ABSTRACT
The understanding of the pathogenesis of unstable angina and acute myocardial infarction has advanced greatly over the past two decades. Because of these advances, many effective new treatment strategies have been developed. Despite these significant advances, ischemic heart disease remains the number one cause of mortality in the world (1). It is known that the vast majority of acute coronary syndromes are due to thrombosis developing on a culprit atherosclerotic plaque (2). These vulnerable lesions upon which thrombosis occurs have certain characteristics, including a large cholesterol-containing lipid core, a thin fibrous cap, and an increased number of lipid-filled macrophages (foam cells) (3). The mechanism from which coronary arterial thrombosis occurs takes on two main forms. The most common form is plaque disruption, accounting for approximately three quarters of cases (4). A tear in the cap exposes circulating blood to the highly thrombogenic lipid core, leading to thrombus formation on the plaque itself, then into the arterial lumen. The second mechanism responsible for coronary artery thrombosis is endothelial erosion, accounting for the remaining one quarter of thrombotic episodes. In this circumstance, denudation and erosion of the endothelium lead to thrombus formation on the plaque surface.
