Unit Title: Ischemic Cardiomyopathy and Coronary Artery Disease Report

This report delves into the complexities of coronary artery disease (CAD) and its related condition, ischemic cardiomyopathy. It begins by defining CAD as an inflammatory condition characterized by arterial lining inflammation, often accelerated by factors such as high blood pressure, smoking, and genetics. The report explores the pathophysiology of CAD, detailing how arterial walls thicken due to plaque buildup, leading to narrowed arterial lumens. It discusses the role of inflammation, the accumulation of atheroma, and the subsequent damage to the endothelium, resulting in the accumulation of substances like cholesterol and lipoproteins. Furthermore, the report describes how the accumulation of oxidized lipoproteins attracts leukocytes, forming fatty streaks and fibrous plaques. It then transitions into ischemic cardiomyopathy, describing it as a condition where the heart muscles weaken due to CAD or heart attacks. The report outlines the signs, symptoms, and risk factors associated with ischemic cardiomyopathy, emphasizing the importance of diagnosis through various methods. The report draws on multiple references, including Ambrose and Singh (2015), Madder et al. (2013), and Jia et al. (2013), to support its findings.

Running head: CORONARY ARTERY DISEASE 1
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Title: Ischemic Cardiomyopathy

CORONARY ARTERY DISEASE 2
Ambrose and Singh (2015) acute myocardial infarction and sudden cardiac death are the most
serious cardiac disorders and account for a lot of deaths every year. The pathophysiologic
mechanism of these diseases start with the coronary artery disease (CAD). They describe CAD
as an inflammatory condition of the arterial lining and is accelerated by high blood pressure,
smoking, high cholesterol levels, diabetes and genetic factors. The gradual thickening of the
coronary artery walls lead to narrowing of the arterial lumen. Madder et al. (2013) claim that
previously coronary artery disease was thought to be a cholesterol storage infection but after
successive researches they found out that it was a complex interaction between risk factors,
blood and the molecular signals they exchange.
Jia et al. (2013) claim that inflammation plays a role in every stage of CAD. The interaction
between arterial endothelium, risk factor or some bacteria, molecule coagulate and blood
leukocytes stick on the arterial wall. This deposit of substances on the arterial wall is called
atheroma. Its accumulation leads to damage of the endothelium. Once the endothelium is
damaged, substances such as cholesterol and lipoproteins start accumulating on the injured sites.
The deposited lipoproteins penetrate the damaged inner arterial wall then undergoes a chemical
process of oxidation (Mandal, 2019). The oxidized lipoproteins attracts leukocytes to engulf it
forming foam cells known as fatty streak. The fatty streak attracts smooth muscle cells where
they accumulate to form an extracellular matrix. This matrix forms the fibrous plaque which
causes bulging of the arterial walls hence the lumen narrows.
References
Ambrose, J. A., & Singh, M. (2015). Pathophysiology of coronary artery disease leading to acute
coronary syndromes. F1000prime reports, 7, 08. doi:10.12703/P7-08

CORONARY ARTERY DISEASE 3
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(2017). Patient education in the management of coronary heart disease. The Cochrane
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Jia, H., Abtahian, F., Aguirre, A. D., Lee, S., Chia, S., Lowe, H. & Tian, J. (2013). In vivo
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Madder, R. D., Goldstein, J. A., Madden, S. P., Puri, R., Wolski, K., Hendricks, M. & Brilakis,
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CORONARY ARTERY DISEASE 4
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