TY - JOUR
T1 - Vorapaxar in the Secondary Prevention of Atherothrombotic Events
AU - the TRA 2P–TIMI 50 Steering Committee and Investigators
AU - Morrow, David A
AU - Braunwald, Eugene
AU - Bonaca, Marc P
AU - Ameriso, Sebastian F
AU - Dalby, Anthony J
AU - Fish, Mary Polly
AU - Fox, Keith A A
AU - Lipka, Leslie J
AU - Liu, Xuan
AU - Nicolau, José Carlos
AU - Oude Ophuis, A J
AU - Paolasso, Ernesto
AU - Scirica, Benjamin M
AU - Spinar, Jindrich
AU - Theroux, Pierre
AU - Wiviott, Stephen D
AU - Strony, John
AU - Murphy, Sabina A
PY - 2012/4
Y1 - 2012/4
N2 - 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
AB - 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
UR - http://www.scopus.com/inward/record.url?scp=84859555815&partnerID=8YFLogxK
U2 - 10.1056/NEJMoa1200933
DO - 10.1056/NEJMoa1200933
M3 - Article
C2 - 22443427
SN - 1533-4406
VL - 366
SP - 1404
EP - 1413
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 15
ER -