May 5;19:289-301. doi: 10.2147/VHRM.S405039. PMID: 37179817; PMCID: PMC10167955.
  • 145
    Marrzoq LF, Sharif FA, Abed AA. Relationship between ApoE gene polymorphism and coronary heart disease in Gaza Strip. J Cardiovasc Dis Res. 2011 Jan;2(1):29-35. doi: 10.4103/0975-3583.78584. PMID: 21716749; PMCID: PMC3120269.
  • 146
    Zaghloul A, Iorgoveanu C, Desai A, Balakumaran K, Chen K. Methylenetetrahydrofolate Reductase Polymorphism and Premature Coronary Artery Disease. Cureus. 2019 Jun 27;11(6):e5014. doi: 10.7759/cureus.5014. PMID: 31497444; PMCID: PMC6716763.
  • 147
    Chaudhary R, Garg J, Shah N, Sumner A. PCSK9 inhibitors: A new era of lipid lowering therapy. World J Cardiol. 2017 Feb 26;9(2):76-91. doi: 10.4330/wjc.v9.i2.76. PMID: 28289523; PMCID: PMC5329749.
  • 148
    Holmes MV, Smith GD. Dyslipidaemia: Revealing the effect of CETP inhibition in cardiovascular disease. Nat Rev Cardiol. 2017 Nov;14(11):635-636. doi: 10.1038/nrcardio.2017.156. Epub 2017 Oct 5. PMID: 28980665; PMCID: PMC5644574.
  • 149
    Liu T, Yoon WS, Lee SR. Recent Updates of Lipoprotein(a) and Cardiovascular Disease. Chonnam Med J. 2021 Jan;57(1):36-43. doi: 10.4068/cmj.2021.57.1.36. Epub 2021 Jan 25. PMID: 33537217; PMCID: PMC7840349.
  • 150
    Šuran D, Blažun Vošner H, Završnik J, Kokol P, Sinkovič A, Kanič V, Kokol M, Naji F, Završnik T. Lipoprotein(a) in Cardiovascular Diseases: Insight From a Bibliometric Study. Front Public Health. 2022 Jul 5;10:923797. doi: 10.3389/fpubh.2022.923797. PMID: 35865239; PMCID: PMC9294325.
  • 151
    Alwan A, Youhanna SC, Platt DE, El-Sibai M, Yerezian JS, Deeb ME, Khazen G, Saadé S, Zreik TG, El Bayeh H, Maalouf A, Abchee A, Zalloua PA. ALOX5AP gene variants show differential association with coronary artery disease in different populations. J Community Genet. 2010 Sep;1(3):107-15. doi: 10.1007/s12687-010-0015-z. Epub 2010 Aug 18. PMID: 22460243; PMCID: PMC3185993.
  • 152
    Kunz R, Kreutz R, Beige J, Distler A, Sharma AM. Association between the angiotensinogen 235T-variant and essential hypertension in whites: a systematic review and methodological appraisal. Hypertension. 1997 Dec;30(6):1331-7. doi: 10.1161/01.hyp.30.6.1331. PMID: 9403549.
  • 153
    Tanaka T, Narazaki M, Kishimoto T. IL-6 in inflammation, immunity, and disease. Cold Spring Harb Perspect Biol. 2014 Sep 4;6(10):a016295. doi: 10.1101/cshperspect.a016295. PMID: 25190079; PMCID: PMC4176007.
  • 154
    Zhao M, Ma J, Li M, Zhang Y, Jiang B, Zhao X, Huai C, Shen L, Zhang N, He L, Qin S. Cytochrome P450 Enzymes and Drug Metabolism in Humans. Int J Mol Sci. 2021 Nov 26;22(23):12808. doi: 10.3390/ijms222312808. PMID: 34884615; PMCID: PMC8657965.
  • 155
    Roberts R. Genetics of coronary artery disease: an update. Methodist Debakey Cardiovasc J. 2014 Jan-Mar;10(1):7-12. doi: 10.14797/mdcj-10-1-7. PMID: 24932356; PMCID: PMC4051327.
  • 156
    Samani, N. J., & Schunkert, H. (2008). Chromosome 9p21 and cardiovascular disease. Circulation: Cardiovascular Genetics, 1(2), 81–84. https://doi.org/10.1161/circgenetics.108.832527
  • 157
    Patel RS, Asselbergs FW, Quyyumi AA, Palmer TM, Finan CI, Tragante V, Deanfield J, Hemingway H, Hingorani AD, Holmes MV. Genetic variants at chromosome 9p21 and risk of first versus subsequent coronary heart disease events: a systematic review and meta-analysis. J Am Coll Cardiol. 2014 Jun 3;63(21):2234-45. doi: 10.1016/j.jacc.2014.01.065. Epub 2014 Mar 7. PMID: 24607648; PMCID: PMC4035794.
  • 158
    Shunmoogam N, Naidoo P, Chilton R. Paraoxonase (PON)-1: a brief overview on genetics, structure, polymorphisms and clinical relevance. Vasc Health Risk Manag. 2018 Jun 18;14:137-143. doi: 10.2147/VHRM.S165173. PMID: 29950852; PMCID: PMC6014389.
  • 159
    Durrington PN, Bashir B, Soran H. Paraoxonase 1 and atherosclerosis. Front Cardiovasc Med. 2023 Feb 16;10:1065967. doi: 10.3389/fcvm.2023.1065967. PMID: 36873390; PMCID: PMC9977831.
  • 160
    Shih DM, Lusis AJ. The roles of PON1 and PON2 in cardiovascular disease and innate immunity. Curr Opin Lipidol. 2009 Aug;20(4):288-92. doi: 10.1097/MOL.0b013e32832ca1ee. PMID: 19474728; PMCID: PMC3869948.
  • 161
    Yapijakis C, Papakosta V, Vassiliou S. ACE Gene Variant Causing High Blood Pressure May Be Associated With Medication-related Jaw Osteonecrosis. In Vivo. 2019 Mar-Apr;33(2):559-562. doi: 10.21873/invivo.11510. PMID: 30804141; PMCID: PMC6506304.
  • 162
    Enas EA, Varkey B, Dharmarajan TS, Pare G, Bahl VK. Lipoprotein(a): An independent, genetic, and causal factor for cardiovascular disease and acute myocardial infarction. Indian Heart J. 2019 Mar-Apr;71(2):99-112. doi: 10.1016/j.ihj.2019.03.004. Epub 2019 Mar 20. PMID: 31280836; PMCID: PMC6620428.
  • 163
    Franceschini N, Muallem H, Rose KM, Boerwinkle E, Maeda N. Low density lipoprotein receptor polymorphisms and the risk of coronary heart disease: the Atherosclerosis Risk in Communities Study. J Thromb Haemost. 2009 Mar;7(3):496-8. doi: 10.1111/j.1538-7836.2008.03262.x. PMID: 19087220; PMCID: PMC2656439.
  • 164
    Morrison, A. C., Bray, M. S., Folsom, A. R., & Boerwinkle, E. (2002). 460W allele associated with cardiovascular disease in hypertensive individuals. Hypertension, 39(6), 1053–1057. https://doi.org/10.1161/01.hyp.0000019128.94483.3a
  • 165
    Tran N, Garcia T, Aniqa M, Ali S, Ally A, Nauli SM. Endothelial Nitric Oxide Synthase (eNOS) and the Cardiovascular System: in Physiology and in Disease States. Am J Biomed Sci Res. 2022;15(2):153-177. Epub 2022 Jan 4. PMID: 35072089; PMCID: PMC8774925.
  • 166
    Brown SA, Pereira N. Pharmacogenomic Impact of CYP2C19 Variation on Clopidogrel Therapy in Precision Cardiovascular Medicine. J Pers Med. 2018 Jan 30;8(1):8. doi: 10.3390/jpm8010008. PMID: 29385765; PMCID: PMC5872082.
  • 167
    Thomas, C. D., Williams, A. K., Lee, C. R., & Cavallari, L. H. (2023). Pharmacogenetics of P2Y12 receptor inhibitors. Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy, 43(2), 158–175. https://doi.org/10.1002/phar.2758
  • 168
    Galasso G, Santulli G, Piscione F, De Rosa R, Trimarco V, Piccolo R, Cassese S, Iaccarino G, Trimarco B, Chiariello M. The GPIIIA PlA2 polymorphism is associated with an increased risk of cardiovascular adverse events. BMC Cardiovasc Disord. 2010 Sep 16;10:41. doi: 10.1186/1471-2261-10-41. PMID: 20846430; PMCID: PMC2954874.
  • 169
    Surma S, Banach M. Fibrinogen and Atherosclerotic Cardiovascular Diseases-Review of the Literature and Clinical Studies. Int J Mol Sci. 2021 Dec 24;23(1):193. doi: 10.3390/ijms23010193. PMID: 35008616; PMCID: PMC8745133.
  • 170
    Jung RG, Motazedian P, Ramirez FD, Simard T, Di Santo P, Visintini S, Faraz MA, Labinaz A, Jung Y, Hibbert B. Association between plasminogen activator inhibitor-1 and cardiovascular events: a systematic review and meta-analysis. Thromb J. 2018 Jun 5;16:12. doi: 10.1186/s12959-018-0166-4. PMID: 29991926; PMCID: PMC5987541.
  • 171
    Hernández-Díaz Y, Tovilla-Zárate CA, Juárez-Rojop I, López-Narváez ML, Álvarez-Cámara JF, González-Castro TB. Association between CRP and TNF-α genes Variants and Cardiovascular Heart Disease in a Mexican Population: Protocol for a Case-Control Study. Int J Environ Res Public Health. 2016 Jan 6;13(1):103. doi: 10.3390/ijerph13010103. PMID: 26751459; PMCID: PMC4730494.
  • 172
    Wang X, Khalil RA. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. Adv Pharmacol. 2018;81:241-330. doi: 10.1016/bs.apha.2017.08.002. Epub 2017 Sep 19. PMID: 29310800; PMCID: PMC5765875.
  • 173
    Zhang Q, Shen Y, Niloy SI, O’Rourke ST, Sun C. Chronic Effects of Apelin on Cardiovascular Regulation and Angiotensin II-Induced Hypertension. Pharmaceuticals (Basel). 2023 Apr 17;16(4):600. doi: 10.3390/ph16040600. PMID: 37111357; PMCID: PMC10145143.
  • 174
    Gruzdeva O, Borodkina D, Uchasova E, Dyleva Y, Barbarash O. Leptin resistance: underlying mechanisms and diagnosis. Diabetes Metab Syndr Obes. 2019 Jan 25;12:191-198. doi: 10.2147/DMSO.S182406. PMID: 30774404; PMCID: PMC6354688.
  • 175
    Tavoosi Z, Moradi-Sardareh H, Saidijam M, Yadegarazari R, Borzuei S, Soltanian A, Goodarzi MT. Cholesterol Transporters ABCA1 and ABCG1 Gene Expression in Peripheral Blood Mononuclear Cells in Patients with Metabolic Syndrome. Cholesterol. 2015;2015:682904. doi: 10.1155/2015/682904. Epub 2015 Dec 15. PMID: 26788366; PMCID: PMC4692991.
