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@article{980953,
author = {Morrow, D.A. and Braunwald, Eugene and Bonaca, M.P. and Ameriso, S.F. and Dalby, A.J. and Fish, M.P. and Fox, K.A.A. and Lipka, L.J. and Liu, Xian and Nicolau, J.C. and Ophuis, Oude and Paolasso, E. and Scirica, B.M. and Špinar, Jindřich and Theroux, T. and Wiviott, S.D. and Strony, J. and Murphy, S.A.},
article_number = {15},
doi = {http://dx.doi.org/10.1056/nejmoa1200933},
keywords = {ACUTE CORONARY SYNDROMES; PROTEASE-ACTIVATED RECEPTORS; ANTITHROMBOTIC AGENTS; DOUBLE-BLIND; CLOPIDOGREL; SAFETY; TRIAL; ASPIRIN; STROKE; TOLERABILITY},
language = {eng},
issn = {0028-4793},
journal = {New England Journal of Medicine},
title = {Vorapaxar in the Secondary Prevention of Atherothrombotic Events},
volume = {366},
year = {2012}
}
TY - JOUR
ID - 980953
AU - Morrow, D.A. - Braunwald, Eugene - Bonaca, M.P. - Ameriso, S.F. - Dalby, A.J. - Fish, M.P. - Fox, K.A.A. - Lipka, L.J. - Liu, Xian - Nicolau, J.C. - Ophuis, Oude - Paolasso, E. - Scirica, B.M. - Špinar, Jindřich - Theroux, T. - Wiviott, S.D. - Strony, J. - Murphy, S.A.
PY - 2012
TI - Vorapaxar in the Secondary Prevention of Atherothrombotic Events
JF - New England Journal of Medicine
VL - 366
IS - 15
SP - 1404-1413
EP - 1404-1413
SN - 00284793
KW - ACUTE CORONARY SYNDROMES
KW - PROTEASE-ACTIVATED RECEPTORS
KW - ANTITHROMBOTIC AGENTS
KW - DOUBLE-BLIND
KW - CLOPIDOGREL
KW - SAFETY
KW - TRIAL
KW - ASPIRIN
KW - STROKE
KW - TOLERABILITY
N2 - 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<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P = 0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). Conclusions Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage.
ER -
MORROW, D.A., Eugene BRAUNWALD, M.P. BONACA, S.F. AMERISO, A.J. DALBY, M.P. FISH, K.A.A. FOX, L.J. LIPKA, Xian LIU, J.C. NICOLAU, Oude OPHUIS, E. PAOLASSO, B.M. SCIRICA, Jindřich ŠPINAR, T. THEROUX, S.D. WIVIOTT, J. STRONY and S.A. MURPHY. Vorapaxar in the Secondary Prevention of Atherothrombotic Events. \textit{New England Journal of Medicine}. 2012, vol.~366, No~15, p.~1404-1413. ISSN~0028-4793. Available from: https://dx.doi.org/10.1056/nejmoa1200933.
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