Despite significant strides towards an understanding of the initiation and progression of atherosclerosis and the influence of risk factors, coronary heart disease remains the principal killer in the western world. 1 If progress in the field is to continue in the 21st century, one must focus on high risk patients with lesions that are vulnerable to thrombosis together with the triggering mechanisms that cause plaques to rupture at a precise location and time. Although animal studies have helped define the molecular mechanisms of atherosclerosis, a convincing model of plaque rupture still does not exist. Therefore, the development of future treatments targeted against plaque instability is contingent upon our ability to confidently recognise precursor lesions likely to thrombose; this will be primarily achieved via improved imaging modalities. Insights into the mechanisms of coronary thrombosis extend from detailed analyses of underlying plaque morphologies in necropsy specimens from sudden death victims. 2 3 In 50–75% of these cases, the culprit lesion (fatal plaque) shows a coronary thrombus whereas the remainder without thrombi exhibit stable coronary plaques with. 75% cross sectional area luminal narrowing. 4 The major cause of acute coronary thrombosis is plaque rupture, and the precursor lesion has been termed vulnerable plaque (fig 1) or, as defined by our laboratory, the thin cap fibroatheroma (TCFA). In this review, we will critically analyse the pathology of plaque rupture with emphasis on its relation to TCFAs and healed plaque ruptures to gain a better understanding of the lesion most responsible for coronary morbidity and mortality.