[Physiopathology of acute coronary syndromes]

Coronary atherosclerosis and its thrombotic complications represent one of the leading causes of lesions usually consists of successive acute episodes, either silent or in the form of an acute coronary syndrome such as unstable angina, non-Q-wave myocardial infarctions, transmural myocardial infarctions or sudden death. This mode of progression does not exclude phases of regression, or more frequently stabilization of plaques, which, depending on their haemodynamic repercussions, are then responsible for chronic myocardial ischaemia. Acute coronary syndrome (ACS) correspond to the same pathophysiological process: rupture of an atheromatous plaque initiating harmful thrombotic, inflammatory and vasomotor phenomena. This is not a new concept, but progress over recent years suggests that the composition and biology of the plaque are factors involved more in the initiation of ACS than the size of the plaque. "Soft" lesions, rich in lipids, are clearly not only the most unstable lesions, but also the most thrombogenic because of their large tissue factor content. After describing the structure of vulnerable plaques, the authors discuss the causes of their rupture and the resulting cascade or events, responsible for life-threatening clinical situations.