Clopidogrel has significantly reduced the incidence of recurrent atherothrombotic\nevents in patients with acute coronary syndrome (ACS) and in those undergoing percutaneous\ncoronary intervention (PCI). However, recurrence events still remain, which may be partly due to\ninadequate platelet inhibition by standard clopidogrel therapy. Genetic polymorphisms involved\nin clopidogrel�s absorption, metabolism, and the P2Y12 receptor may interfere with its antiplatelet\nactivity. Recent evidence indicated that epigenetic modification may also affect clopidogrel response.\nIn addition, non-genetic factors such as demographics, disease complications, and drug-drug\ninteractions can impair the antiplatelet effect of clopidogrel. The identification of factors contributing\nto the variation in clopidogrel response is needed to improve platelet inhibition and to reduce risk\nfor cardiovascular events. This review encompasses the most recent updates on factors influencing\npharmacokinetic and pharmacodynamic responses to clopidogrel.
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