Plaque stabilisation in acute coronary syndromes: clinical considerations

he large secondary prevention trials of statin treatment in coronary artery disease were characterised by separation of the survival curves in the first 6-18 months after randomisation. w1-3 This was too soon to be fully explained by changes in disease progression, so the concept of plaque stabilisation arose, described largely in terms of cap strength and lipid pool. w4 w5 This concept, however, has no direct parallel in acute coronary syndromes because the plaque has, by definition, already ruptured and thrombosis has occurred with variable obstruction of the arterial lumen. 1 2 The process of plaque rupture occurs against a background of inflammation and endothelial dysfunction which are generalised throughout the coronary arteries, accounting for recent intravascular ultrasound findings of multiple ruptured plaques in patients with acute coronary syndromes, often located remotely from the index artery. In order to achieve plaque stabilisation, therefore, with healing of the ruptured plaque and restoration of luminal patency, the following targets must be achieved: c Dissolution of thrombus c Reduction of inflammatory activity c Passivation of the coronary endothelium.