Hyperlipidemia and atherosclerosis

Hyperlipidemia and atherosclerosis

Elevated LDL is a major risk factor for the development of atherosclerosis. This pathology can result in coronary artery disease (CAD), myocardial infarction, angina pectoris, strokes, and transient cerebral ischemia. The formation of early lesions is due to accumulation of LDL in the tunica interna of the arterial wall resulting from high circulating levels of LDL. In the intima, the LDLs undergo chemical modifications such as oxidation. Oxidized LDL directly harms the endothelial cells and vascular function. Oxidized LDL also induces an

inflammatory response starting with penetration of monocytes and lymphocytes into the intima. Once resident within the tunica interna, the monocytes differentiate into macrophages, which - combined with oxidized LDL- transform into lipid-laden foam cells. Oxidized LDL is able to stimulate necrosis of the foam cells. Their proteolytic enzymes damage the endothelial cells as well. Macrophages may produce cytokines and growth factors that can further signal some of the cellular events in atherosclerotic plaque evolution and complication.

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Atherogenic dyslipidemia is a triad of lipid abnormalities includes