[The hemostatic system in the acute coronary syndromes: physiopathological and therapeutic implications].

The interaction between the vulnerable atherosclerotic plaque prone to disruption and thrombus formation is the cornerstone of acute coronary syndromes (ACS): unstable angina and acute myocardial infarction with and without ST-segment elevation. Platelet adhesion and aggregation and clotting activation, at the level of injured endothelium lacking thromborresistance properties, and directly implicated in the pathogenesis of atherothrombosis. Tissue factor emerges as the initial mechanism leading to thrombin generation and fibrin formation to stabilize the platelet-rich thrombus. The combination of several antithrombotic strategies, including fibrinolytics, antiplatelets (aspirin, clopidogrel, and GpIIb/IIIa antagonists), and anticoagulants (mainly low-molecular-weight heparins) has proven to be of great benefit in the reduction of ischemic events and in the prevention of recurrences after ACS.