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Atherosclerosis follows the deposition, retention, and oxidative modification of lipoproteins, especially low-density lipoprotein (LDL) in the walls of large arteries. Uptake of oxidized LDL results in the formation of macrophage foam cells. Proliferation of vascular smooth muscle cells and secretion of extracellular matrix contribute "fibrous" components of the plaque, whereas ongoing accumulation of lipid and inflammatory cell debris forms the necrotic lipid core of the mature atherosclerotic plaque. Both the size and composition of plaques determine the clinical course. In particular, a large lipid core, thin fibrous cap, dense inflammatory cell infiltrate, and proteolytic enzyme activity are associated with adverse risk. Atherosclerosis has often been considered a relentlessly progressive disease. However, new imaging techniques that can quantify plaque burden and provide insights into some of the specific plaque components have allowed regression to be mapped for the first time. In this article, drugs targeting atherosclerosis that have potential or proven benefit in atherosclerosis regression are discussed. |
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