Failure of CT coronary imaging to identify plaque erosion: a resetting of expectations

This editorial refers to ‘Coronary CT angiography characteristics of culprit lesions in acute coronary syndromes not related to plaque rupture as defined by optical coherence tomography and angioscopy’, by Y. Ozaki et al. doi:10.1093/eurheartj/ehr189. Prospective identification of high-risk plaque (or vulnerable plaque) prior to the occurrence of coronary thrombosis has for years been compared with the quest for the Holy Grail, since this would be the necessary initial step for the focal treatment of the high-risk lesion and subsequent prevention of progression to an acute coronary syndrome (ACS).1–3The most common cause of coronary thrombosis is plaque rupture (in 55–60% of cases) or plaque erosion (in 30–35% of cases) and much less frequently calcific nodules.4 From post-mortem studies we know that ruptured plaques have specific features: a thin fibrous cap ( 10% of the plaque area) that is inflamed and often accompanied by expansive remodelling.4–6 These plaques usually have a stenosis diameter < 50% and contain spotty calcifications. The precursor lesion of the ruptured plaque is the thin cap fibroatheroma (TCFA), which resembles the morphology of the ruptured plaque except that there is no rupture or thrombosis. The ruptured plaque is distinct from the eroded plaque, and retrospective pathological studies of plaque erosion found that an acute thrombus was in direct contact with the intima in an area of absent endothelium. This plaque is often rich in proteoglycans, a lipid pool or necrotic core is often lacking, the fibrous cap is thick and rich in smooth muscle cells, and constrictive remodelling of the plaque is often seen.4 The precursor lesions of the …