Chronic ulcerated plaques: new insights into the pathogenesis of acute coronary disease.

Ulcerated atherosclerotic plaques form the substrate for the vast majority of coronary thrombi, but this association does not prove that either one or both of these lesions represents a recent development. Recent reports suggest ulcerated plaques may exist for weeks, months, and possibly years without resolving and reestablishing endothelial integrity. The coronary arteries of 83 patients dying of acute coronary disease were extensively examined, histologically, to determine the pathologic features associated with ulcerated plaques but not associated with an intraluminal thrombus. These findings were then correlated with the degree of luminal stenosis, the presence of inflammatory cell infiltrates, calcification, and necrotic atherosclerotic plaques. The results show ulcerated plaques without thrombosis are ubiquitous, multiple, are unrelated to the degree of luminal stenosis, and are consistently associated with inflammatory cell infiltrates, calcification, and necrotic plaques. Our observations suggest acute coronary disease may result from thrombosis and possibly other biochemical reactions, superimposed on chronic, rather than on recent, ulcerated plaques that have been present for an indeterminate length of time before the onset of acute symptoms. These observations form the basis for an alternative approach to the understanding of the pathogenesis of acute coronary disease and have implications for the prevention of thrombosis.