A major factor invoking coronary thrombosis is disruption of an atherosclerotic plaque. Studies comparing intact and disrupted plaques have been used to define the characteristics of vulnerable plaques i.e. those at risk of disruption. The characteristics are a lipid core occupying over 50% of overall plaque volume, a thin plaque cap, a large absolute number and density of macrophages, and a reduction in the smooth muscle content of the plaque. Such vulnerable plaques make up a small proportion of all the plaques present in most individuals. Angiographic stenosis, however, does not predict vulnerability because there is no relation between core size or plaque size with stenosis A large proportion of disruption episodes go unnoticed clinically because the thrombus does not sufficiently encroach on the lumen to cause ischaemia These subclinical episodes, however, will invoke plaque growth. Plaque disruption is followed by a smooth muscle proliferative repair response analogous to that occurring after angioplasty. In both situations exuberant repair leads to post event stenosis Reconstruction of coronary lesions at autopsy shows that 70% of high grade stenosis (angiographic >50% diameter) have had an episode of healed disruption. Such data highlight the role of plaque disruption in the generation of advanced stenotic lesions irrespective of whether an acute clinical event occurred. Any therapeutic intervention which increases plaque stability, i.e. resistance to disruption, would reduce the acute ischaemic event rate but also slow the generation of new high grade stenoses.