  • 176
    Hu S, Hu D, Wei H, Li SY, Wang D, Li CZ, Jiang J, Wang D, Cui G, Wang D. Functional Deletion/Insertion Promoter Variants in SCARB1 Associated With Increased Susceptibility to Lipid Profile Abnormalities and Coronary Heart Disease. Front Cardiovasc Med. 2022 Jan 13;8:800873. doi: 10.3389/fcvm.2021.800873. PMID: 35097019; PMCID: PMC8793335.
  • 177
    Zhou J, Shao L, Yu J, Huang J, Feng Q. PDGF-BB promotes vascular smooth muscle cell migration by enhancing Pim-1 expression via inhibiting miR-214. Ann Transl Med. 2021 Dec;9(23):1728. doi: 10.21037/atm-21-5638. PMID: 35071422; PMCID: PMC8743727.
  • 178
    Zhang X, Cheng M, Tong F, Su X. Association between RAGE variants and the susceptibility to atherosclerotic lesions in Chinese Han population. Exp Ther Med. 2019 Mar;17(3):2019-2030. doi: 10.3892/etm.2019.7163. Epub 2019 Jan 9. PMID: 30783474; PMCID: PMC6364181.
  • 179
    Allingham-Hawkins D, Lea A, Levine S. KIF6 p.Trp719Arg Testing to Assess Risk of Coronary Artery Disease and/or Statin Response. PLoS Curr. 2010 Oct 21;2:RRN1191. doi: 10.1371/currents.RRN1191. PMID: 20975779; PMCID: PMC2959200.
  • 180
    Sheikhvatan M, Boroumand MA, Behmanesh M, Ziaee S, Cheraghee S. Integrin Beta-3 Gene Polymorphism and Risk for Myocardial Infarction in Premature Coronary Disease. Iran J Biotechnol. 2019 Apr 20;17(2):e1921. doi: 10.21859/ijb.1921. PMID: 31457051; PMCID: PMC6697842.
  • 181
    Iyer D, Zhao Q, Wirka R, Naravane A, Nguyen T, Liu B, Nagao M, Cheng P, Miller CL, Kim JB, Pjanic M, Quertermous T. Coronary artery disease genes SMAD3 and TCF21 promote opposing interactive genetic programs that regulate smooth muscle cell differentiation and disease risk. PLoS Genet. 2018 Oct 11;14(10):e1007681. doi: 10.1371/journal.pgen.1007681. PMID: 30307970; PMCID: PMC6198989.
  • 182
    Zhang, X., Cao, Y.J., Zhang, H.Y. et al. Associations between ADIPOQ polymorphisms and coronary artery disease: a meta-analysis. BMC Cardiovasc Disord 19, 63 (2019). https://doi.org/10.1186/s12872-019-1041-3
  • 183
    Askin L, Tibilli H, Tanriverdi O, Turkmen S. The relationship between coronary artery disease and SIRT1 protein. North Clin Istanb. 2020 Oct 1;7(6):631-635. doi: 10.14744/nci.2020.31391. PMID: 33381707; PMCID: PMC7754863.
  • 184
    Assimes TL, Knowles JW, Priest JR, Basu A, Volcik KA, Southwick A, Tabor HK, Hartiala J, Allayee H, Grove ML, Tabibiazar R, Sidney S, Fortmann SP, Go A, Hlatky M, Iribarren C, Boerwinkle E, Myers R, Risch N, Quertermous T. Common polymorphisms of ALOX5 and ALOX5AP and risk of coronary artery disease. Hum Genet. 2008 May;123(4):399-408. doi: 10.1007/s00439-008-0489-5. Epub 2008 Mar 28. PMID: 18369664; PMCID: PMC4023692.
  • 185
    Meens MJPMT, Pfenniger A, Kwak BR. Risky communication in atherosclerosis and thrombus formation. Swiss Med Wkly [Internet]. 2012 Mar. 25 [cited 2023 Jul. 26];142(1314):w13553.
  • 186
    Zhu M, Lin J, Wang C, Yang M, Lv H, Yang M, Xu B, Chen X, Jiang J. The relationship among angiotensinogen genes polymorphisms and hs-CRP and coronary artery disease. J Clin Lab Anal. 2019 Jun;33(5):e22881. doi: 10.1002/jcla.22881. Epub 2019 Mar 26. PMID: 30912862; PMCID: PMC6595333.
  • 187
    Malinowski D, Bochniak O, Luterek-Puszyńska K, Puszyński M, Pawlik A. Genetic Risk Factors Related to Coronary Artery Disease and Role of Transforming Growth Factor Beta 1 Polymorphisms. Genes. 2023; 14(7):1425. https://doi.org/10.3390/genes14071425
  • 188
    Holloway JW, Yang IA, Ye S. Variation in the toll-like receptor 4 gene and susceptibility to myocardial infarction. Pharmacogenet Genomics. 2005 Jan;15(1):15-21. doi: 10.1097/01213011-200501000-00003. PMID: 15864121.
  • 189
    Li X, Wu N, Ji H, Huang Y, Hu H, Li J, Mi S, Duan S, Chen X. A male-specific association between AGTR1 hypermethylation and coronary heart disease. Bosn J Basic Med Sci. 2020 Feb 5;20(1):31-36. doi: 10.17305/bjbms.2019.4321. PMID: 31538912; PMCID: PMC7029202.
  • 190
    Normaznah Y, Azizah MR, Kuak SH, Rosli MA. CYP11B2 gene polymorphism among coronary heart disease patients and blood donors in Malaysia. Malays J Pathol. 2015 Apr;37(1):45-7. PMID: 25890613.
  • 191
    Li YY, Wang H, Wu JJ, Kim HJ, Yang XX, Geng HY, Gong G. ALDH2 gene G487A polymorphism and coronary artery disease: a meta-analysis including 5644 participants. J Cell Mol Med. 2018 Mar;22(3):1666-1674. doi: 10.1111/jcmm.13443. Epub 2017 Dec 26. PMID: 29278292; PMCID: PMC5824379.
  • 192
    Medina, M. W., Gao, F., Naidoo, D., Rudel, L. L., Temel, R. E., McDaniel, A. L., Marshall, S. M., & Krauss, R. M. (2011). Coordinately Regulated Alternative Splicing of Genes Involved in Cholesterol Biosynthesis and Uptake. PLOS ONE, 6(4), e19420. https://doi.org/10.1371/journal.pone.0019420
  • 193
    Bharath, G., Vishnuprabu, D. P., Preethi, L., Nagappan, A. S., Dhianeshwaran Isravanya, R. T., Bhaskar, L. V., Swaminathan, N., & Munirajan, A. K. (2022). slco1b1 and abcb1 variants synergistically influence the atorvastatin treatment response in south Indian coronary artery disease patients. Pharmacogenomics, 23(12), 683–694. https://doi.org/10.2217/pgs-2022-0044
  • 194
    Song W, Wang H, Wu Q. Atrial natriuretic peptide in cardiovascular biology and disease (NPPA). Gene. 2015 Sep 10;569(1):1-6. doi: 10.1016/j.gene.2015.06.029. Epub 2015 Jun 12. PMID: 26074089; PMCID: PMC4496260.
  • 195
    Muckian C, Fitzgerald A, O’Neill A, O’Byrne A, Fitzgerald DJ, Shields DC. Genetic variability in the extracellular matrix as a determinant of cardiovascular risk: association of type III collagen COL3A1 polymorphisms with coronary artery disease. Blood. 2002 Aug 15;100(4):1220-3. doi: 10.1182/blood-2002-01-0283. PMID: 12149201.
  • 196
    Huang K, Zhong J, Li Q, Zhang W, Chen Z, Zhou Y, Wu M, Zhong Z, Lu S, Zhang S. Effects of CDKN2B-AS1 polymorphisms on the susceptibility to coronary heart disease. Mol Genet Genomic Med. 2019 Nov;7(11):e955. doi: 10.1002/mgg3.955. Epub 2019 Sep 8. PMID: 31496134; PMCID: PMC6825846.
  • 197
    Döring Y, van der Vorst EPC, Duchene J, Jansen Y, Gencer S, Bidzhekov K, Atzler D, Santovito D, Rader DJ, Saleheen D, Weber C. CXCL12 Derived From Endothelial Cells Promotes Atherosclerosis to Drive Coronary Artery Disease. Circulation. 2019 Mar 5;139(10):1338-1340. doi: 10.1161/CIRCULATIONAHA.118.037953. PMID: 30865486; PMCID: PMC6417827.
  • 198
    Thorsten Kessler and others, Association of the coronary artery disease risk gene GUCY1A3 with ischaemic events after coronary intervention, Cardiovascular Research, Volume 115, Issue 10, 1 August 2019, Pages 1512–1518, https://doi.org/10.1093/cvr/cvz015
  • 199
    Kessler T, Wobst J, Wolf B, Eckhold J, Vilne B, Hollstein R, von Ameln S, Dang TA, Sager HB, Moritz Rumpf P, Aherrahrou R, Kastrati A, Björkegren JLM, Erdmann J, Lusis AJ, Civelek M, Kaiser FJ, Schunkert H. Functional Characterization of the GUCY1A3 Coronary Artery Disease Risk Locus. Circulation. 2017 Aug 1;136(5):476-489. doi: 10.1161/CIRCULATIONAHA.116.024152. Epub 2017 May 9. PMID: 28487391; PMCID: PMC5560301.
  • 200
    Anand SS, Hawkes C, de Souza RJ, Mente A, Dehghan M, Nugent R, Zulyniak MA, Weis T, Bernstein AM, Krauss RM, Kromhout D, Jenkins DJA, Malik V, Martinez-Gonzalez MA, Mozaffarian D, Yusuf S, Willett WC, Popkin BM. Food Consumption and its Impact on Cardiovascular Disease: Importance of Solutions Focused on the Globalized Food System: A Report From the Workshop Convened by the World Heart Federation. J Am Coll Cardiol. 2015 Oct 6;66(14):1590-1614. doi: 10.1016/j.jacc.2015.07.050. PMID: 26429085; PMCID: PMC4597475.
  • 201
    Gholizadeh E, Ayremlou P, Nouri Saeidlou S. The association between dietary pattern and coronary artery disease: A case-control study. J Cardiovasc Thorac Res. 2020;12(4):294-302. doi: 10.34172/jcvtr.2020.48. Epub 2020 Nov 28. PMID: 33510878; PMCID: PMC7828759.
  • 202
    Nystoriak MA, Bhatnagar A. Cardiovascular Effects and Benefits of Exercise. Front Cardiovasc Med. 2018 Sep 28;5:135. doi: 10.3389/fcvm.2018.00135. PMID: 30324108; PMCID: PMC6172294.
  • 203
    Tian D, Meng J. Exercise for Prevention and Relief of Cardiovascular Disease: Prognoses, Mechanisms, and Approaches. Oxid Med Cell Longev. 2019 Apr 9;2019:3756750. doi: 10.1155/2019/3756750. PMID: 31093312; PMCID: PMC6481017.
