The Formation and Impact of the Atheromatous Condition

Pathophysiology of Coronary Artery Disease
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Pathophysiology of Coronary Artery Disease
Cardiovascular diseases comprise a wide range of heart diseases such as heart attack, angina, stroke, coronary heart and congenital heart diseases. The coronary artery disease is normally caused by a buildup of plaques or cholesterol inside the walls of the artery linings. The plaques which are also called atheromatous causes the thickening of arterial walls narrowing the arterial space in the process.The coronary artery is involved in transporting oxygen and nutrients rich blood to the heart. However, in the presence of atheromatous or atheromatous plaque, there is a decrease of blood reaching the heart muscle due to a narrow arterial space (NHLBI, 2015).
The formation of the atheromatous condition usually starts to develop as a result of injuries or damage in the innermost arterial lining called the endothelium. Once arterial walls are damaged, fats, lipoproteins, and cholesterol start to build up along the intima or the wall of the artery. High concentration of lipoprotein (low-density lipoprotein) penetrates the injured endothelium from where it undergoes oxidation process. The oxidized low-density lipoprotein hence attracts leukocytes making them migrate and engulf the lipoproteins resulting in the formation of foam cells. These foam cells are the earliest visible signs of atheromatous and are referred to as fatty freaks. Once fatty freaks are formed, smooth muscle cells are then attracted to the site and start to multiple hence producing an extracellular matrix comprising of proteoglycan and collagen accelerating the development of atherosclerosis plaque. As such, fatty freaks start to calcify (calcium deposits) around the plaque (NHLBI, 2015). The resulting plaque is made up of a core rich in lipids and dead cells. As a result, the region becomes prone to rupture exposing the underlying lipids and dead cells to blood thrombogenic factors, further narrowing th...