Abstract
Atherosclerosis is a complex process involving the deposition of plasma lipoproteins and the proliferation of cellular elements in the artery wall. This chronic condition advances through a series of stages beginning with fatty streak lesions composed largely of lipid-engorged macrophage foam cells and ultimately progressing to complex plaques consisting of a core of lipid and necrotic cell debris covered by a fibrous cap.1 These plaques provide a barrier to arterial blood flow and may precipitate clinical events, particularly under conditions that favor plaque rupture and thrombus formation.