  • 204
    Warburton DE, Nicol CW, Bredin SS. Health benefits of physical activity: the evidence. CMAJ. 2006 Mar 14;174(6):801-9. doi: 10.1503/cmaj.051351. PMID: 16534088; PMCID: PMC1402378.
  • 205
    Albarrati AM, Alghamdi MSM, Nazer RI, Alkorashy MM, Alshowier N, Gale N. Effectiveness of Low to Moderate Physical Exercise Training on the Level of Low-Density Lipoproteins: A Systematic Review. Biomed Res Int. 2018 Nov 1;2018:5982980. doi: 10.1155/2018/5982980. PMID: 30515408; PMCID: PMC6236809.
  • 206
    Basso JC, Suzuki WA. The Effects of Acute Exercise on Mood, Cognition, Neurophysiology, and Neurochemical Pathways: A Review. Brain Plast. 2017 Mar 28;2(2):127-152. doi: 10.3233/BPL-160040. PMID: 29765853; PMCID: PMC5928534.
  • 207
    Salehi N, Janjani P, Tadbiri H, Rozbahani M, Jalilian M. Effect of cigarette smoking on coronary arteries and pattern and severity of coronary artery disease: a review. J Int Med Res. 2021 Dec;49(12):3000605211059893. doi: 10.1177/03000605211059893. PMID: 34855538; PMCID: PMC8647272.
  • 208
    Tasnim S, Tang C, Wright JM. Effect of alcohol on blood pressure. Cochrane Database Syst Rev. 2017 Sep 1;2017(9):CD012787. doi: 10.1002/14651858.CD012787. PMCID: PMC6483609.
  • 209
    Wipfli H, Avila-Tang E, Navas-Acien A, Kim S, Onicescu G, Yuan J, Breysse P, Samet JM; Famri Homes Study Investigators. Secondhand smoke exposure among women and children: evidence from 31 countries. Am J Public Health. 2008 Apr;98(4):672-9. doi: 10.2105/AJPH.2007.126631. Epub 2008 Feb 28. PMID: 18309121; PMCID: PMC2376995.
  • 210
    Gallucci G, Tartarone A, Lerose R, Lalinga AV, Capobianco AM. Cardiovascular risk of smoking and benefits of smoking cessation. J Thorac Dis. 2020 Jul;12(7):3866-3876. doi: 10.21037/jtd.2020.02.47. PMID: 32802468; PMCID: PMC7399440.
  • 211
    Piano MR. Alcohol’s Effects on the Cardiovascular System. Alcohol Res. 2017;38(2):219-241. PMID: 28988575; PMCID: PMC5513687.
  • 212
    Hoek AG, van Oort S, Mukamal KJ, Beulens JWJ. Alcohol Consumption and Cardiovascular Disease Risk: Placing New Data in Context. Curr Atheroscler Rep. 2022 Jan;24(1):51-59. doi: 10.1007/s11883-022-00992-1. Epub 2022 Feb 7. PMID: 35129737; PMCID: PMC8924109.
  • 213
    Ferreira VR, Jardim TV, Sousa ALL, Rosa BMC, Jardim PCV. Smoking, alcohol consumption and mental health: Data from the Brazilian study of Cardiovascular Risks in Adolescents (ERICA). Addict Behav Rep. 2018 Nov 22;9:100147. doi: 10.1016/j.abrep.2018.100147. PMID: 31193769; PMCID: PMC6542299.
  • 214
    Liu YZ, Wang YX, Jiang CL. Inflammation: The Common Pathway of Stress-Related Diseases. Front Hum Neurosci. 2017 Jun 20;11:316. doi: 10.3389/fnhum.2017.00316. PMID: 28676747; PMCID: PMC5476783.
  • 215
    De Hert M, Detraux J, Vancampfort D. The intriguing relationship between coronary heart disease and mental disorders. Dialogues Clin Neurosci. 2018 Mar;20(1):31-40. doi: 10.31887/DCNS.2018.20.1/mdehert. PMID: 29946209; PMCID: PMC6016051.
  • 216
    Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension. Heart. 2003 Sep;89(9):1104-9. doi: 10.1136/heart.89.9.1104. PMID: 12923045; PMCID: PMC1767863.
  • 217
    Aronow WS. Hypertension and left ventricular hypertrophy. Ann Transl Med. 2017 Aug;5(15):310. doi: 10.21037/atm.2017.06.14. PMID: 28856150; PMCID: PMC5555990.
  • 218
    Picariello C, Lazzeri C, Attanà P, Chiostri M, Gensini GF, Valente S. The impact of hypertension on patients with acute coronary syndromes. Int J Hypertens. 2011;2011:563657. doi: 10.4061/2011/563657. Epub 2011 Jun 22. PMID: 21747979; PMCID: PMC3124673.
  • 219
    Poznyak AV, Sadykhov NK, Kartuesov AG, Borisov EE, Melnichenko AA, Grechko AV, Orekhov AN. Hypertension as a risk factor for atherosclerosis: Cardiovascular risk assessment. Front Cardiovasc Med. 2022 Aug 22;9:959285. doi: 10.3389/fcvm.2022.959285. PMID: 36072873; PMCID: PMC9441708.
  • 220
    Mensah GA. Commentary: Hypertension Phenotypes: The Many Faces of a Silent Killer. Ethn Dis. 2019 Oct 17;29(4):545-548. doi: 10.18865/ed.29.4.545. PMID: 31641321; PMCID: PMC6802171.
  • 221
    Leon BM, Maddox TM. Diabetes and cardiovascular disease: Epidemiology, biological mechanisms, treatment recommendations and future research. World J Diabetes. 2015 Oct 10;6(13):1246-58. doi: 10.4239/wjd.v6.i13.1246. PMID: 26468341; PMCID: PMC4600176.
  • 222
    Rahman MS, Hossain KS, Das S, Kundu S, Adegoke EO, Rahman MA, Hannan MA, Uddin MJ, Pang MG. Role of Insulin in Health and Disease: An Update. Int J Mol Sci. 2021 Jun 15;22(12):6403. doi: 10.3390/ijms22126403. PMID: 34203830; PMCID: PMC8232639.
  • 223
    Yagihashi S, Mizukami H, Sugimoto K. Mechanism of diabetic neuropathy: Where are we now and where to go? J Diabetes Investig. 2011 Jan 24;2(1):18-32. doi: 10.1111/j.2040-1124.2010.00070.x. PMID: 24843457; PMCID: PMC4008011.
  • 224
    Petrie JR, Guzik TJ, Touyz RM. Diabetes, Hypertension, and Cardiovascular Disease: Clinical Insights and Vascular Mechanisms. Can J Cardiol. 2018 May;34(5):575-584. doi: 10.1016/j.cjca.2017.12.005. Epub 2017 Dec 11. PMID: 29459239; PMCID: PMC5953551.
  • 225
    Poznyak A, Grechko AV, Poggio P, Myasoedova VA, Alfieri V, Orekhov AN. The Diabetes Mellitus-Atherosclerosis Connection: The Role of Lipid and Glucose Metabolism and Chronic Inflammation. Int J Mol Sci. 2020 Mar 6;21(5):1835. doi: 10.3390/ijms21051835. PMID: 32155866; PMCID: PMC7084712.
  • 226
    Shariq OA, McKenzie TJ. Obesity-related hypertension: a review of pathophysiology, management, and the role of metabolic surgery. Gland Surg. 2020 Feb;9(1):80-93. doi: 10.21037/gs.2019.12.03. PMID: 32206601; PMCID: PMC7082272.
  • 227
    Klop B, Elte JW, Cabezas MC. Dyslipidemia in obesity: mechanisms and potential targets. Nutrients. 2013 Apr 12;5(4):1218-40. doi: 10.3390/nu5041218. PMID: 23584084; PMCID: PMC3705344.
  • 228
    Poelman M, Strak M, Schmitz O, Hoek G, Karssenberg D, Helbich M, Ntarladima AM, Bots M, Brunekreef B, Grobbee R, Dijst M, Vaartjes I. Relations between the residential fast-food environment and the individual risk of cardiovascular diseases in The Netherlands: A nationwide follow-up study. Eur J Prev Cardiol. 2018 Sep;25(13):1397-1405. doi: 10.1177/2047487318769458. Epub 2018 Apr 24. PMID: 29688759; PMCID: PMC6130123.
  • 229
    Phillips JE, Klein WM. Socioeconomic Status and Coronary Heart Disease Risk: The Role of Social Cognitive Factors. Soc Personal Psychol Compass. 2010 Sep;4(9):704-727. doi: 10.1111/j.1751-9004.2010.00295.x. PMID: 21785652; PMCID: PMC3140045.
  • 230
    Graham G. Disparities in cardiovascular disease risk in the United States. Curr Cardiol Rev. 2015;11(3):238-45. doi: 10.2174/1573403×11666141122220003. PMID: 25418513; PMCID: PMC4558355.
  • 231
    Sara JD, Prasad M, Eleid MF, Zhang M, Widmer RJ, Lerman A. Association Between Work-Related Stress and Coronary Heart Disease: A Review of Prospective Studies Through the Job Strain, Effort-Reward Balance, and Organizational Justice Models. J Am Heart Assoc. 2018 Apr 27;7(9):e008073. doi: 10.1161/JAHA.117.008073. PMID: 29703810; PMCID: PMC6015274.
  • 232
    Gecaite-Stonciene J, Hughes BM, Burkauskas J, Bunevicius A, Kazukauskiene N, van Houtum L, Brozaitiene J, Neverauskas J, Mickuviene N. Fatigue Is Associated With Diminished Cardiovascular Response to Anticipatory Stress in Patients With Coronary Artery Disease. Front Physiol. 2021 Aug 17;12:692098. doi: 10.3389/fphys.2021.692098. PMID: 34483954; PMCID: PMC8416171.
  • 233
    Barnett LA, Prior JA, Kadam UT, Jordan KP. Chest pain and shortness of breath in cardiovascular disease: a prospective cohort study in UK primary care. BMJ Open. 2017 May 25;7(5):e015857. doi: 10.1136/bmjopen-2017-015857. PMID: 28550024; PMCID: PMC5726088.
  • 234
    Sai Ravi Shanker A, Phanikrishna B, Bhaktha Vatsala Reddy C. Association between erectile dysfunction and coronary artery disease and its severity. Indian Heart J. 2013 Mar-Apr;65(2):180-6. doi: 10.1016/j.ihj.2013.02.013. Epub 2013 Feb 24. PMID: 23647898; PMCID: PMC3861235.
  • 235
    Yüksel F, Karataş D, Türkdoğan FT, Yüksel Ö. Increased Atherosclerosis Correlates with Subjective Tinnitus Severity. Indian J Otolaryngol Head Neck Surg. 2018 Mar;70(1):119-124. doi: 10.1007/s12070-015-0845-4. Epub 2015 Apr 28. PMID: 29456955; PMCID: PMC5807274.
