A Thin Slice of Pie: Vorapaxar for Secondary Prevention After Myocardial Infarction

Vorapaxar inhibits platelet activation by blocking protease-activated receptor 1, the main thrombin receptor. The TRA 2P–TIMI 50 study demonstrated that, in 26,449 patients with prior myocardial infarction (MI), ischemic stroke, or peripheral arterial disease, vorapaxar significantly decreased the risk for cardiovascular death, MI, or stroke by 13% and increased the risk for moderate or severe bleeding by 66%, with a doubling in the rate of intracerebral hemorrhage (JW Cardiol Mar 25 2012). Almost all patients were also receiving aspirin and a lipid-lowering agent, and most were receiving a thienopyridine.

Now, the TRA 2P–TIMI 50 investigators present the results of a prespecified analysis of the subgroup of 17,779 patients with prior MI. During a median follow-up of 2.5 years, the composite endpoint occurred in 8.1% of the vorapaxar group and 9.7% of the placebo group (hazard ratio, 0.80; 95% confidence interval, 0.72–0.89; P<0.001). The risk for moderate or severe bleeding was increased with vorapaxar by 61% (3.4% vs. 2.1%; 95% CI, 1.31–1.97; P<0.001). Intracerebral hemorrhage was more common in the vorapaxar group (0.6% vs. 0.4%; HR, 1.54; 95% CI, 0.96–2.48; P=0.076).