Aspirin and Clopidogrel: Lessons from PCI-CLARITY, COMMIT & CHARISMA
DOI:
https://doi.org/10.2015/hc.v1i1%20sup.44Abstract
Platelet activation plays a critical role both in spontaneous coronary artery thrombosis due to atherosclerotic plaque rupture and in thrombotic complications following percutaneous coronary intervention (PCI) with coronary artery stenting. Aspirin use has been shown to safely reduce ischemic events throughout the spectrum of clinical conditions of coronary artery disease (CAD). Therefore, aspirin is part of the standard treatment given to patients with CAD, including those undergoing PCI. Despite the inhibition of cyclooxygenase by aspirin, however, platelet activation can still occur through thromboxane-independent pathways, leading to the aggregation of platelets and the formation of thrombin. For that reason, a more potent antiplatelet effect was sought by using other agents ??? thienopyridines (ticlopidine, clopidogrel) and glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors, usually in combination with aspirin. Indeed, depending on the clinical scenario and the concomitant anticoagulants used, regimens combining 2 or more of these antiplatelet agents have resulted in fewer ischemic events and sometimes more bleeding events compared with aspirin alone.
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