  • 236
    British Heart Foundation. (2021, May 3). The heart-kidney link. BHF. https://www.bhf.org.uk/informationsupport/heart-matters-magazine/medical/kidney-heart-link
  • 237
    Shahjehan RD, Bhutta BS. Coronary Artery Disease. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564304/
  • 238
    Sattar Y, Chhabra L. Electrocardiogram. [Updated 2023 Apr 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549803/
  • 239
    Walker RW, Dewhurst M, Gray WK, Jusabani A, Aris E, Unwin N, Swai M, Adams PC, Mugusi F. Electrocardiographic assessment of coronary artery disease and stroke risk factors in rural and urban Tanzania: a case-control study. J Stroke Cerebrovasc Dis. 2014 Feb;23(2):315-20. doi: 10.1016/j.jstrokecerebrovasdis.2013.03.002. Epub 2013 Mar 30. PMID: 23545320; PMCID: PMC4185096.
  • 240
    Sattar Y, Chhabra L. Electrocardiogram. [Updated 2023 Apr 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK549803/
  • 241
    Warner MJ, Tivakaran VS. Inferior Myocardial Infarction. [Updated 2023 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470572/
  • 242
    de Hartog-Keyzer JML, El Messaoudi S, Harskamp R, Vart P, Ringoir L, Pop V, Nijveldt R. Electrocardiography for the detection of left ventricular hypertrophy in an elderly population with long-standing hypertension in primary care: a secondary analysis of the CHELLO cohort study. BMJ Open. 2020 Aug 20;10(8):e038824. doi: 10.1136/bmjopen-2020-038824. PMID: 32819998; PMCID: PMC7443300.
  • 243
    Mahmoodzadeh S, Moazenzadeh M, Rashidinejad H, Sheikhvatan M. Diagnostic performance of electrocardiography in the assessment of significant coronary artery disease and its anatomical size in comparison with coronary angiography. J Res Med Sci. 2011 Jun;16(6):750-5. PMID: 22091303; PMCID: PMC3214392.
  • 244
    Ananthasubramaniam G, Ananthasubramaniam K. Stress electrocardiography testing in coronary artery disease: Is it time for its swan song or to redefine its role in the modern era? Indian Heart J. 2022 Mar-Apr;74(2):81-85. doi: 10.1016/j.ihj.2022.02.003. Epub 2022 Feb 12. PMID: 35167825; PMCID: PMC9039687.
  • 245
    Ananthasubramaniam G, Ananthasubramaniam K. Stress electrocardiography testing in coronary artery disease: Is it time for its swan song or to redefine its role in the modern era ? Indian Heart J. 2022 Mar-Apr;74(2):81-85. doi: 10.1016/j.ihj.2022.02.003. Epub 2022 Feb 12. PMID: 35167825; PMCID: PMC9039687.
  • 246
    Rafie N, Kashou AH, Noseworthy PA. ECG Interpretation: Clinical Relevance, Challenges, and Advances. Hearts. 2021; 2(4):505-513. https://doi.org/10.3390/hearts2040039
  • 247
    Vermeir P, Vandijck D, Degroote S, Peleman R, Verhaeghe R, Mortier E, Hallaert G, Van Daele S, Buylaert W, Vogelaers D. Communication in healthcare: a narrative review of the literature and practical recommendations. Int J Clin Pract. 2015 Nov;69(11):1257-67. doi: 10.1111/ijcp.12686. Epub 2015 Jul 6. PMID: 26147310; PMCID: PMC4758389.
  • 248
    Chokkalingam Mani B, Chaudhari SS. Right Heart Cardiac Catheterization. [Updated 2023 Apr 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557404/
  • 249
    Ralston BH, Waberski AT, Kanter JP, Schick JW, Downing TE. Measured Oxygen Consumption During Pediatric Cardiac Catheterization is More Accurate than Assumed Oxygen Consumption. Pediatr Cardiol. 2023 May 27. doi: 10.1007/s00246-023-03186-x. Epub ahead of print. PMID: 37243747.
  • 250
    Manda YR, Baradhi KM. Cardiac Catheterization Risks and Complications. [Updated 2023 Jan 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK531461/
  • 251
    Kosova E, Ricciardi M. Cardiac Catheterization. JAMA. 2017;317(22):2344. doi:10.1001/jama.2017.0708
  • 252
    Chokkalingam Mani B, Chaudhari SS. Right Heart Cardiac Catheterization. [Updated 2023 Apr 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557404/
  • 253
    NHS. (2022, October 4). Cardiac catheterisation and coronary angiography. NHS choices. https://www.nhs.uk/conditions/coronary-angiography/
  • 254
    Chhabra L, Zain MA, Siddiqui WJ. Angioplasty. [Updated 2023 Jan 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499894/
  • 255
    Hemmerling, Thomas M.; Cyr, Shantale; Terrasini, Nora. Epidural catheterization in cardiac surgery: The 2012 risk assessment. Annals of Cardiac Anaesthesia 16(3):p 169-177, July–September 2013. | DOI: 10.4103/0971-9784.114237
  • 256
    Kiamanesh O, Toma M. The State of the Heart Biopsy: A Clinical Review. CJC Open. 2020 Dec 1;3(4):524-531. doi: 10.1016/j.cjco.2020.11.017. PMID: 34027357; PMCID: PMC8129478.
  • 257
    Shah SM, Pfau SE. Coronary Physiology in the Cardiac Catheterization Laboratory. J Clin Med. 2019 Feb 18;8(2):255. doi: 10.3390/jcm8020255. PMID: 30781631; PMCID: PMC6406799.
  • 258
    Darshan Doshi, M. (2020, May 21). Are there benefits of cardiac catheterization for stable coronary artery disease?. Harvard Health. https://www.health.harvard.edu/blog/are-there-benefits-of-cardiac-catheterization-for-stable-coronary-artery-disease-2020052119817
  • 259
    Serruys PW, Hara H, Garg S, Kawashima H, Nørgaard BL, Dweck MR, Bax JJ, Knuuti J, Nieman K, Leipsic JA, Mushtaq S, Andreini D, Onuma Y. Coronary Computed Tomographic Angiography for Complete Assessment of Coronary Artery Disease: JACC State-of-the-Art Review. J Am Coll Cardiol. 2021 Aug 17;78(7):713-736. doi: 10.1016/j.jacc.2021.06.019. PMID: 34384554.
  • 260
    Sun Z. Coronary CT angiography: Beyond morphological stenosis analysis. World J Cardiol. 2013 Dec 26;5(12):444-52. doi: 10.4330/wjc.v5.i12.444. PMID: 24392188; PMCID: PMC3879698.
  • 261
    Ramjattan NA, Lala V, Kousa O, et al. Coronary CT Angiography. [Updated 2023 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470279/
  • 262
    Ramjattan NA, Lala V, Kousa O, et al. Coronary CT Angiography. [Updated 2023 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470279/
  • 263
    Mueller J, Jeudy J, Poston R, White CS. Cardiac CT angiography after coronary bypass surgery: prevalence of incidental findings. AJR Am J Roentgenol. 2007 Aug;189(2):414-9. doi: 10.2214/AJR.06.0736. PMID: 17646469; PMCID: PMC4146433.
  • 264
    Shreya D, Zamora DI, Patel GS, Grossmann I, Rodriguez K, Soni M, Joshi PK, Patel SC, Sange I. Coronary Artery Calcium Score – A Reliable Indicator of Coronary Artery Disease? Cureus. 2021 Dec 3;13(12):e20149. doi: 10.7759/cureus.20149. PMID: 35003981; PMCID: PMC8723785.
  • 265
    Stark M, Kerndt CC, Sharma S. Troponin. [Updated 2023 Apr 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507805/
  • 266
    Emerging Risk Factors Collaboration; Kaptoge S, Di Angelantonio E, Lowe G, Pepys MB, Thompson SG, Collins R, Danesh J. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet. 2010 Jan 9;375(9709):132-40. doi: 10.1016/S0140-6736(09)61717-7. Epub 2009 Dec 22. PMID: 20031199; PMCID: PMC3162187.
  • 267
    Gherasim L. Troponins in Heart Failure – a Perpetual Challenge. Maedica (Bucur). 2019 Dec;14(4):371-377. doi: 10.26574/maedica.2019.14.4.371. PMID: 32153668; PMCID: PMC7035435.
  • 268
    Chaikijurajai T, Tang WHW. Myeloperoxidase: a potential therapeutic target for coronary artery disease. Expert Opin Ther Targets. 2020 Jul;24(7):695-705. doi: 10.1080/14728222.2020.1762177. Epub 2020 May 7. PMID: 32336171; PMCID: PMC7387188.
  • 269
    Sofogianni A, Alkagiet S, Tziomalos K. Lipoprotein-associated Phospholipase A2 and Coronary Heart Disease. Curr Pharm Des. 2018;24(3):291-296. doi: 10.2174/1381612824666180111110550. PMID: 29332572.
  • 270
    Goyal BM, Sharma SM, Walia M. B-type natriuretic peptide levels predict extent and severity of coronary artery disease in non-ST elevation acute coronary syndrome and normal left ventricular function. Indian Heart J. 2014 Mar-Apr;66(2):183-7. doi: 10.1016/j.ihj.2013.12.015. Epub 2013 Dec 26. PMID: 24814112; PMCID: PMC4017577.
  • 271
    Weber M, Mitrovic V, Hamm C. B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide – Diagnostic role in stable coronary artery disease. Exp Clin Cardiol. 2006 Summer;11(2):99-101. PMID: 18651043; PMCID: PMC2274852.
  • 272
    Toth, P. P. (2004). High-density lipoprotein and cardiovascular risk. Circulation, 109(15), 1809–1812. https://doi.org/10.1161/01.cir.0000126889.97626.b8
  • 273
    Ganguly P, Alam SF. Role of homocysteine in the development of cardiovascular disease. Nutr J. 2015 Jan 10;14:6. doi: 10.1186/1475-2891-14-6. PMID: 25577237; PMCID: PMC4326479.
  • 274
    Shi Y, Wu Y, Bian C, Zhang W, Yang J, Xu G. Predictive value of plasma fibrinogen levels in patients admitted for acute coronary syndrome. Tex Heart Inst J. 2010;37(2):178-83. PMID: 20401290; PMCID: PMC2851424.
  • 275
    Mellwig KP, Horstkotte D, van Buuren F. Lipoprotein (a) and coronary heart disease – is there an efficient secondary prevention? Clin Res Cardiol Suppl. 2017 Mar;12(Suppl 1):18-21. doi: 10.1007/s11789-017-0088-x. PMID: 28233270; PMCID: PMC5352755.
