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The treatment of acute coronary syndromes, including acute myocardial infarction and unstable angina, has been one of the most successful contributions in the last 20 years to the improvement of medicine. However, we are still unable to predict them, and therefore to prevent occurrence of acute myocardial infarction and/or death. Major improvements have been made in an effort to understand the mechanism(s) which might lead to acute coronary occlusion: the concept of vulnerable plaque has helped us to understand better the cascade resulting in acute occlusion. Why does a stable plaque become vulnerable, and is it possible to reverse/prevent this process?
The contribution of pathologists has been critical in pointing out the role of the vulnerable plaque in the pathogenesis of acute coronary syndromes, and the major role of thrombus formation.1,2 Initially, plaque rupture has been defined as the mechanism responsible for the evolution from vulnerable plaque to acute occlusion.3 Although plaque rupture remains a major cause of plaque complications, other mechanisms have emerged—that is, plaque erosion, and less frequently calcified nodules protruding into the artery lumen.4 The fact that coronary thrombosis may occur without plaque rupture is a phenomenon that will have to be taken into account in the definition of vulnerability (table 1). These potentially independent mechanisms leading to acute coronary syndromes represent nowadays the new basis to approaching the treatment and prevention of vulnerable plaque. However, this does not eliminate the possibility of other unknown mechanisms undetectable at necropsy. Does a plaque become locally vulnerable or does the patient become vulnerable? The new concept of widespread coronary inflammatory processes during unstable angina has to be integrated into our strategies, provided it is recognised we are not just fighting the culprit vulnerable lesion, but facing a disease involving multiple lesions.5 This review will …
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