Pathophysiology of Coronary Artery Disease

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September 1, 2019
Coronary artery disease, one of the most debilitating diseases worldwide, is characterized by plaque or atheromatous blockage of a blood vessel, resulting to a decrease in blood supply to the heart, and consequently, to other organ systems, leading to ischemia and other complications CITATION BMJ03 \l 1033 (BMJ, 2003).
Blood vessels, especially the arteries, are susceptible to injury when the following risk factors are present: 1) Hypertension; 2) Hyperlipidemia; 3) Hypercholesterolemia; and 4) Hyperglycemia or Diabetes Mellitus. Damage to the blood vessels precipitates an inflammatory reaction which leads to the recruitment of proinflammatory cytokines derived from excess adipose tissue which leads to the release of adhesion molecules that promote platelet aggregation to the endothelial wall to prevent bleeding from the endothelial wall damage CITATION Lib05 \l 1033 (Libby & Theroux, 2005). Initial vessel wall injury results to initial vasoconstriction followed by vasodilation secondary to histamine, kinin, and other inflammatory agent release, to increase the blood flow in the area. Histamine also increases vascular permeability. Consequently, it results in the migration secondary to chemotaxis, rolling, margination, and transmigration of leukocytes to the endothelial wall CITATION Vin15 \l 1033 (Vinay, Abbas, & Aster, 2015).
Oxidized Low Density Lipoprotein (LDL) or bad cholesterol causes this vascular injury. Adhesion of monocytes to the endothelial cells and subsequent migration to the subendothelium (tunica intima) results in their transformation as macrophages. These macrophages utilize and modify the oxidized LDL (oxLDL) or modified LDL and become foam cells. These foam cells gather at the site of injury and express growth factors and cytokines that stimulate the passage of smooth muscle cells (SMCs) from the tunica media to the tunica intima. These SMCs will then proliferate, produce collagen, an...