  • 276
    Miller, M., Stone, N. J., Ballantyne, C., Bittner, V., Criqui, M. H., Ginsberg, H. N., Goldberg, A. C., Howard, W. J., Jacobson, M. S., Kris-Etherton, P. M., Lennie, T. A., Levi, M., Mazzone, T., & Pennathur, S. (2011). Triglycerides and cardiovascular disease. Circulation, 123(20), 2292–2333. https://doi.org/10.1161/cir.0b013e3182160726
  • 277
    Madjid M, Ali M, Willerson JT. Lipoprotein-associated phospholipase A2 as a novel risk marker for cardiovascular disease: a systematic review of the literature. Tex Heart Inst J. 2010;37(1):25-39. PMID: 20200624; PMCID: PMC2829807.
  • 278
    Su JH, Luo MY, Liang N, Gong SX, Chen W, Huang WQ, Tian Y, Wang AP. Interleukin-6: A Novel Target for Cardio-Cerebrovascular Diseases. Front Pharmacol. 2021 Aug 24;12:745061. doi: 10.3389/fphar.2021.745061. PMID: 34504432; PMCID: PMC8421530.
  • 279
    Mittal B, Mishra A, Srivastava A, Kumar S, Garg N. Matrix metalloproteinases in coronary artery disease. Adv Clin Chem. 2014;64:1-72. doi: 10.1016/b978-0-12-800263-6.00001-x. PMID: 24938016.
  • 280
    Zhang J, Chen Z, Ma M, He Y. Soluble ST2 in coronary artery disease: Clinical biomarkers and treatment guidance. Front Cardiovasc Med. 2022 Sep 26;9:924461. doi: 10.3389/fcvm.2022.924461. PMID: 36225958; PMCID: PMC9548599.
  • 281
    Behbodikhah J, Ahmed S, Elyasi A, Kasselman LJ, De Leon J, Glass AD, Reiss AB. Apolipoprotein B and Cardiovascular Disease: Biomarker and Potential Therapeutic Target. Metabolites. 2021 Oct 8;11(10):690. doi: 10.3390/metabo11100690. PMID: 34677405; PMCID: PMC8540246.
  • 282
    van der Laan SW, Fall T, Soumaré A, Teumer A, Sedaghat S, Baumert J, Zabaneh D, van Setten J, Isgum I, Galesloot TE, Arpegård J, Amouyel P, Trompet S, Waldenberger M, Dörr M, Magnusson PK, Giedraitis V, Larsson A, Morris AP, Felix JF, Morrison AC, Franceschini N, Bis JC, Kavousi M, O’Donnell C, Drenos F, Tragante V, Munroe PB, Malik R, Dichgans M, Worrall BB, Erdmann J, Nelson CP, Samani NJ, Schunkert H, Marchini J, Patel RS, Hingorani AD, Lind L, Pedersen NL, de Graaf J, Kiemeney LA, Baumeister SE, Franco OH, Hofman A, Uitterlinden AG, Koenig W, Meisinger C, Peters A, Thorand B, Jukema JW, Eriksen BO, Toft I, Wilsgaard T, Onland-Moret NC, van der Schouw YT, Debette S, Kumari M, Svensson P, van der Harst P, Kivimaki M, Keating BJ, Sattar N, Dehghan A, Reiner AP, Ingelsson E, den Ruijter HM, de Bakker PI, Pasterkamp G, Ärnlöv J, Holmes MV, Asselbergs FW. Cystatin C and Cardiovascular Disease: A Mendelian Randomization Study. J Am Coll Cardiol. 2016 Aug 30;68(9):934-45. doi: 10.1016/j.jacc.2016.05.092. PMID: 27561768; PMCID: PMC5451109.
  • 283
    Gao Z, Liu Z, Wang R, Zheng Y, Li H, Yang L. Galectin-3 Is a Potential Mediator for Atherosclerosis. J Immunol Res. 2020 Feb 14;2020:5284728. doi: 10.1155/2020/5284728. PMID: 32149158; PMCID: PMC7042544.
  • 284
    Wollert KC, Kempf T, Wallentin L. Growth Differentiation Factor 15 as a Biomarker in Cardiovascular Disease. Clin Chem. 2017 Jan;63(1):140-151. doi: 10.1373/clinchem.2016.255174. Epub 2016 Oct 25. PMID: 28062617.
  • 285
    Rezar R, Jirak P, Gschwandtner M, Derler R, Felder TK, Haslinger M, Kopp K, Seelmaier C, Granitz C, Hoppe UC, Lichtenauer M. Heart-Type Fatty Acid-Binding Protein (H-FABP) and its Role as a Biomarker in Heart Failure: What Do We Know So Far? J Clin Med. 2020 Jan 7;9(1):164. doi: 10.3390/jcm9010164. PMID: 31936148; PMCID: PMC7019786.
  • 286
    Eggers KM, Hammarsten O, Lindahl B. Differences between high-sensitivity cardiac troponin T and I in stable populations: underlying causes and clinical implications. Clin Chem Lab Med. 2022 Nov 28;61(3):380-387. doi: 10.1515/cclm-2022-0778. PMID: 36424851.
  • 287
    Mayyas F, Al-Jarrah M, Ibrahim K, Mfady D, Van Wagoner DR. The significance of circulating endothelin-1 as a predictor of coronary artery disease status and clinical outcomes following coronary artery catheterization. Cardiovasc Pathol. 2015 Jan-Feb;24(1):19-25. doi: 10.1016/j.carpath.2014.08.004. Epub 2014 Aug 15. PMID: 25213716; PMCID: PMC5831113.
  • 288
    Hong CG, Florida E, Li H, Parel PM, Mehta NN, Sorokin AV. Oxidized low-density lipoprotein associates with cardiovascular disease by a vicious cycle of atherosclerosis and inflammation: A systematic review and meta-analysis. Front Cardiovasc Med. 2023 Jan 16;9:1023651. doi: 10.3389/fcvm.2022.1023651. PMID: 36727024; PMCID: PMC9885196.
  • 289
    Ismail Oran, Bulent Oran, “Ischemia-Modified Albumin as a Marker of Acute Coronary Syndrome: The Case for Revising the Concept of “N-Terminal Modification” to “Fatty Acid Occupation” of Albumin”, Disease Markers, vol. 2017, Article ID 5692583, 8 pages, 2017. https://doi.org/10.1155/2017/5692583
  • 290
    Melak T, Baynes HW. Circulating microRNAs as possible biomarkers for coronary artery disease: a narrative review. EJIFCC. 2019 Jun 24;30(2):179-194. PMID: 31263392; PMCID: PMC6599194.
  • 291
    Khan FR, Ali J, Ullah R, Hassan Z, Khattak S, Lakhta G, Gul N. Relationship Between High Glycated Hemoglobin and Severity of Coronary Artery Disease in Type II Diabetic Patients Hospitalized With Acute Coronary Syndrome. Cureus. 2021 Mar 6;13(3):e13734. doi: 10.7759/cureus.13734. PMID: 33842112; PMCID: PMC8021276.
  • 292
    Pregnancy-Associated Plasma Protein-A (PAPP-A)
  • 293
    Farinacci M, Krahn T, Dinh W, Volk HD, Düngen HD, Wagner J, Konen T, von Ahsen O. Circulating endothelial cells as biomarker for cardiovascular diseases. Res Pract Thromb Haemost. 2018 Oct 26;3(1):49-58. doi: 10.1002/rth2.12158. PMID: 30656276; PMCID: PMC6332781.
  • 294
    Boulanger CM, Loyer X, Rautou PE, Amabile N. Extracellular vesicles in coronary artery disease. Nat Rev Cardiol. 2017 May;14(5):259-272. doi: 10.1038/nrcardio.2017.7. Epub 2017 Feb 2. PMID: 28150804.
  • 295
    Angeli, Fabio, Verdecchia, Paolo, Savonitto, Stefano, Cavallini, Sara, Santucci, Andrea, Coiro, Stefano, Sclafani, Rocco, Riccini, Clara, De Servi, Stefano and Cavallini, Claudio. “Soluble CD40 ligand and outcome in patients with coronary artery disease undergoing percutaneous coronary intervention” Clinical Chemistry and Laboratory Medicine (CCLM), vol. 60, no. 1, 2022, pp. 118-126. https://doi.org/10.1515/cclm-2021-0817
  • 296
    Chu Y, Teng J, Feng P, Liu H, Wang F, Li X. Pentraxin-3 in coronary artery disease: A meta-analysis. Cytokine. 2019 Jul;119:197-201. doi: 10.1016/j.cyto.2019.03.017. Epub 2019 Apr 4. PMID: 30954865.
  • 297
    Orlando A, Nava E, Giussani M, Genovesi S. Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents. Int J Mol Sci. 2019 Jun 30;20(13):3228. doi: 10.3390/ijms20133228. PMID: 31262082; PMCID: PMC6651242.
  • 298
    Orlando A, Nava E, Giussani M, Genovesi S. Adiponectin and Cardiovascular Risk. From Pathophysiology to Clinic: Focus on Children and Adolescents. Int J Mol Sci. 2019 Jun 30;20(13):3228. doi: 10.3390/ijms20133228. PMID: 31262082; PMCID: PMC6651242.
  • 299
    Aggarwal R, Akhthar T, Jain SK. Coronary artery disease and its association with Vitamin D deficiency. J Midlife Health. 2016 Apr-Jun;7(2):56-60. doi: 10.4103/0976-7800.185334. PMID: 27499590; PMCID: PMC4960940.
  • 300
    Ghayour-Mobarhan M, Ayati N, Sahebkar A, Moohebati M, Ayati N, Elyasi S, Mohammadpour AH. Evaluation of serum Asymmetric Dimethyl Arginine concentrations in coronary artery disease patients without traditional cardiovascular risk factors. Acta Biomed. 2018 Jun 7;89(2):203-208. doi: 10.23750/abm.v89i2.5335. PMID: 29957752; PMCID: PMC6179032.
  • 301
    Larsson, S.C., Michaëlsson, K. & Burgess, S. IGF-1 and cardiometabolic diseases: a Mendelian randomisation study. Diabetologia 63, 1775–1782 (2020). https://doi.org/10.1007/s00125-020-05190-9
  • 302
    Askin L, Abus S, Tanriverdi O. Resistin and Cardiovascular Disease: A Review of the Current Literature Regarding Clinical and Pathological Relationships. Curr Cardiol Rev. 2022;18(1):e290721195114. doi: 10.2174/1573403X17666210729101120. PMID: 34325643; PMCID: PMC9241124.
  • 303
    Rahimi-Sakak, F., Maroofi, M., Rahmani, J. et al. Serum uric acid and risk of cardiovascular mortality: a systematic review and dose-response meta-analysis of cohort studies of over a million participants. BMC Cardiovasc Disord 19, 218 (2019). https://doi.org/10.1186/s12872-019-1215-z
  • 304
    Batra J, Buttar RS, Kaur P, Kreimerman J, Melamed ML. FGF-23 and cardiovascular disease: review of literature. Curr Opin Endocrinol Diabetes Obes. 2016 Dec;23(6):423-429. doi: 10.1097/MED.0000000000000294. PMID: 27652999; PMCID: PMC6936216.
