Pharmacological Options in Atherosclerosis: A Review of the Existing Evidence

a Atherogenic lipoproteins such as low-density lipoproteins (LDLs) entering the intima are modified, by oxidation or enzymatic activity, and aggregate within the extracellular intimal space. Unregulated uptake of these lipoproteins by macrophages generates foam cells and fatty streaks. These are usually asymptomatic. b Vascular smooth muscle cells secrete large amounts of extracellular-matrix components, such as collagen, which increase the retention and aggregation of atherogenic lipoproteins. The inflammatory state is potentiated by monocyte and leukocyte recruitment. As the plaque grows, compensatory remodeling (adaptive intimal thickening) occurs to preserve the lumen diameter. c Foam cells eventually die and release cellular debris, which forms a necrotic core. Smooth muscle cells form a fibrous cap beneath the endothelium, which walls off the plaque from the blood. d The advanced lesion can either rupture or continue to grow, eventually leading to clinically significant obstructive disease