Patients taking any thienopyridine within 5 days of randomization were excluded. Prasugrel was associated with a significant 2.2% abso- lute reduction and a 19% relative reduction in the primary efficacy endpoint, a composite of the rate of death due to cardiovascular causes (including arrhythmia, congestive heart failure, shock, and sudden or unwitnessed death), nonfatal myocardial infarction (MI), or nonfatal stroke during the follow-up period (see Online Data Supplement). The primary efficacy endpoint occurred in 9.9% of patients receiving prasugrel and 12.1% of patients receiving clopi- dogrel (HR for prasugrel versus clopidogrel: 0.81; 95% CI: lar death, MI, and stroke by 138 events (number needed to treat 46). The difference in the primary endpoint was largely related to the difference in rates of nonfatal MI (7.3% for prasugrel versus 9.5% for clopidogrel; HR: 0.76; death (2.1% versus 2.4%; P 0.31) and nonfatal stroke (1.0% versus 1.0%; P 0.93) were not reduced by prasu- grel relative to clopidogrel. Rates of stent thrombosis were significantly reduced from 2.4% to 1.1% (P 0.001) by prasugrel. Prasugrel was associated with a significant increase in the rate of bleeding, notably TIMI (Thrombolysis In Myocardial Infarction) major hemorrhage, which was ob- served in 2.4% of patients taking prasugrel and in 1.8% of patients taking clopidogrel (HR for prasugrel versus clopi- was associated with a significant increase in fatal bleeding compared with clopidogrel (0.4% versus 0.1%; P 0.002). 