  • 305
    El-Ashmawy HM, Roshdy HS, Saad Z, Ahmed AM. Serum endostatin level as a marker for coronary artery calcification in type 2 diabetic patients. J Saudi Heart Assoc. 2019 Jan;31(1):24-31. doi: 10.1016/j.jsha.2018.09.001. Epub 2018 Sep 20. PMID: 30364696; PMCID: PMC6197639.
  • 306
    Gorący J, Kaczmarczyk M, Ciechanowicz A, Safranow K, Gorący J, Jakubowska K, Chlubek D, Gorący I. E-selectin gene haplotypes are associated with the risk of myocardial infarction. Arch Med Sci. 2019 Sep;15(5):1223-1231. doi: 10.5114/aoms.2019.84413. Epub 2019 Apr 9. PMID: 31572467; PMCID: PMC6764297.
  • 307
    Jung, R.G., Motazedian, P., Ramirez, F.D. et al. Association between plasminogen activator inhibitor-1 and cardiovascular events: a systematic review and meta-analysis. Thrombosis J 16, 12 (2018). https://doi.org/10.1186/s12959-018-0166-4
  • 308
    Karjalainen MK, Holmes MV, Wang Q, Anufrieva O, Kähönen M, Lehtimäki T, Havulinna AS, Kristiansson K, Salomaa V, Perola M, Viikari JS, Raitakari OT, Järvelin MR, Ala-Korpela M, Kettunen J. Apolipoprotein A-I concentrations and risk of coronary artery disease: A Mendelian randomization study. Atherosclerosis. 2020 Apr;299:56-63. doi: 10.1016/j.atherosclerosis.2020.02.002. Epub 2020 Feb 14. PMID: 32113648.
  • 309
    Kaur, G., Sharma, D., Bisen, S. et al. Vascular cell-adhesion molecule 1 (VCAM-1) regulates JunB-mediated IL-8/CXCL1 expression and pathological neovascularization. Commun Biol 6, 516 (2023). https://doi.org/10.1038/s42003-023-04905-z
  • 310
    Rathcke, C.N., Vestergaard, H. YKL-40 – an emerging biomarker in cardiovascular disease and diabetes. Cardiovasc Diabetol 8, 61 (2009). https://doi.org/10.1186/1475-2840-8-61
  • 311
    Pacileo M, Cirillo P, De Rosa S, Ucci G, Petrillo G, Musto D’Amore S, Sasso L, Maietta P, Spagnuolo R, Chiariello M. The role of neopterin in cardiovascular disease. Monaldi Arch Chest Dis. 2007 Jun;68(2):68-73. doi: 10.4081/monaldi.2007.454. PMID: 17886766.
  • 312
    Zhang K, Li M, Yin L, Fu G, Liu Z. Role of thrombospondin‑1 and thrombospondin‑2 in cardiovascular diseases (Review). Int J Mol Med. 2020 May;45(5):1275-1293. doi: 10.3892/ijmm.2020.4507. Epub 2020 Feb 20. PMID: 32323748; PMCID: PMC7138268.
  • 313
    Herder C, Peeters W, Illig T, Baumert J, de Kleijn DP, Moll FL, Poschen U, Klopp N, Müller-Nurasyid M, Roden M, Preuss M; CARDIoGRAM Consortium; Karakas M, Meisinger C, Thorand B, Pasterkamp G, Koenig W, Assimes TL, Deloukas P, Erdmann J, Holm H, Kathiresan S, König IR, McPherson R, Reilly MP, Roberts R, Samani NJ, Schunkert H, Stewart AF. RANTES/CCL5 and risk for coronary events: results from the MONICA/KORA Augsburg case-cohort, Athero-Express and CARDIoGRAM studies. PLoS One. 2011;6(12):e25734. doi: 10.1371/journal.pone.0025734. Epub 2011 Dec 6. PMID: 22162987; PMCID: PMC3232218.
  • 314
    Zhang, X., Hu, C., Wu, Hm. et al. Fibronectin type III domain-containing 5 in cardiovascular and metabolic diseases: a promising biomarker and therapeutic target. Acta Pharmacol Sin 42, 1390–1400 (2021). https://doi.org/10.1038/s41401-020-00557-5
  • 315
    Pockley AG, Frostegård J. Heat shock proteins in cardiovascular disease and the prognostic value of heat shock protein related measurements. Heart. 2005 Sep;91(9):1124-6. doi: 10.1136/hrt.2004.059220. PMID: 16103532; PMCID: PMC1769066.
  • 316
    Hammoud RA, Vaccari CS, Nagamia SH, Khan BV. Regulation of the renin-angiotensin system in coronary atherosclerosis: a review of the literature. Vasc Health Risk Manag. 2007;3(6):937-45. PMID: 18200812; PMCID: PMC2350139.
  • 317
    Jing Y, Shi J, Lu B, Zhang W, Yang Y, Wen J, Hu R, Yang Z, Wang X. Association of Circulating Cathepsin S and Cardiovascular Disease Among Patients With Type 2 Diabetes: A Cross-Sectional Community-Based Study. Front Endocrinol (Lausanne). 2021 Mar 5;12:615913. doi: 10.3389/fendo.2021.615913. PMID: 33746900; PMCID: PMC7973458.
  • 318
    Ikeda U, Matsui K, Murakami Y, Shimada K. Monocyte chemoattractant protein-1 and coronary artery disease. Clin Cardiol. 2002 Apr;25(4):143-7. doi: 10.1002/clc.4960250403. PMID: 12000070; PMCID: PMC6654294.
  • 319
    Maria Philippova and others, T-cadherin is present on endothelial microparticles and is elevated in plasma in early atherosclerosis, European Heart Journal, Volume 32, Issue 6, March 2011, Pages 760–771, https://doi.org/10.1093/eurheartj/ehq206
  • 320
    Matsui M, Uemura S, Takeda Y, Samejima K, Matsumoto T, Hasegawa A, Tsushima H, Hoshino E, Ueda T, Morimoto K, Okamoto K, Okada S, Onoue K, Okayama S, Kawata H, Kawakami R, Maruyama N, Akai Y, Iwano M, Shiiki H, Saito Y; NARA-CKD Investigators. Placental Growth Factor as a Predictor of Cardiovascular Events in Patients with CKD from the NARA-CKD Study. J Am Soc Nephrol. 2015 Nov;26(11):2871-81. doi: 10.1681/ASN.2014080772. Epub 2015 Mar 18. PMID: 25788536; PMCID: PMC4625670.
  • 321
    Lunde IG, Herum KM, Carlson CC, Christensen G. Syndecans in heart fibrosis. Cell Tissue Res. 2016 Sep;365(3):539-52. doi: 10.1007/s00441-016-2454-2. Epub 2016 Jul 14. PMID: 27411689.
  • 322
    Cheong KI, Leu HB, Wu CC, Yin WH, Wang JH, Lin TH, Tseng WK, Chang KC, Chu SH, Yeh HI, Chen JW, Wu YW; National Taiwan Biosignature Research Investigators. The clinical significance of osteopontin on the cardiovascular outcomes in patients with stable coronary artery disease. J Formos Med Assoc. 2023 Apr;122(4):328-337. doi: 10.1016/j.jfma.2022.11.011. Epub 2022 Dec 7. PMID: 36494313.
  • 323
    Ma B, Jia J, Wang X, Zhang R, Niu S, Ni L, Di X, Liu C. Differential roles of Scavenger receptor class B type I: A protective molecule and a facilitator of atherosclerosis (Review). Mol Med Rep. 2020 Oct;22(4):2599-2604. doi: 10.3892/mmr.2020.11383. Epub 2020 Jul 28. PMID: 32945418; PMCID: PMC7453654.
  • 324
    Zhong J, Chen X, Ye H, Wu N, Chen X, Duan S. CDKN2A and CDKN2B methylation in coronary heart disease cases and controls. Exp Ther Med. 2017 Dec;14(6):6093-6098. doi: 10.3892/etm.2017.5310. Epub 2017 Oct 16. PMID: 29285163; PMCID: PMC5740815.
  • 325
    Kurano M, Yatomi Y. Sphingosine 1-Phosphate and Atherosclerosis. J Atheroscler Thromb. 2018 Jan 1;25(1):16-26. doi: 10.5551/jat.RV17010. Epub 2017 Jul 20. PMID: 28724841; PMCID: PMC5770220.
  • 326
    Ni J, Ma X, Zhou M, Pan X, Tang J, Hao Y, Lu Z, Gao M, Bao Y, Jia W. Serum lipocalin-2 levels positively correlate with coronary artery disease and metabolic syndrome. Cardiovasc Diabetol. 2013 Dec 21;12:176. doi: 10.1186/1475-2840-12-176. PMID: 24359145; PMCID: PMC3878105.
  • 327
    von Jeinsen, B., Ritzen, L., Vietheer, J. et al. The adipokine fatty-acid binding protein 4 and cardiac remodeling. Cardiovasc Diabetol 19, 117 (2020). https://doi.org/10.1186/s12933-020-01080-x
  • 328
    Rabbani N, Godfrey L, Xue M, Shaheen F, Geoffrion M, Milne R, Thornalley PJ. Glycation of LDL by methylglyoxal increases arterial atherogenicity: a possible contributor to increased risk of cardiovascular disease in diabetes. Diabetes. 2011 Jul;60(7):1973-80. doi: 10.2337/db11-0085. Epub 2011 May 26. PMID: 21617182; PMCID: PMC3121424.
  • 329
    Satish M, Agrawal DK. Pro-resolving lipid mediators in the resolution of neointimal hyperplasia pathogenesis in atherosclerotic diseases. Expert Rev Cardiovasc Ther. 2019 Mar;17(3):177-184. doi: 10.1080/14779072.2019.1563483. Epub 2019 Jan 9. PMID: 30582389; PMCID: PMC6679914.
  • 330
    İnci S, Aksan G, Doğan P. Chemerin as an independent predictor of cardiovascular event risk. Ther Adv Endocrinol Metab. 2016 Apr;7(2):57-68. doi: 10.1177/2042018816629894. Epub 2016 Feb 8. PMID: 27092231; PMCID: PMC4820999.
  • 331
    Cao RY, Li Q, Miao Y, Zhang Y, Yuan W, Fan L, Liu G, Mi Q, Yang J. The Emerging Role of MicroRNA-155 in Cardiovascular Diseases. Biomed Res Int. 2016;2016:9869208. doi: 10.1155/2016/9869208. Epub 2016 Nov 27. PMID: 28018919; PMCID: PMC5149600.
  • 332
    Semenza GL. Hypoxia-inducible factor 1 and cardiovascular disease. Annu Rev Physiol. 2014;76:39-56. doi: 10.1146/annurev-physiol-021113-170322. Epub 2013 Aug 21. PMID: 23988176; PMCID: PMC4696033.
  • 333
    Møller PL, Rohde PD, Winther S, Breining P, Nissen L, Nykjaer A, Bøttcher M, Nyegaard M, Kjolby M. Sortilin as a Biomarker for Cardiovascular Disease Revisited. Front Cardiovasc Med. 2021 Apr 16;8:652584. doi: 10.3389/fcvm.2021.652584. PMID: 33937362; PMCID: PMC8085299.
