Vorapaxar in the Secondary Prevention of Atherothrombotic Events

the TRA 2P–TIMI 50 Steering Committee and Investigators, David A Morrow, Eugene Braunwald, Marc P Bonaca, Sebastian F Ameriso, Anthony J Dalby, Mary Polly Fish, Keith A A Fox, Leslie J Lipka, Xuan Liu, José Carlos Nicolau, A J Oude Ophuis, Ernesto Paolasso, Benjamin M Scirica, Jindrich Spinar, Pierre Theroux, Stephen D Wiviott, John Strony, Sabina A Murphy

Research output: Contribution to journalArticlepeer-review


Background Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. Methods We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. Results At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P
Original languageEnglish
Pages (from-to)1404-1413
JournalNew England Journal of Medicine
Issue number15
Publication statusPublished - Apr 2012


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