BackgroundCardiovascular diseases (CVDs) are considered a leading cause of death worldwide. Allelic variation in theCYP2C19gene leads to a dysfunctional enzyme, and patients with this loss-of-function allele will have an impaired clopidogrel metabolism, which eventually results in major adverse cardiovascular events (MACE). Ischemic heart disease patients (n= 102) who underwent percutaneous cardiac intervention (PCI) followed by clopidogrel were enrolled in the present study.MethodsThe genetic variations in theCYP2C19gene were identified using the TaqMan chemistry-based qPCR technique. Patients were followed up for 1 year to monitor MACE, and the correlations between the allelic variations inCYP2C19and MACE were recorded.ResultsDuring the follow-up, we reported 64 patients without MACE (29 with unstable angina (UA), 8 with myocadiac infarction (MI), 1 patient with non-STEMI, and 1 patient with ischemic dilated cardiomyopathy (IDC)). Genotyping ofCYP2C19in the patients who underwent PCI and were treated with clopidogrel revealed that 50 patients (49%) were normal metabolizers for clopidogrel with genotypeCYP2C19*1/*1and 52 patients (51%) were abnormal metabolizers, with genotypesCYP2C19*1/*2(n= 15),CYP2C19*1/*3(n= 1),CYP2C19*1/*17(n= 35), andCYP2C19*2/*17(n= 1). Demographic data indicated that age and residency were significantly associated with abnormal clopidogrel metabolism. Moreover, diabetes, hypertension, and cigarette smoking were significantly associated with the abnormal metabolism of clopidogrel. These data shed light on the inter-ethnic variation in metabolizing clopidogrel based on theCYP2C19allelic distribution.ConclusionThis study, along with other studies that address genotype variation of clopidogrel-metabolizing enzymes, might pave the way for further understanding of the pharmacogenetic background of CVD-related drugs.