TY - JOUR
T1 - Peripheral Revascularization in Patients With Peripheral Artery Disease With Vorapaxar
T2 - Insights From the TRA 2°P–TIMI 50 Trial
AU - Bonaca, Marc P.
AU - Creager, Mark A.
AU - Olin, Jeffrey
AU - Scirica, Benjamin M.
AU - Gilchrist, Ian C.
AU - Murphy, Sabina A.
AU - Goodrich, Erica L.
AU - Braunwald, Eugene
AU - Morrow, David A.
N1 - Funding Information:
The TRA 2°P–TIMI 50 trial was supported by a grant from Merck to Brigham and Women's Hospital. Dr. Bonaca was supported by a Research Career Development Award (K12 HL083786) from the National Heart, Lung, and Blood Institute. The TIMI Study Group has received significant research grant support from Accumetrics, Amgen, AstraZeneca, Beckman Coulter, Bristol-Myers Squibb, CV Therapeutics, Daiichi-Sankyo, Eli Lilly, GlaxoSmithKline, Integrated Therapeutics, Merck, Nanosphere, Novartis Pharmaceuticals, Nuvelo, Ortho-Clinical Diagnostics, Pfizer, Roche Diagnostics, Sanofi, Sanofi-Synthelabo, Siemens Medical Solutions, and Singulex. Dr. Bonaca has received consulting fees from Merck, AstraZeneca, and Bayer. Dr. Olin is on the medical advisory board and Steering Committee TRA-2P for Merck and is also on the medical advisory board and the International Steering Committee EUCLID Trial for AstraZeneca. Dr. Scirica received research grants from Merck, AstraZeneca, Daiichi-Sankyo, Gilead, Eisai, Poxel, Biogen Idec, Boehringer Ingelheim, Dr. Reddy's Laboratory, Forest Pharmaceuticals, GlaxoSmithKline, Lexicon, and St. Jude Medical; and received consulting fees from AstraZeneca and Merck. Ms. Murphy has received consulting fees from Eli Lilly and Amarin Pharmaceuticals and has received speaking fees from Merck. Dr. Braunwald received research grant support from Merck. Dr. Morrow has received consulting fees from Beckman-Coulter, Boehringer Ingelheim, Critical Diagnostics, Genentech, Gilead, Instrumentation Laboratory, Merck, Roche Diagnostics, AstraZeneca, GlaxoSmithKline, Novartis, and Servier; and has also received research grant support from Merck, Amgen, AstraZeneca, Daiichi-Sankyo, Eisai, GlaxoSmithKline, and Novartis. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Publisher Copyright:
© 2016 American College of Cardiology Foundation
PY - 2016/10/24
Y1 - 2016/10/24
N2 - Objectives The aim of this study was to determine whether the reduction in peripheral revascularization with vorapaxar in patients with peripheral artery disease (PAD) is directionally consistent across indications, including acute limb ischemia, progressively disabling symptoms, or both. Background The protease-activated receptor–1 antagonist vorapaxar reduces peripheral revascularization in patients with PAD. Methods The TRA 2°P–TIMI 50 (Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events–Thrombolysis in Myocardial Infarction 50) trial randomized 26,449 patients with histories of myocardial infarction, stroke, or symptomatic PAD to vorapaxar or placebo on a background of standard therapy. A total of 5,845 patients had a known history of PAD at randomization. Peripheral revascularization procedures reported by the site were a pre-specified outcome. We explored whether the benefit of vorapaxar was consistent across indication and type of procedure. Results Of the 5,845 patients with known PAD, a total of 934 (16%) underwent at least 1 peripheral revascularization over 2.5 years (median). More than one-half (55%) were for worsening claudication, followed by critical limb ischemia (24%), acute limb ischemia (16%), and asymptomatic severe stenosis (4%). Vorapaxar significantly reduced peripheral revascularization (19.3% for placebo, 15.4% for vorapaxar; hazard ratio: 0.82; 95% confidence interval: 0.72 to 0.93; p = 0.003), with a consistent pattern of efficacy across indication. Conclusions Vorapaxar reduces peripheral revascularization in patients with PAD. This benefit of vorapaxar is directionally consistent across type of procedure and indication. (Trial to Assess the Effects of Vorapaxar [SCH 530348; MK-5348] in Preventing Heart Attack and Stroke in Patients With Atherosclerosis [TRA 2°P - TIMI 50] [P04737]; NCT00526474)
AB - Objectives The aim of this study was to determine whether the reduction in peripheral revascularization with vorapaxar in patients with peripheral artery disease (PAD) is directionally consistent across indications, including acute limb ischemia, progressively disabling symptoms, or both. Background The protease-activated receptor–1 antagonist vorapaxar reduces peripheral revascularization in patients with PAD. Methods The TRA 2°P–TIMI 50 (Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events–Thrombolysis in Myocardial Infarction 50) trial randomized 26,449 patients with histories of myocardial infarction, stroke, or symptomatic PAD to vorapaxar or placebo on a background of standard therapy. A total of 5,845 patients had a known history of PAD at randomization. Peripheral revascularization procedures reported by the site were a pre-specified outcome. We explored whether the benefit of vorapaxar was consistent across indication and type of procedure. Results Of the 5,845 patients with known PAD, a total of 934 (16%) underwent at least 1 peripheral revascularization over 2.5 years (median). More than one-half (55%) were for worsening claudication, followed by critical limb ischemia (24%), acute limb ischemia (16%), and asymptomatic severe stenosis (4%). Vorapaxar significantly reduced peripheral revascularization (19.3% for placebo, 15.4% for vorapaxar; hazard ratio: 0.82; 95% confidence interval: 0.72 to 0.93; p = 0.003), with a consistent pattern of efficacy across indication. Conclusions Vorapaxar reduces peripheral revascularization in patients with PAD. This benefit of vorapaxar is directionally consistent across type of procedure and indication. (Trial to Assess the Effects of Vorapaxar [SCH 530348; MK-5348] in Preventing Heart Attack and Stroke in Patients With Atherosclerosis [TRA 2°P - TIMI 50] [P04737]; NCT00526474)
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U2 - 10.1016/j.jcin.2016.07.034
DO - 10.1016/j.jcin.2016.07.034
M3 - Article
C2 - 27765312
AN - SCOPUS:84994013957
VL - 9
SP - 2157
EP - 2164
JO - JACC: Cardiovascular Interventions
JF - JACC: Cardiovascular Interventions
SN - 1936-8798
IS - 20
ER -