Essay on Coronary Artery Disease: A Comprehensive Overview

This essay provides a comprehensive overview of Coronary Artery Disease (CAD), beginning with an introduction to the disease, also known as ischemic heart disease. It describes the normal physiology of coronary arteries, which supply blood and oxygen to the cardiac muscles, and explains how disruptions in blood flow due to plaque buildup can lead to myocardial ischemia and heart attacks. The essay then delves into the pathophysiology of CAD, detailing the process of atherosclerosis, including plaque formation, and the role of inflammation in the development of the disease. It further explores the pharmacology of CAD, focusing on the use of beta blockers in managing chest pain and improving blood supply to the myocardium. The essay concludes with a summary of the key points and highlights the effectiveness of beta blockers in the pharmacological treatment of CAD. The essay also includes relevant references to support the information presented.

Running head: CORONARY ARTERY DISEASE
Coronary Artery Disease
Name of the Student
Name of the University
Author Note

1CORONARY ARTERY DISEASE
Introduction
Coronary Heart Disease (CAD) is also referred to as ischemic heart disease (IHD) and
this disease is associated with the blockage of the blood vessels due to the atherosclerosis.
Due to the blockage in the coronary blood vessels, the blood supply is disrupted to the
cardiac muscles. As result, there is lack of oxygen supply in those region of cardiac muscles.
It is a usually reported that, there are several factors that can promote the risks of CAD
among patients. For example, it can be said that, the patients with high blood pressures,
obesity, diabetes, high level of blood cholesterol, smoking behaviour, family history of CAD,
lack of exercise have the higher chances of developing CAD. Due to restricted blood flow to
the cardiac muscles, the cells of the cardiac muscles may die due to less amount of oxygen
supply (Mack & Gopal, 2016). This condition is generally referred to as myocardial ischemia
or heart attack. Generally CAD takes place only when, the smooth muscles of the coronary
artery develops plaques that may contain deposition of calcium, fatty lipids and a few specific
type of abnormal inflammatory cells in that region. In the treatment of the CAD, beta
blockers, calcium channel blockers, blood thinner, ACE inhibitors can be used (American
Diabetes Association, 2016). In this essay, the overview of the coronary artery disease,
underlying pathophysiology of the disease, pharmacology of CAD along with relevant
clinical practice are discussed in a brief manner.
Overview of Coronary Artery Disease (CAD)
Coronary arteries general supplies blood to the heart, specifically to the cardiac
muscles of the heart. During the normal supply of the blood vessels, adequate amount of
oxygen is supplied to those region of cardiac muscles and this causes continuation of normal
activities of myocardium. Therefore, the local regulatory mechanism of the cardiac muscles
will control the blood flow through the vasodilation and vasoconstriction mechanism. In case

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of the coronary artery disease (CAD), it is reported that, the both structure and function of the
coronary artery is altered due to the deposition of plaque inside the walls of the coronary
arteries that supplies oxygenated blood to the myocardium. The right and left coronary
arteries of the heart is associated with supplying the blood to heart. The left and right
coronary arteries divides the small and large arteries into arterioles which also can supply
oxygen to myocardium. On the other hand, the left coronary artery supplies blood to the
anterior septum and left ventricle of the heart. The right coronary artery supply blood to the
right ventricle, AV node and myocardial walls of the heart. Hence, any disruption in the
blood supply to those areas can cause serious consequences such as cardiac arrhythmia,
myocardial ischemia. Such problems are due to reduced blood flow in those areas and
simultaneously less amount of oxygen reach in those areas ( Hall, 2015). The due to oxygen
the myocardium become infarcted and promotes the myocardium to die. A specific type of
CAD is STEMI that is ST elevated myocardial ischemia and in this condition, the coronary
artery is completely almost completely blocked by blood clots or plaques. In such cases, it
may happen that, the heart stops to work and leads to the condition refers to heart failure
( Moretti et al., 2015).
Pathophysiology of CAD
The coronary artery disease is associated with the deposition of vessel occluding
lipids inside the blood vessels. The underlying pathophysiology of this CAD starts with the
formation of atherosclerosis inside the blood vessels. The process of atherosclerosis can be
defined as a low grade inflammated condition of the inner lining myocardial cells of the
coronary arteries. These condition can be more serious in case of association of various risk
factors such as high cholesterol, smoking, diabetes, genetics and high blood pressure. In
case of CAD, the slow process of plaque formation inside the walls of coronary arteries
promotes the thickening of the artery walls and that results in gradual narrowness of the

