Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction: A prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial

Benjamin M. Scirica, Marc P. Bonaca, Eugene Braunwald, Gaetano M. De Ferrari, Daniel Isaza, Basil S. Lewis, Felix Mehrhof, Piera A. Merlini, Sabina A. Murphy, Marc S. Sabatine, Michal Tendera, Frans Van De Werf, Robert Wilcox, David A. Morrow

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Abstract

Background Vorapaxar inhibits platelet activation by antagonising thrombin-mediated activation of the proteaseactivated receptor 1 on human platelets. The effect of adding other antiplatelet drugs to aspirin for long-term secondary prevention of thrombotic events in stable patients with previous myocardial infarction is uncertain. We tested this effect in a subgroup of patients from the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-TIMI 50 trial. Methods In TRA 2°P-TIMI 50 - a randomised, placebo-controlled, parallel trial - we randomly assigned patients with a history of atherothrombosis to receive vorapaxar (2 5 mg daily) or matching placebo in a 1:1 ratio. Patients, and those giving treatment, assessing outcomes, and analysing results were masked to treatment allocation. Patients with a qualifying myocardial infarction within the previous 2 weeks to 12 months were analysed as a pre-defined subgroup. The primary efficacy endpoint was cardiovascular death, myocardial infarction, or stroke, analysed by intention to treat. We analysed events by Kaplan-Meier analysis and compared groups with a Cox proportional hazard model. TRA 2°P-TIMI 50 is registered at ClinicalTrials.gov (NCT00526474). Findings 17 779 of 26 449 patients had a qualifying myocardial infarction and were assigned treatment (8898 to vorapaxar and 8881 to placebo). Median follow-up was 2 5 years (IQR 2 0-2 9). Cardiovascular death, myocardial infarction, or stroke occurred in 610 of 8898 patients in the vorapaxar group and 750 of 8881 in the placebo group ( 3-year Kaplan-Meier estimates 8 1% vs 9 7%, HR 0 80, 95% CI 0 72-0 89; p

Original languageEnglish
Pages (from-to)1317-1324
Number of pages8
JournalLancet
Volume380
Issue number9850
DOIs
Publication statusPublished - Oct 2012

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Secondary Prevention
Myocardial Infarction
Placebos
Kaplan-Meier Estimate
Stroke
Thrombin Receptors
Platelet Aggregation Inhibitors
Platelet Activation
vorapaxar
Proportional Hazards Models
Thrombin
Aspirin
Blood Platelets
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

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Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction : A prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial. / Scirica, Benjamin M.; Bonaca, Marc P.; Braunwald, Eugene; De Ferrari, Gaetano M.; Isaza, Daniel; Lewis, Basil S.; Mehrhof, Felix; Merlini, Piera A.; Murphy, Sabina A.; Sabatine, Marc S.; Tendera, Michal; Van De Werf, Frans; Wilcox, Robert; Morrow, David A.

In: Lancet, Vol. 380, No. 9850, 10.2012, p. 1317-1324.

Research output: Contribution to journalArticle

Scirica, BM, Bonaca, MP, Braunwald, E, De Ferrari, GM, Isaza, D, Lewis, BS, Mehrhof, F, Merlini, PA, Murphy, SA, Sabatine, MS, Tendera, M, Van De Werf, F, Wilcox, R & Morrow, DA 2012, 'Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction: A prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial', Lancet, vol. 380, no. 9850, pp. 1317-1324. https://doi.org/10.1016/S0140-6736(12)61269-0
Scirica, Benjamin M. ; Bonaca, Marc P. ; Braunwald, Eugene ; De Ferrari, Gaetano M. ; Isaza, Daniel ; Lewis, Basil S. ; Mehrhof, Felix ; Merlini, Piera A. ; Murphy, Sabina A. ; Sabatine, Marc S. ; Tendera, Michal ; Van De Werf, Frans ; Wilcox, Robert ; Morrow, David A. / Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction : A prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial. In: Lancet. 2012 ; Vol. 380, No. 9850. pp. 1317-1324.
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abstract = "Background Vorapaxar inhibits platelet activation by antagonising thrombin-mediated activation of the proteaseactivated receptor 1 on human platelets. The effect of adding other antiplatelet drugs to aspirin for long-term secondary prevention of thrombotic events in stable patients with previous myocardial infarction is uncertain. We tested this effect in a subgroup of patients from the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-TIMI 50 trial. Methods In TRA 2°P-TIMI 50 - a randomised, placebo-controlled, parallel trial - we randomly assigned patients with a history of atherothrombosis to receive vorapaxar (2 5 mg daily) or matching placebo in a 1:1 ratio. Patients, and those giving treatment, assessing outcomes, and analysing results were masked to treatment allocation. Patients with a qualifying myocardial infarction within the previous 2 weeks to 12 months were analysed as a pre-defined subgroup. The primary efficacy endpoint was cardiovascular death, myocardial infarction, or stroke, analysed by intention to treat. We analysed events by Kaplan-Meier analysis and compared groups with a Cox proportional hazard model. TRA 2°P-TIMI 50 is registered at ClinicalTrials.gov (NCT00526474). Findings 17 779 of 26 449 patients had a qualifying myocardial infarction and were assigned treatment (8898 to vorapaxar and 8881 to placebo). Median follow-up was 2 5 years (IQR 2 0-2 9). Cardiovascular death, myocardial infarction, or stroke occurred in 610 of 8898 patients in the vorapaxar group and 750 of 8881 in the placebo group ( 3-year Kaplan-Meier estimates 8 1{\%} vs 9 7{\%}, HR 0 80, 95{\%} CI 0 72-0 89; p",
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T1 - Vorapaxar for secondary prevention of thrombotic events for patients with previous myocardial infarction

