Coronary atherosclerosis is mainly characterized by build-up of plaques in artery wall , which formed by lipids, cholesterol, macrophages , and smooth muscle cells accumulation as intimate plaques in the large and medium-sized epicardial coronary arteries.(1,2,3)
The development of atherosclerosis usually follows the endothelial dysfunction, which increase the permeability to and accumulation of oxidized lipoproteins which are taken by macrophages at focal sites within the endothelium to produce lipid laden foam cells.
Release of cytokines, macrophages or the damaged endothelium promote further accumulation of macrophages and smooth muscle cells migration and …show more content…
Subendocardial connective tissue matrix is then exposed and platelet adhesion occurs because of reaction of collagen. The thrombus is adherent to the surface of plaque.
2- the second process is deep endothelial fissuring, the plaque cap tears ( ulcerates, fissures or ruptures), allowing blood from the lumen to enter the inside of the plaque itself. The core with lamellar lipid surface, tissue factor ( which triggers platelet adhesion and activation ) produced by macrophages and exposed collagen, is highly thrombogenic. Thrombus forms within the plaque, expanding its volume and distorting its shape. Thrombosis may then extend into the lumen and cause reduction in lumenial diameter which then develop into stenosis or blockage in the arteries that supply blood and oxygen to the heart. In this case, the smaller distal intramyocardial arteries and arterioles are maximally dilated and any increase in myocardial oxygen demand provokes ischemia, which can contribute to many coronary heart diseases as angina or heart