Abstract

The platelet response to endothelial injury is central to the process of atherothrombosis, the pathophysiologic hallmark of acute coronary syndromes (ACS). Multiple antiplatelet agents have been developed to inhibit key components of this platelet activity. The use of two or more antiplatelet agents in patients with ACS reduces ischemic events but increases bleeding risk. Triple antiplatelet therapy utilizing aspirin, P2Y12 antagonists and glycoprotein IIb/IIIa inhibitors, remains indicated in select ACS populations. In ST-elevation myocardial infarction, triple antiplatelet therapy may be beneficial in subjects receiving percutaneous coronary intervention without adequate thienopyridine preloading and in those with large thrombus burden. In subjects with non-ST elevation ACS, triple antiplatelet therapy is reserved for those at highest ischemic risk (e.g., elevated troponin or refractory ischemia) and for those with thrombotic complications at the time of percutaneous coronary intervention. The focus of ...

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