| Contributors: |
Tricoci, P; Huang, Z; Held, C; Moliterno, Dj; Armstrong, Pw; Van de Werf, F; White, Hd; Aylward, Pe; Wallentin, L; Chen, E; Lokhnygina, Y; Pei, J; Leonardi, S; Rorick, Tl; Kilian, Am; Jennings, Lh; Ambrosio, G; Bode, C; Cequier, A; Cornel, Jh; Diaz, R; Erkan, A; Huber, K; Hudson, Mp; Jiang, L; Jukema, Jw; Lewis, B; Lincoff, Am; Montalescot, G; Nicolau, Jc; Ogawa, H; Pfisterer, M; Prieto, Jc; Ruzyllo, W; Sinnaeve, Pr; Storey, Rf; Valgimigli, M; Whellan, Dj; Widimsky, P; Strony, J; Harrington, Ra; Mahaffey, Kw; Huo, Y; Lixin, J; Isaza, D; Grande, P; Laine, M; Wong, L; Ofner, P; Yamaguchi, T; Park, Sj; Nordrehaug, Je; Providencia, L; Cheem, Th; Dalby, A; Betriu, A; Chen, Mf; Verheugt, F |
| Description: |
BACKGROUND Vorapaxar is a new oral protease-activated–receptor 1 (PAR-1) antagonist that inhibits thrombin-induced platelet activation. METHODS In this multinational, double-blind, randomized trial, we compared vorapaxar with placebo in 12,944 patients who had acute coronary syndromes without ST-segment elevation. The primary end point was a composite of death from cardiovascular causes, myocardial infarction, stroke, recurrent ischemia with rehospitalization, or urgent coronary revascularization. RESULTS Follow-up in the trial was terminated early after a safety review. After a median follow-up of 502 days (interquartile range, 349 to 667), the primary end point occurred in 1031 of 6473 patients receiving vorapaxar versus 1102 of 6471 patients receiving placebo (Kaplan–Meier 2-year rate, 18.5% vs. 19.9%; hazard ratio, 0.92; 95% confidence interval [CI], 0.85 to 1.01; P = 0.07). A composite of death from cardiovascular causes, myocardial infarction, or stroke occurred in 822 patients in the vorapaxar group versus 910 in the placebo group (14.7% and 16.4%, respectively; hazard ratio, 0.89; 95% CI, 0.81 to 0.98; P = 0.02). Rates of moderate and severe bleeding were 7.2% in the vorapaxar group and 5.2% in the placebo group (hazard ratio, 1.35; 95% CI, 1.16 to 1.58; P |