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Introduction The Ruptured Atherosclerotic Plaque. It has been learned from research during the last decades that thrombosis, rather than gradual occlusion of an artery, is mainly responsible for acute coronary syndromes such as unstable angina pectoris, myocardial infarction, and sudden coronary death. Atherosclerosis could be considered as a relatively benign disease as long as plaque is compensated for by arterial enlargement and until thrombosis superimposes mature plaques. Plaque rupture, or erosion, is the most frequent cause of acute intraluminal thrombus formation. When the fibrous cap of a plaque ruptures, the highly thrombogenic, soft lipid‐rich core is exposed to circulating blood coagulation factors. Plaque composition (“vulnerability”) is more important than plaque size and luminal stenosis in determining those plaques that are prone to acute clinical syndromes. Pathology studies revealed three histological determinants that are associated with rupture. The first determinant thought to be associated with plaque rupture is a large atheromatous core. In a postmortem study of 17 infarct‐related arteries, it appeared that the atheromatous lipid‐rich cores in 39 segments with plaque rupture were larger than those in 229 segments revealing intact plaque surface (32% and 5–12% of plaque area, respectively). In aortic plaques, Davies et al. observed a
Journal of Interventional Cardiology – Wiley
Published: Apr 1, 2003
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