Atherosclerosis Essay
Atherosclerosis can affect the arteries of the heart and it’s called coronary artery disease.
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…
proliferation .The formation of smooth muscle and the layer of cells covering the extra cellular lipid separates it from the adaptive smooth muscle thickening in the endothelium. Excessive production of collagen by smooth muscle will occur. After that, advanced or raised fibrolipid plaque with a soft, yellow, grumous core of lipid covered by white fibrous cap will formed , which then grow gradually and encroach in the lumen or become unstable, undergo thrombosis and produce obstruction(1,4)
Two mechanisms are responsible for thrombosis formation(1,5) :
1- the first process is superficial endothelial injury, which involve denudation of the endothelial covering over the plaque.
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
attack.
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…
proliferation .The formation of smooth muscle and the layer of cells covering the extra cellular lipid separates it from the adaptive smooth muscle thickening in the endothelium. Excessive production of collagen by smooth muscle will occur. After that, advanced or raised fibrolipid plaque with a soft, yellow, grumous core of lipid covered by white fibrous cap will formed , which then grow gradually and encroach in the lumen or become unstable, undergo thrombosis and produce obstruction(1,4)
Two mechanisms are responsible for thrombosis formation(1,5) :
1- the first process is superficial endothelial injury, which involve denudation of the endothelial covering over the plaque.
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
attack.