  • 334
    Seki M, Powers JC, Maruyama S, Zuriaga MA, Wu CL, Kurishima C, Kim L, Johnson J, Poidomani A, Wang T, Muñoz E, Rajan S, Park JY, Walsh K, Recchia FA. Acute and Chronic Increases of Circulating FSTL1 Normalize Energy Substrate Metabolism in Pacing-Induced Heart Failure. Circ Heart Fail. 2018 Jan;11(1):e004486. doi: 10.1161/CIRCHEARTFAILURE.117.004486. PMID: 29317401; PMCID: PMC5765881.
  • 335
    Papagianni M, Tziomalos K. Cardiovascular effects of dipeptidyl peptidase-4 inhibitors. Hippokratia. 2015 Jul-Sep;19(3):195-9. PMID: 27418775; PMCID: PMC4938463.
  • 336
    Regmi M, Siccardi MA. Coronary Artery Disease Prevention. [Updated 2023 Feb 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK547760/
  • 337
    Xu J, Lo S. Fundamentals and role of intravascular ultrasound in percutaneous coronary intervention. Cardiovasc Diagn Ther. 2020 Oct;10(5):1358-1370. doi: 10.21037/cdt.2020.01.15. PMID: 33224762; PMCID: PMC7666933.
  • 338
    Tebaldi M, Campo G, Biscaglia S. Fractional flow reserve: Current applications and overview of the available data. World J Clin Cases. 2015 Aug 16;3(8):678-81. doi: 10.12998/wjcc.v3.i8.678. PMID: 26301228; PMCID: PMC4539407.
  • 339
    Zong J, He Q, Liu Y, Qiu M, Wu J, Hu B. Advances in the development of biodegradable coronary stents: A translational perspective. Mater Today Bio. 2022 Jul 19;16:100368. doi: 10.1016/j.mtbio.2022.100368. PMID: 35937578; PMCID: PMC9352968.
  • 340
    Padmanabhan S, Hastie C, Prabhakaran D, Dominczak AF. Genomic approaches to coronary artery disease. Indian J Med Res. 2010 Nov;132(5):567-78. PMID: 21150009; PMCID: PMC3028944.
  • 341
    Tada, H., Fujino, N., Nomura, A. et al. Personalized medicine for cardiovascular diseases. J Hum Genet 66, 67–74 (2021). https://doi.org/10.1038/s10038-020-0818-7
  • 342
    Ambesh P, Campia U, Obiagwu C, Bansal R, Shetty V, Hollander G, Shani J. Nanomedicine in coronary artery disease. Indian Heart J. 2017 Mar-Apr;69(2):244-251. doi: 10.1016/j.ihj.2017.02.007. Epub 2017 Feb 24. PMID: 28460774; PMCID: PMC5414944.
  • 343
    Dhingra LS, Aminorroaya A, Oikonomou EK, et al. Use of Wearable Devices in Individuals With or at Risk for Cardiovascular Disease in the US, 2019 to 2020. JAMA Netw Open. 2023;6(6):e2316634. doi:10.1001/jamanetworkopen.2023.16634
  • 344
    Mahmud S, Alam S, Emon NU, Boby UH, Kamruzzaman, Ahmed F, Monjur-Al-Hossain ASM, Tahamina A, Rudra S, Ajrin M. Opportunities and challenges in stem cell therapy in cardiovascular diseases: Position standing in 2022. Saudi Pharm J. 2022 Sep;30(9):1360-1371. doi: 10.1016/j.jsps.2022.06.017. Epub 2022 Jun 22. PMID: 36249945; PMCID: PMC9563042.
  • 345
    Li Y, Gong Y, Zheng B, Fan F, Yi T, Zheng Y, He P, Fang J, Jia J, Zhu Q, Jiang J, Huo Y. Effects on Adherence to a Mobile App-Based Self-management Digital Therapeutics Among Patients With Coronary Heart Disease: Pilot Randomized Controlled Trial. JMIR Mhealth Uhealth. 2022 Feb 15;10(2):e32251. doi: 10.2196/32251. PMID: 34906924; PMCID: PMC8889473.
  • 346
    Semmlow J, Rahalkar K. Acoustic detection of coronary artery disease. Annu Rev Biomed Eng. 2007;9:449-69. doi: 10.1146/annurev.bioeng.9.060906.151840. PMID: 17425468.
  • 347
    Du S, Kim H, Rebholz CM. Higher Ultra-Processed Food Consumption Is Associated with Increased Risk of Incident Coronary Artery Disease in the Atherosclerosis Risk in Communities Study. J Nutr. 2021 Dec 3;151(12):3746-3754. doi: 10.1093/jn/nxab285. PMID: 34494108; PMCID: PMC8643602.
  • 348
    Aune D, Giovannucci E, Boffetta P, Fadnes LT, Keum N, Norat T, Greenwood DC, Riboli E, Vatten LJ, Tonstad S. Fruit and vegetable intake and the risk of cardiovascular disease, total cancer and all-cause mortality-a systematic review and dose-response meta-analysis of prospective studies. Int J Epidemiol. 2017 Jun 1;46(3):1029-1056. doi: 10.1093/ije/dyw319. PMID: 28338764; PMCID: PMC5837313.
  • 349
    Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017 Aug 30;16(1):53. doi: 10.1186/s12937-017-0271-4. PMID: 28854932; PMCID: PMC5577766.
  • 350
    Barbiellini Amidei C, Trevisan C, Dotto M, et alAssociation of physical activity trajectories with major cardiovascular diseases in elderly peopleHeart 2022;108:360-366
  • 351
    Gallucci G, Tartarone A, Lerose R, Lalinga AV, Capobianco AM. Cardiovascular risk of smoking and benefits of smoking cessation. J Thorac Dis. 2020 Jul;12(7):3866-3876. doi: 10.21037/jtd.2020.02.47. PMID: 32802468; PMCID: PMC7399440.
  • 352
    Rehm J. The risks associated with alcohol use and alcoholism. Alcohol Res Health. 2011;34(2):135-43. PMID: 22330211; PMCID: PMC3307043.
  • 353
    Assadi SN. What are the effects of psychological stress and physical work on blood lipid profiles? Medicine (Baltimore). 2017 May;96(18):e6816. doi: 10.1097/MD.0000000000006816. PMID: 28471984; PMCID: PMC5419930.
  • 354
    Nagai M, Hoshide S, Kario K. Sleep duration as a risk factor for cardiovascular disease- a review of the recent literature. Curr Cardiol Rev. 2010 Feb;6(1):54-61. doi: 10.2174/157340310790231635. PMID: 21286279; PMCID: PMC2845795.
  • 355
    Manoharan MP, Raja R, Jamil A, Csendes D, Gutlapalli SD, Prakash K, Swarnakari KM, Bai M, Desai DM, Desai A, Penumetcha SS. Obesity and Coronary Artery Disease: An Updated Systematic Review 2022. Cureus. 2022 Sep 23;14(9):e29480. doi: 10.7759/cureus.29480. PMID: 36299943; PMCID: PMC9588166.
  • 356
    Wang YJ, Yeh TL, Shih MC, Tu YK, Chien KL. Dietary Sodium Intake and Risk of Cardiovascular Disease: A Systematic Review and Dose-Response Meta-Analysis. Nutrients. 2020 Sep 25;12(10):2934. doi: 10.3390/nu12102934. PMID: 32992705; PMCID: PMC7601012.
  • 357
    De Hert M, Detraux J, Vancampfort D. The intriguing relationship between coronary heart disease and mental disorders. Dialogues Clin Neurosci. 2018 Mar;20(1):31-40. doi: 10.31887/DCNS.2018.20.1/mdehert. PMID: 29946209; PMCID: PMC6016051.
  • 358
    Thachil J. Antiplatelet therapy – a summary for the general physicians. Clin Med (Lond). 2016 Apr;16(2):152-60. doi: 10.7861/clinmedicine.16-2-152. PMID: 27037385; PMCID: PMC4952969.
  • 359
    Ornelas A, Zacharias-Millward N, Menter DG, Davis JS, Lichtenberger L, Hawke D, Hawk E, Vilar E, Bhattacharya P, Millward S. Beyond COX-1: the effects of aspirin on platelet biology and potential mechanisms of chemoprevention. Cancer Metastasis Rev. 2017 Jun;36(2):289-303. doi: 10.1007/s10555-017-9675-z. PMID: 28762014; PMCID: PMC5557878.
  • 360
    Damman P, Woudstra P, Kuijt WJ, de Winter RJ, James SK. P2Y12 platelet inhibition in clinical practice. J Thromb Thrombolysis. 2012 Feb;33(2):143-53. doi: 10.1007/s11239-011-0667-5. PMID: 22183178; PMCID: PMC3269569.
  • 361
    Shoeb M, Fang MC. Assessing bleeding risk in patients taking anticoagulants. J Thromb Thrombolysis. 2013 Apr;35(3):312-9. doi: 10.1007/s11239-013-0899-7. PMID: 23479259; PMCID: PMC3888359.
  • 362
    Bularga A, Meah MN, Doudesis D, Shah ASV, Mills NL, Newby DE, Lee KK. Duration of dual antiplatelet therapy and stability of coronary heart disease: a 60 000-patient meta-analysis of randomised controlled trials. Open Heart. 2021 Jul;8(2):e001707. doi: 10.1136/openhrt-2021-001707. PMID: 34341097; PMCID: PMC8330558.
  • 363
    Volney C, Collins A, Adams S. Ticagrelor versus clopidogrel in the management of acute myocardial infarction. J Community Hosp Intern Med Perspect. 2019 Sep 5;9(4):314-318. doi: 10.1080/20009666.2019.1644915. PMID: 31531213; PMCID: PMC6737723.
  • 364
    Tummala R, Rai MP. Glycoprotein IIb/IIIa Inhibitors. [Updated 2022 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554376/
  • 365
    Lim SY. Role of statins in coronary artery disease. Chonnam Med J. 2013 Apr;49(1):1-6. doi: 10.4068/cmj.2013.49.1.1. Epub 2013 Apr 25. PMID: 23678470; PMCID: PMC3651980.
  • 366
    Lim SY. Role of statins in coronary artery disease. Chonnam Med J. 2013 Apr;49(1):1-6. doi: 10.4068/cmj.2013.49.1.1. Epub 2013 Apr 25. PMID: 23678470; PMCID: PMC3651980.
  • 367
    Diamantis E, Kyriakos G, Quiles-Sanchez LV, Farmaki P, Troupis T. The Anti-Inflammatory Effects of Statins on Coronary Artery Disease: An Updated Review of the Literature. Curr Cardiol Rev. 2017;13(3):209-216. doi: 10.2174/1573403X13666170426104611. PMID: 28462692; PMCID: PMC5633715.
