Abstract
Smoking, elevated levels of plasma lipids, and hypertension are known to increase the number of atherosclerotic plaques in the aorta and coronary arteries.1,2 The influence of these cardiovascular risk factors on the structure and composition of individual plaques has been less well studied.The common factor precipitating acute cardiac events in patients with coronary artery disease is thrombosis. Thrombosis develops on a plaque either because the overlying endothelium undergoes denudation (erosion) or because the plaque tears open (rupture), exposing the highly thrombogenic core to blood in the arterial lumen.3 The two processes differ in that after endothelial erosion the . . .