Abstract

To the Editor: Rioufol et al1 recently reported a lower incidence of plaque rupture in culprit arteries than in non-culprit arteries (37.5% versus 79%) in acute coronary syndrome (ACS). The low incidence in culprit arteries was explained by thrombi that masked underlying ulcerations, but findings suggest that plaque rupture/thromboses do not directly induce symptoms in ACS (or ACS/infarction). There are other problems with the plaque rupture/thromboses mechanism. These include low (around 25%) incidences of thromboses in ACS,2,3 failure of thrombolysis to benefit non-ST-segment elevation infarction,3 rising incidence of thromboses over time in infarction,2,3 common occurrence of asymptomatic plaque rupture,3 failure of platelet glycoprotein IIb/IIIa receptor blockade to benefit most cases of ACS,4 and apparent inability of thromboses in very stenotic arteries to explain infarction.2,3 To my knowledge, nobody has seen plaque rupture …

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