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artery. The deposition of plaques can be classified into various degrees such as first degree
blockage, 2nd degree blockage and 3rd degree blockage. This formation of atherosclerosis
plaques comprises of cellular debris, inflammatory cells, smooth muscle cells, cholesterol
ester. The formation of thrombus inside the coronary artery is dependent on various factors
such as plaque composition, plaque volume and the degree of luminal narrowing and this
thrombus is gradually incorporated on the walls of coronary artery. It is reported in various
studies, that progression of atherosclerosis is mediated by proinflammatory cytokines and it is
observed that, the T- lymphocytes and monocytes are present in all the stages of plaque
formation that results in active inflammation of that region during this atherosclerosis
development. Low amount of chronic inflammation can enhance the deposition of
atherosclerosis plaque inside the coronary artery (Alexopoulos, Katritsis, & Raggi, 2014). In
a study by Ambrose and Singh (2015), it is reported that, in case of fatal coronary
thrombosis, almost 66% to 75% cases are associated with rupture of plaque. In addition to
this, it is observed in angiograms performed among the patients with acute myocardial
infarction (AMI) that, almost 84% of the total patients have occlusions in the coronary artery.
Due to the atherosclerosis related inflammation in coronary artery, level of C-reactive protein
(CRP) is also elevated. Moreover, presence of high level of IL-6, CD40 may also promote the
risk of CAD among patients (Hartman & Frishman, 2014). Not only this, but the presence of
soluble human heat-shock protein (HSP-60), HSP-65 can also promote the risk of
atherosclerosis which is the reason of CAD ( Wick et al., 2014).
Pharmacology of CAD
CAD generally restricts the blood flow to cardiac muscles that results in chest pain
generally known as angina and acute coronary syndrome. In CAD, it is 0observed that, the
due to blockage, coronary artery fails to supply adequate amount of blood to heart muscles.
So, reducing this chest pain and managing blood supply to the myocardium are the primary

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area of concern for patients. The use of beta blockers in the treatment of CAD is quite
common. The usage of beta blockers will help to relieve the CAD patients. Administration of
beta blockers helps in reducing the heart rate and thereby repairs the tissue damages lowing
the work load of heart muscles ( Hall, 2015). After administering this drugs, it generally
binds with the β1 and β2 adrenergic receptors of the cardiac muscles and this causes reduction
in heart rate by reducing the cardiac contractility. As a part of their action, beta blockers also
increases the diastolic filling time of heart. In addition to this, the demand of myocardial
oxygen is also reduced by negative chronotropic and inotropic effect. It is assumed that, use
of beta blockers also can enhances the coronary blood supply by augmentation of collateral
blood flow. Moreover, beta blocker administration helps to supply more bloods to the
ischemic areas of the heart (Hall, 2015). According to Irfan and Hirsch (2015), it is observed
that, beta blockers are very efficient in management of CAD. In this study, almost 26,973
patients were included as subject population. Among them, 19843 patients were given beta
blocker treatment on their discharge, 3819 patients initiated beta blocker treatment after one
year of their discharge and 3131 patients did not use this treatment method. In this study, it
was reported that, the patients had 3.7 years of average follow up and 16% of total patients
died and 26% of patients reported about cardiac attacks during this time. The author
concluded that, the use of beta blockers among the patients of CAD had proven
advantageous. It was observed that, the patients who used beta blockers as part of the
medication process, those patients had lower mortality rates and cardiac problems, than of the
patients who did not use beta blockers. The beta blocker treatment was associated with
significantly lower risks of deaths and acute myocardial infarction.
Conclusion
Hence it can be concluded that, CAD is one of the major cardiac problems that is
associated with the blockage of coronary arteries and thereby reducing the blood flow to the

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myocardium. Due to lack of adequate oxygen supply, problem of myocardial ischemia, chest
pain, acute myocardial infarction may be faced by patients. However, use of beta blockers
can reduce the workload of heart that results in reduced demand of myocardial oxygen
demand. So, it can be said that, the use of beta blockers can be used as effective
pharmacological treatment of this disease.

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References
Alexopoulos, N., Katritsis, D., & Raggi, P. (2014). Visceral adipose tissue as a source of
inflammation and promoter of atherosclerosis. Atherosclerosis, 233(1), 104-112.
Ambrose, J. A., & Singh, M. (2015). Pathophysiology of coronary artery disease leading to
acute coronary syndromes. F1000prime reports, 7.
American Diabetes Association. (2016). 8. Cardiovascular disease and risk
management. Diabetes care, 39(Supplement 1), S60-S71.
Hall, J. E. (2015). Guyton & Hall Physiology Review E-Book. Elsevier Health Sciences.
Hartman, J., & Frishman, W. H. (2014). Inflammation and atherosclerosis: a review of the
role of interleukin-6 in the development of atherosclerosis and the potential for targeted
drug therapy. Cardiology in review, 22(3), 147-151.
Irfan, A. & Hirsch, A., G. (2015). Beta-Blocker Therapy in Patients With Stable Coronary
Artery Disease. American College of Cardiology. Retrieved from-
https://www.acc.org/latest-in-cardiology/articles/2015/04/13/10/13/beta-blocker-therapy-
in-patients-with-stable-coronary-artery-disease
Mack, M., & Gopal, A. (2016). Epidemiology, traditional and novel risk factors in coronary
artery disease. Heart failure clinics, 12(1), 1-10.
Moretti, C., D'Ascenzo, F., Quadri, G., Omedè, P., Montefusco, A., Taha, S., ... & Gaita, F.
(2015). Management of multivessel coronary disease in STEMI patients: a systematic
review and meta-analysis. International journal of cardiology, 179, 552-557.
Wick, G., Jakic, B., Buszko, M., Wick, M. C., & Grundtman, C. (2014). The role of heat
shock proteins in atherosclerosis. Nature Reviews Cardiology, 11(9), 516.