Inflammation, Chronic Ulcerated Plaques, and Unstable Coronary Syndromes

Abstract

Inflammation is a well-recognized component of active atherosclerotic disease, believed to play a major role in plaque ulceration and the development of acute coronary events. Although ulcerated plaque lesions underlie the development of acute coronary thrombosis and acute coronary disease, the ulceration may not be a sudden or recent event. Our studies, based on extensive histologic study of the coronary tree in patients who died of acute coronary disease, suggest that ulcerated plaques may exist as chronic, unrecognized lesions. Clinical studies indicate that ulcerated plaques may exist, silent and unrecognized, for weeks, months, or even years without resolving and reestablishing endothelial integrity. In addition, pathologic studies show that patients with acute coronary disease often have multiple, ubiquitous plaques in all stages of plaque development, which are not associated with luminal stenosis or thrombosis but are consistently associated with inflammation. Because inflammation is a marker of active atherosclerotic disease, and because ulcerated plaques are consistently associated with inflammation, ulcerated plaques appear to be a component of active inflammatory atherosclerotic disease. Ulcerated plaques, and the associated exposure of subendothelial collagen to flowing blood, are potentially unstable lesions until endothelial integrity is restored. Patients with unstable coronary syndromes may harbor unstable lesions, such as chronic ulcerated plaques, that play an important role in the pathogenesis of such syndromes. Recognition and treatment of ulcerated plaques before the onset of acute coronary events may prevent acute coronary syndromes by eliminating the pathologic substrate responsible for coronary thrombosis.