Abstract
Atherosclerosis develops as a result of a chronic arterial inflammation and intimal fibrosis. The disease represents in many respects a vascular repair process activated in response to injury caused by toxic breakdown products of aggregated and oxidized lipoproteins. The initial response of the artery involves expression of adhesion molecules and recruitment of leukocytes. Degenerated lipoproteins are removed from the extracellular space by macrophages. If lipoproteins continue to accumulate, the inflammatory process becomes chronic and cytokines stimulate smooth muscle to migrate into the intima. These cells proliferate and form an atherosclerotic plaque. Plaque cell death and inflammation in response to oxidized lipids and other toxic factors may cause plaques to rupture.
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