Journal
EUROPEAN HEART JOURNAL
Volume 34, Issue 23, Pages 1723-1731Publisher
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/eht104
Keywords
Myocardial infarction; Trials; Thrombosis
Categories
Funding
- Merck Co., Inc.
- Sanofi-Aventis
- Eli Lilly
- The Medicines Company
- National Institutes of Health
- Pfizer
- Roche
- Johnson Johnson
- Merck Sharpe Dohme
- AstraZeneca
- GlaxoSmithKline
- Daiichi Sankyo Pharma Development
- Bristol-Myers Squibb
- Merck Sharp Dohme Corp
- Boehringer Ingelheim
- Sanofi-Aventis Canada
- Regado Biosciences
- Amylin
- Novartis
- Schering-Plough
- Bayer/Johnson Johnson
- Merck
- Portola
- Bayer
- Pozen
- Regado
- Daiichi Sankyo
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Aims The TRA.CER trial compared vorapaxar, a novel platelet protease-activated receptor (PAR)-1 antagonist, with placebo in 12 944 patients with high-risk non-ST-segment elevation acute coronary syndromes (NSTE ACS). In this analysis, we explored the effect of vorapaxar on myocardial infarction (MI). Methods and results A blinded, independent central endpoint adjudication committee prospectively defined and classified MI according to the universal MI definition, including peak cardiac marker value (creatine kinase-MB [CK-MB] and/or troponin). Because the trial failed to meet its primary endpoint, these analyses are considered exploratory. During a median follow-up of 502 days, 1580 MIs occurred in 1319 patients. The majority (n = 1025, 64.9) were type 1 (spontaneous) MI, followed by type 4a [percutaneous coronary intervention (PCI)-related] MI (n = 352; 22.3). Compared with placebo, vorapaxar reduced the hazard of a first MI of any type by 12 [hazard ratio (HR), 0.88; 95 confidence interval (CI), 0.79-0.98; P = 0.021] and the hazard of total number of MIs (first and subsequent) by 14 (HR, 0.86; 95 CI, 0.77-0.97; P = 0.014), an effect that was sustained over time. Vorapaxar reduced type 1 MI by 17 (HR, 0.83; 95 CI, 0.73-0.95; P = 0.007). Type 4a MIs were not significantly reduced by vorapaxar (HR, 0.90; 95 CI, 0.73-1.12; P = 0.35). Vorapaxar effect was consistent across MI sizes defined by peak cardiac marker elevations and across key clinical subgroups; however, in patients not treated with thienopyridine at baseline (HR, 0.65; 95 CI, 0.46-0.92) compared with patients who received thienopyridine (HR, 0.91; 95 CI, 0.81-1.02), there was a trend towards a higher effect (P-int = 0.077). Conclusion The PAR-1 antagonist vorapaxar was associated with a reduction of MI, including total number of infarctions. This reduction was sustained over time and was mostly evident in type 1 MI, the most common type of MI observed.
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