Abstract
Clopidogrel is an antiplatelet drug that is administered in the form of prodrug that has to be converted to its active metabolite by hepatic cytochrome P450 (CYP) isoenzymes in the liver. There exists individual response variability of platelets inhibition by clopidogrel that is an indication that genetic factors are involved in clopidogrel responsiveness. Combining aspirin and clopidogrel is considered as gold standard therapy for patients who develop acute coronary syndromes (ACS) or are undergoing percutaneous coronary intervention (PCI). However, despite the administration of dual antiplatelet therapy, some patients face recurrent cardiovascular ischemic events, the most catastrophic is stent thrombosis. It is well established that the antiplatelet response to clopidogrel varies widely among patients. Patients who display little attenuation of platelet reactivity under clopidogrel therapy are recognized as low-or non-responders, or clopidogrelresistant. Different alleles of cytochrome P450 gene and a number of other genes are involved in the pharmacokinetics and pharmacodynamics of clopidogrel. Herein we discussed the mode of action of clopidogrel, mechanism of clopidogrel resistance and relation of genetic polymorphisms of CYP and other genes to clopidogrel resistance in patients using clopidogrel.