These agents are continued in a maintenance dose for 1 year after PCI with a stent (BMS or DES) in the absence of bleeding. A 600-mg loading dose of clopidogrel is preferred to a 300-mg loading dose, given the more extensive and rapid platelet inhibition achieved with the higher dose, as well as the beneficial effects reported in a CURRENT-OASIS 7 subgroup analysis.259 The underpow- ered ARMYDA-6 MI (Antiplatelet Therapy for Reduction of Myocardial Damage During Angioplasty Myocardial Infarction) study also reported beneficial surrogate outcomes with the higher clopidogrel loading dose.258 The antiplatelet response to clopidogrel may vary as a function of patient phenotype (obesity, diabetes mellitus), enteric ABCB 1 polymorphisms, hepatic CYP450 enzyme system polymorphisms (predominantly CYP 2C19*2), and medications that interfere with clopidogrel biotransforma- tion. Approximately 25% to 30% of patients may harbor a reduced-function CYP2C19 allele. In TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel Thrombolysis In Myocardial Infarction)285 patients who were carriers of the reduced-function CYP2C19*2 allele had significantly lower levels of the active metabolite of clopi- dogrel, diminished platelet inhibition, and increased rates of major adverse cardiovascular events and stent thrombosis.285 The US Food and Drug Administration has changed clopido- grel s prescribing information to highlight the potential impact of CYP2C19 genotype on clopidogrel pharmacokinetics and Nevertheless, other studies have not con- firmed associations between CYP2C19 polymorphisms and adverse outcomes in clopidogrel-treated patients.290 Future studies are needed to further clarify the risk associated with these genetic polymorphisms and to develop effective thera- peutic strategies for carriers of allelic variants of responsible enzyme systems. 