by Mark Lin

Created on: December 17, 2008

Atherosclerosis, the formation of certain bumps composed of connective tissues and fat, is generated by various ill-formed lifestyle habits and numerous genetic predispositions. Atherosclerosis is generally composed of a lipid-rich core commonly generously enriched with cholesterol and low density lipoprotein (LDL), commonly called the "bad cholesterol" because it is the bulk constituent of an atherosclerotic plague upon oxidation. Other constituents of the plague include smooth muscle cells and macrophages, as well as a capsule made from fibrin polymers.

LDL can produce atherosclerotic plagues in two ways. Firstly, the engulfment of the lipoprotein by specialized white blood cells in the blood stream known as "macrophages" can produce the so-called "foam cells," named from their lipid-laden appearance. These foam cells then migrate towards possible sites of vessel damage, and move into the interior of the vessels, contributing to the formation of the plague by mechanically giving rise to an inward bulge into the lumen. Secondly, LDL can mediate the migration of smooth muscle cells from the middle layer of a blood vessel, known as the tunica media, into the lumen of the vessel. The migration of the smooth muscle cells directly causes mechanical obstruction of the vessel lumen.

Most atherosclerotic plagues can lead to severe complications, with or without its ruptures. From time to time the fibrous capsule of the plague, formed from fibrin deposits, can be deficit in tensile strength and become prone to rupturing. Upon rupture, the plague triggers local blood clotting (thrombosis) by exposing the underlying connective tissue of the vessel lumen. The collagen fibers of the vessel are powerful mediators for blood clotting. On the other hand, thrombus may be formed in the mechanism described below. As well known in pathology, three factors can well expose an individual to thrombosis: turbulence in blood flow, hypercoagulability, and endothelial cell injury. Endothelial cells are cells lining the interiors of a blood vessel. The three factors have come to be known collectively as the Virchow's triad, named after the pathologist who discovered the links between such. Of the three, an unruptured atherosclerotic plague can produce the latter two, since the plague is a mechanical obstacle in nature in the lumen; one may well perceive that its formation causes turbulence in blood flow. Its presence also covers the cells underlying it, causing endothelial injury. An atherosclerotic plague can contribute to thrombus formation by the pathomechanisms listed above.

Having said this, the reader is highly advised to prevent atherosclerosis formation through careful controls by diet and lifestyle. Since genetic factors are naturally determined and cannot be changed, emphasis should be placed more on the former two.

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