ABSTRACT

During recent years, our understanding of the pathophysiology of acute ischaemic syndromes has undergone dramatic changes. Vascular fissures, erosions and plaque rupture have been identified as precipitants of thrombosis in acute myocardial infarction (MI), unstable angina, sudden death, and stroke. Whereas cardiologists tended to believe that the extent of the stenosis was related to the risk of an acute event, postmortem studies and angiographic studies showed that approximately two-thirds of cases of acute MI arise from atherosclerotic lesions that are minimal to moderate in severity.1 These observations, together with results from serial analyses of angiographic studies demonstrating the unpredictable rapid progression of a number of mild coronary lesions to severe stenoses or even to total occlusions, have led to the concept of the ‘unstable’ or ‘vulnerable’ plaque.