约4％～30％的缺血性心血管疾病患者并未从氯吡格雷抗血小板治疗中获益。氯吡格雷抵抗(低或无反应性)反映氯吡格雷抗血小板治疗失败,但尚未明确定义。氯吡格雷抵抗的可能机制分为内源性和外源性。内源性机制包括P2Y_(12)受体和CYP3A的基因多态性。外源性机制概括为氯吡格雷剂量偏低或给药不当、生物利用度下降和有关CYP3A4参与的药物间相互作用以及血小板过度激活。 About 4% to 30% of patients with ischemic cardiovascular disease did not benefit from antiplatelet therapy with clopidogrel. Clopidogrel resistance (low or no response) reflects the failure of clopidogrel antiplatelet therapy, but has not yet been clearly defined. The possible mechanisms of clopidogrel resistance are divided into endogenous and exogenous. Endogenous mechanisms include the P2Y_ (12) receptor and CYP3A gene polymorphisms. Exogenous mechanisms are summarized as low or improper dosing of clopidogrel, decreased bioavailability, and drug-related interactions involving CYP3A4 and platelet over-activation.