Pathology of Atherosclerotic Plaque
The modern consensus of the genesis and pathology of atherosclerosis differs from both older and recent chelation theories. In brief, arterial atheromas begin as low-density lipoproteins (LDL), cross the endothelial cell layer of the artery at a point of local injury or oxidant damage, and are deposited in the subendothelial layer. Monocytes, attracted to the injured area and subendothelial layers, engulf LDL and become foam cells, collectively forming a fatty streak on the arterial wall. The accumulation of foam cells ruptures the arterial endothelial cell layer, and platelets aggregate at the site and release growth factors, stimulating smooth-muscle cells to proliferate. During repair, cells produce collagen and form a fibrous, collagen-rich cap over the site (plaque). This plaque contains cholesterol, lipid particles, fibrous protein, and debris. The plaque enlarges as the process repeats. Calcium deposition inside the atheroma is a late event, and is not intrinsic to the genesis or maintenance of the atheroma's structure. Calcium rarely occupies more than a small fraction of the plaque's volume [6].