Thrombin-receptor antagonist vorapaxar in acute coronary syndromes
Author
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Tricoci, Pierluigi
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Huang, Zhen
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Held, Claes
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Moliterno, David J.
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Armstrong, Paul W.
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Van De Werf, Frans
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White, Harvey D.
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Aylward, Philip E.
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Wallentin, Lars
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Chen, Edmond
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Lokhnygina, Yuliya
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Pei, Jinglan
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Leonardi, Sergio
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Rorick, Tyrus L.
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Kilian, Ann M.
Author
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Jennings
Admission date
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2019-03-11T13:03:00Z
Available date
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2019-03-11T13:03:00Z
Publication date
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2012
Cita de ítem
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New England Journal of Medicine, Volumen 366, Issue 1, 2018, Pages 20-33
Identifier
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15334406
Identifier
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00284793
Identifier
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10.1056/NEJMoa1109719
Identifier
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https://repositorio.uchile.cl/handle/2250/165428
Abstract
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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 patient