Summary

Since its approval in 1997, clopidogrel has been a cornerstone of therapy in patients with acute coronary syndrome and in those patients who are undergoing percutaneous coronary intervention. Although the drug reduces the risk of future ischemic events, high variability in the antiplatelet effect between patients has been demonstrated. A number of factors are responsible for this variability, including clinical factors, drug interactions, and the presence of CYP2C19 loss-of-function alleles that hinder the metabolism of clopidogrel to its active form, thus leading to attenuation of its antiplatelet effect [Brandt JT et al. J Thromb Haemost 2007].