  • 368
    Bansal AB, Cassagnol M. HMG-CoA Reductase Inhibitors. [Updated 2022 Jul 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542212/
  • 369
    Young SG, Fong LG. Lowering plasma cholesterol by raising LDL receptors–revisited. N Engl J Med. 2012 Mar 22;366(12):1154-5. doi: 10.1056/NEJMe1202168. PMID: 22435375; PMCID: PMC5611813.
  • 370
    Jiang, SY., Li, H., Tang, JJ. et al. Discovery of a potent HMG-CoA reductase degrader that eliminates statin-induced reductase accumulation and lowers cholesterol. Nat Commun 9, 5138 (2018). https://doi.org/10.1038/s41467-018-07590-3
  • 371
    Suliman I, Batarfi A, Almohammadi H, Aljeraisi H, Alnaserallah H, Alghamdi A. Prevalence of Self-Reported Muscle Pain Among Statin Users From National Guard Hospital, Riyadh. Cureus. 2022 Mar 24;14(3):e23463. doi: 10.7759/cureus.23463. PMID: 35481326; PMCID: PMC9034880.
  • 372
    Fernandes R, Shaikh I, Wegstapel H. Possible association between statin use and bowel dysmotility. BMJ Case Rep. 2012 Feb 25;2012:bcr1020114918. doi: 10.1136/bcr.10.2011.4918. PMID: 22665551; PMCID: PMC3291011.
  • 373
    Cheng T, Li C, Shen L, Wang S, Li X, Fu C, Li T, Liu B, Gu Y, Wang W, Feng B. The Intestinal Effect of Atorvastatin: Akkermansia muciniphila and Barrier Function. Front Microbiol. 2022 Feb 2;12:797062. doi: 10.3389/fmicb.2021.797062. PMID: 35185821; PMCID: PMC8847773.
  • 374
    Averbukh LD, Turshudzhyan A, Wu DC, Wu GY. Statin-induced Liver Injury Patterns: A Clinical Review. J Clin Transl Hepatol. 2022 Jun 28;10(3):543-552. doi: 10.14218/JCTH.2021.00271. Epub 2022 Jan 10. PMID: 35836753; PMCID: PMC9240239.
  • 375
    Fyhrquist F, Metsärinne K, Tikkanen I. Role of angiotensin II in blood pressure regulation and in the pathophysiology of cardiovascular disorders. J Hum Hypertens. 1995 Nov;9 Suppl 5:S19-24. PMID: 8583476.
  • 376
    Haymore BR, Yoon J, Mikita CP, Klote MM, DeZee KJ. Risk of angioedema with angiotensin receptor blockers in patients with prior angioedema associated with angiotensin-converting enzyme inhibitors: a meta-analysis. Ann Allergy Asthma Immunol. 2008 Nov;101(5):495-9. doi: 10.1016/S1081-1206(10)60288-8. PMID: 19055203.
  • 377
    Oemrawsingh, R. M., Akkerhuis, K. M., Van Vark, L. C., Redekop, W. K., Rudez, G., Remme, W. J., Bertrand, M. E., Fox, K. M., Ferrari, R., Danser, A. H. J., de Maat, M., Simoons, M. L., Brugts, J. J., & Boersma, E. (2016). Individualized angiotensin‐converting enzyme (ace)‐inhibitor therapy in stable coronary artery disease based on clinical and pharmacogenetic determinants: The Perindopril Genetic (PERGENE) risk model. Journal of the American Heart Association, 5(3). https://doi.org/10.1161/jaha.115.002688
  • 378
    Boyette LC, Manna B. Physiology, Myocardial Oxygen Demand. [Updated 2022 Jul 11]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499897/
  • 379
    Wu T, Chen X, Deng L. Beta‐blockers for unstable angina. Cochrane Database Syst Rev. 2017 Nov 24;2017(11):CD007050. doi: 10.1002/14651858.CD007050.pub2. PMCID: PMC6486012.
  • 380
    Shahrokhi M, Gupta V. Propranolol. [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557801/
  • 381
    Rehman B, Sanchez DP, Shah S. Atenolol. [Updated 2022 Oct 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539844/
  • 382
    Anık A. Beta-blocker Rebound Phenomenon in an Adolescent with Graves’ Disease. J Clin Res Pediatr Endocrinol. 2022 Dec 1;14(4):490-491. doi: 10.4274/jcrpe.galenos.2022.2022-6-2. Epub 2022 Jul 21. PMID: 35859995; PMCID: PMC9724061.
  • 383
    Anık A. Beta-blocker Rebound Phenomenon in an Adolescent with Graves’ Disease. J Clin Res Pediatr Endocrinol. 2022 Dec 1;14(4):490-491. doi: 10.4274/jcrpe.galenos.2022.2022-6-2. Epub 2022 Jul 21. PMID: 35859995; PMCID: PMC9724061.
  • 384
    Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/
  • 385
    Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/
  • 386
    Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/
  • 387
    Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/
  • 388
    Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/
  • 389
    Ahmad M, Mehta P, Reddivari AKR, et al. Percutaneous Coronary Intervention. [Updated 2022 Sep 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK556123/
  • 390
    Doll, J. A., Hira, R. S., Kearney, K. E., Kandzari, D. E., Riley, R. F., Marso, S. P., Grantham, J. A., Thompson, C. A., McCabe, J. M., Karmpaliotis, D., Kirtane, A. J., & Lombardi, W. (2020). Management of percutaneous coronary intervention complications. Circulation: Cardiovascular Interventions, 13(6). https://doi.org/10.1161/circinterventions.120.008962
  • 391
    Angiolillo DJ, Galli M, Collet JP, Kastrati A, O’Donoghue ML. Antiplatelet therapy after percutaneous coronary intervention. EuroIntervention. 2022 Apr 1;17(17):e1371-e1396. doi: 10.4244/EIJ-D-21-00904. PMID: 35354550; PMCID: PMC9896394.
  • 392
    Blankenship JC, Marshall JJ, Pinto DS, Lange RA, Bates ER, Holper EM, Grines CL, Chambers CE; Society for Cardiovascular Angiography and Interventions. Effect of percutaneous coronary intervention on quality of life: a consensus statement from the Society for Cardiovascular Angiography and Interventions. Catheter Cardiovasc Interv. 2013 Feb;81(2):243-59. doi: 10.1002/ccd.24376. Epub 2012 Apr 27. PMID: 22431260.
  • 393
    Bachar BJ, Manna B. Coronary Artery Bypass Graft. [Updated 2023 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507836/
  • 394
    Diodato M, Chedrawy EG. Coronary artery bypass graft surgery: the past, present, and future of myocardial revascularisation. Surg Res Pract. 2014;2014:726158. doi: 10.1155/2014/726158. Epub 2014 Jan 2. PMID: 25374960; PMCID: PMC4208586.
  • 395
    Bachar BJ, Manna B. Coronary Artery Bypass Graft. [Updated 2023 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507836/
  • 396
    Bachar BJ, Manna B. Coronary Artery Bypass Graft. [Updated 2023 Apr 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507836/
  • 397
    Taylor RS, Dalal HM, McDonagh STJ. The role of cardiac rehabilitation in improving cardiovascular outcomes. Nat Rev Cardiol. 2022 Mar;19(3):180-194. doi: 10.1038/s41569-021-00611-7. Epub 2021 Sep 16. PMID: 34531576; PMCID: PMC8445013.
  • 398
    Tessler J, Bordoni B. Cardiac Rehabilitation. 2023 May 22. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 30725881.
  • 399
    Brown JC, Gerhardt TE, Kwon E. Risk Factors for Coronary Artery Disease. 2023 Jan 23. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 32119297.
  • 400
    Ralapanawa U, Sivakanesan R. Epidemiology and the Magnitude of Coronary Artery Disease and Acute Coronary Syndrome: A Narrative Review. J Epidemiol Glob Health. 2021 Jun;11(2):169-177. doi: 10.2991/jegh.k.201217.001. Epub 2021 Jan 7. PMID: 33605111; PMCID: PMC8242111.
  • 401
    Ferreira-González, I. (2014a, February 1). The epidemiology of coronary heart disease: Revista Española de Cardiología. Revista Española de Cardiología (English Edition). https://www.revespcardiol.org/en-the-epidemiology-coronary-heart-disease-articulo-S1885585713003381
  • 402
    Kandaswamy E, Zuo L. Recent Advances in Treatment of Coronary Artery Disease: Role of Science and Technology. Int J Mol Sci. 2018 Jan 31;19(2):424. doi: 10.3390/ijms19020424. PMID: 29385089; PMCID: PMC5855646.
  • 403
    Graham G. Disparities in cardiovascular disease risk in the United States. Curr Cardiol Rev. 2015;11(3):238-45. doi: 10.2174/1573403×11666141122220003. PMID: 25418513; PMCID: PMC4558355.
  • 404
    Aggarwal A, Srivastava S, Velmurugan M. Newer perspectives of coronary artery disease in young. World J Cardiol. 2016 Dec 26;8(12):728-734. doi: 10.4330/wjc.v8.i12.728. PMID: 28070240; PMCID: PMC5183972.
  • 405
    Mochari-Greenberger H, Mosca L. Differential Outcomes by Race and Ethnicity in Patients with Coronary Heart Disease: A Contemporary Review. Curr Cardiovasc Risk Rep. 2015 May;9(5):20. doi: 10.1007/s12170-015-0447-4. PMID: 25914758; PMCID: PMC4405256.
  • 406
    Kumar R, Singh MC, Singh MC, Ahlawat SK, Thakur JS, Srivastava A, Sharma MK, Malhotra P, Bali HK, Kumari S. Urbanization and coronary heart disease: a study of urban-rural differences in northern India. Indian Heart J. 2006 Mar-Apr;58(2):126-30. PMID: 18989056.
  • 407
    American Heart Association. (2020, April 22). Health disparities in rural us: Higher coronary artery disease death in women under 65 and people with heart failure. Health disparities in rural US: Higher coronary artery disease death in women under 65 and people with heart failure. https://newsroom.heart.org/news/health-disparities-in-rural-us-higher-coronary-artery-disease-death-in-women-under-65-and-people-with-heart-failure
  • 408
    Kelli HM, Mehta A, Tahhan AS, Liu C, Kim JH, Dong TA, Dhindsa DS, Ghazzal B, Choudhary MK, Sandesara PB, Hayek SS, Topel ML, Alkhoder AA, Martini MA, Sidoti A, Ko YA, Lewis TT, Vaccarino V, Sperling LS, Quyyumi AA. Low Educational Attainment is a Predictor of Adverse Outcomes in Patients With Coronary Artery Disease. J Am Heart Assoc. 2019 Sep 3;8(17):e013165. doi: 10.1161/JAHA.119.013165. Epub 2019 Sep 2. PMID: 31476920; PMCID: PMC6755831.
  • 409
    Fioranelli M, Bottaccioli AG, Bottaccioli F, Bianchi M, Rovesti M, Roccia MG. Stress and Inflammation in Coronary Artery Disease: A Review Psychoneuroendocrineimmunology-Based. Front Immunol. 2018 Sep 6;9:2031. doi: 10.3389/fimmu.2018.02031. PMID: 30237802; PMCID: PMC6135895.

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