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Atherosclerosis is the underlying cause of most CVD, starting early in life and progressing slowly and silently for decades before manifesting as acute MI, stroke, or angina pectoris. Plaques are initiated when monocytes from the endothelium migrate into the intima. These monocytes become tissue macrophages. Macrophages containing oxidized lipid (foam cells) form small, isolated groups, accumulating in the intima. Subsequently, foam cells, lipid-containing smooth muscle cells, T lymphocytes, and mast cells collect in the intima to form the earliest recognizable atherosclerotic lesion—the fatty streak. As progression continues, pools of extracellular lipids, the result of the apoptosis of foam cells, disrupt the intimal lining of the vessel. These extracellular lipid pools increase in number over time, eventually converging to form a clearly defined lipid core. Simultaneously, a secretory phenotype develops in the surrounding smooth muscle cells, resulting in stimulated synthesis and decreased resorption of collagen. The result is a collagen-rich fibrous cap separating the lipid-rich contents of the plaque from the vessel lumen. Lesions with a fibrous cap and lipid core are characteristic of advanced atherosclerosis. They are marked by surface defects that may expose the underlying thrombogenic surface to flowing blood, resulting in thrombosis. Pepine CJ. The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: potential role in myocardial ischemia. Am J Cardiol . 1998;82(suppl 10A):23S-27S.