What happens inside an atherosclerotic plaque?

摘要

Atheiogenesis probably begins with endothelial dysfunction, whose diggers include dyslipidemi,smoking, hypertension, and insulin resistance. Endothelial dysfunction may encompass impaired barrier function; induction of endothelial adhesion molecules including VCAM-1; and migration of leukocytes and monocytes into the subendothelial space in response to chemoattractant cytokines such as monocyte chemoattractant protein-1 (MCP-4) Subsequent steps include formation of foam cells, smooth muscle cell migration, T cell activation, and, at sites of plaque disruption, platelet activation and aggregation. The smooth muscle cells form a fibrous cap. Stable plaques have a thick fibrous cap, a small lipid core, and few inflammatory cells.In contrast, lesions with higher risk of rupture have high lipid content, numerous inflammatory cells, and a thin fibrous cap with reduced collagen and vascular smooth muscle cells. Diseased coronary arteries contain multiple such vulnerable plaques, hence the need for systematic therapy to prevent acute coronary events.