Résumé
The most important pathological mechanism in non-ST elevation Acute Coronary Syndrome [ACS] is the formation of a platelet rich thrombus on an atherosclerotic plaque. The understanding of this mechanism has changed the management of ACS with time. Until recently, the combination of aspirin and unfractionated heparin constituted the main antithrombotic therapy in ACS with a 46% reduction in vascular events, as reported by the Antithrombotic Trialists Collaboration. However, even with this regimen the recurrences of ischemic events in patients with ACS remained high. Now with the advent of newer drugs i.e., adenosine diphosphate [ADP] receptor antagonists and glycoprotein IIb/IIIa [GP IIb/IIIa] inhibitors, the out come of patients with ACS have significantly improved. The CURE trial clearly demonstrated the benefits of the combination of aspirin and clopidogrel in reducing major cardiovascular events by 20%. GP IIb/IIIa inhibitors, block the final common pathway of platelet aggregation. Agents like eptifibatide and tirofiban in large studies have demonstrated to cause reduction in 30 days risk of death and myocardial infarction. The risk reduction was greatest in patients with a baseline-elevated troponin, dynamic ST changes, recurrent angina, diabetes and in patients undergoing percutaneous revascularization. In view of the current evidence, appropriate selection of the antiplatelet and antithrombotic agents is the key for reduction in death and major adverse cardiac events in patients with ACS