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Am J Cardiol. 2014 Mar 15;113(6):936-44. doi: 10.1016/j.amjcard.2013.11.052. Epub 2013 Dec 25.

Association of aspirin dose and vorapaxar safety and efficacy in patients with non-ST-segment elevation acute coronary syndrome (from the TRACER Trial).

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Department of Medicine, Stanford University, Stanford, California. Electronic address:
Duke Clinical Research Institute, Durham, North Carolina.
Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala, Sweden.
Department of Cardiovascular Science, University of Sheffield, Sheffield, United Kingdom.
University of Tennessee Health Science Center, Memphis, Tennessee; CirQuest Labs, LLC, Memphis, Tennessee.
Green Lane Cardiovascular Service, Auckland City Hospital, Auckland, New Zealand.
Division of Cardiology, University of Alberta, Edmonton, Alberta, Canada.
South Australian Health and Medical Research Institute, Flinders University and Medical Centre, Adelaide, South Australia, Australia.
Gill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington, Kentucky.
Department of Cardiology, University of Leuven, Leuven, Belgium.
Global Clinical Development, Bayer HealthCare Pharmaceuticals Inc., Whippany, New Jersey.
Duke Clinical Research Institute, Durham, North Carolina; Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Merck, Whitehouse Station, New Jersey.
Department of Medicine, Stanford University, Stanford, California.


Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRACER) trial compared vorapaxar and placebo in 12,944 high-risk patients with non-ST-segment elevation acute coronary syndrome. We explored aspirin (ASA) use and its association with outcomes. Kaplan-Meier event rates were compared in groups defined by ASA dose (low, medium, and high). Landmark analyses with covariate adjustment were performed for 0 to 30, 31 to 180, and 181 to 365 days. Of 12,515 participants, 7,523, 1,049, and 3,943 participants were treated with low-, medium-, and high-dose ASA at baseline, respectively. Participants enrolled in North America versus elsewhere were more often treated with a high dose at baseline (66% vs 19%) and discharge (60% vs 3%). Unadjusted cardiovascular death, myocardial infarction, stroke, hospitalization for ischemia, or urgent revascularization event rates tended to be higher with higher baseline ASA (18.45% low, 19.13% medium, and 20.27% high; p for trend = 0.15573). Unadjusted and adjusted hazard ratios (95% confidence intervals) for effect of vorapaxar on cardiovascular (unadjusted p for interaction = 0.065; adjusted p for interaction = 0.140) and bleeding (unadjusted p for interaction = 0.915; adjusted p for interaction = 0.954) outcomes were similar across groups. Landmark analyses showed similar safety and efficacy outcomes with vorapaxar and placebo by ASA dose at each time point except for 0 to 30 days, when vorapaxar tended to be worse for efficacy (hazard ratio 1.13, 95% confidence interval 0.89 to 1.44, p for interaction = 0.0157). In conclusion, most TRACER participants were treated with low-dose ASA, although a high dose was common in North America. High-dose participants tended to have higher rates of ischemic and bleeding outcomes. Although formal statistical testing did not reveal heterogeneity in vorapaxar's effect across dose subgroups, consistent trends support use of low-dose ASA with other antiplatelet therapies.

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