T2 - A prespecified subgroup analysis of the TRA 2°P-TIMI 50 trial

AU - Scirica, Benjamin M.

AU - Bonaca, Marc P.

AU - Braunwald, Eugene

AU - De Ferrari, Gaetano M.

AU - Isaza, Daniel

AU - Lewis, Basil S.

AU - Mehrhof, Felix

AU - Merlini, Piera A.

AU - Murphy, Sabina A.

AU - Sabatine, Marc S.

AU - Tendera, Michal

AU - Van De Werf, Frans

AU - Wilcox, Robert

AU - Morrow, David A.

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N2 - Background Vorapaxar inhibits platelet activation by antagonising thrombin-mediated activation of the proteaseactivated receptor 1 on human platelets. The effect of adding other antiplatelet drugs to aspirin for long-term secondary prevention of thrombotic events in stable patients with previous myocardial infarction is uncertain. We tested this effect in a subgroup of patients from the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-TIMI 50 trial. Methods In TRA 2°P-TIMI 50 - a randomised, placebo-controlled, parallel trial - we randomly assigned patients with a history of atherothrombosis to receive vorapaxar (2 5 mg daily) or matching placebo in a 1:1 ratio. Patients, and those giving treatment, assessing outcomes, and analysing results were masked to treatment allocation. Patients with a qualifying myocardial infarction within the previous 2 weeks to 12 months were analysed as a pre-defined subgroup. The primary efficacy endpoint was cardiovascular death, myocardial infarction, or stroke, analysed by intention to treat. We analysed events by Kaplan-Meier analysis and compared groups with a Cox proportional hazard model. TRA 2°P-TIMI 50 is registered at ClinicalTrials.gov (NCT00526474). Findings 17 779 of 26 449 patients had a qualifying myocardial infarction and were assigned treatment (8898 to vorapaxar and 8881 to placebo). Median follow-up was 2 5 years (IQR 2 0-2 9). Cardiovascular death, myocardial infarction, or stroke occurred in 610 of 8898 patients in the vorapaxar group and 750 of 8881 in the placebo group ( 3-year Kaplan-Meier estimates 8 1% vs 9 7%, HR 0 80, 95% CI 0 72-0 89; p

AB - Background Vorapaxar inhibits platelet activation by antagonising thrombin-mediated activation of the proteaseactivated receptor 1 on human platelets. The effect of adding other antiplatelet drugs to aspirin for long-term secondary prevention of thrombotic events in stable patients with previous myocardial infarction is uncertain. We tested this effect in a subgroup of patients from the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-TIMI 50 trial. Methods In TRA 2°P-TIMI 50 - a randomised, placebo-controlled, parallel trial - we randomly assigned patients with a history of atherothrombosis to receive vorapaxar (2 5 mg daily) or matching placebo in a 1:1 ratio. Patients, and those giving treatment, assessing outcomes, and analysing results were masked to treatment allocation. Patients with a qualifying myocardial infarction within the previous 2 weeks to 12 months were analysed as a pre-defined subgroup. The primary efficacy endpoint was cardiovascular death, myocardial infarction, or stroke, analysed by intention to treat. We analysed events by Kaplan-Meier analysis and compared groups with a Cox proportional hazard model. TRA 2°P-TIMI 50 is registered at ClinicalTrials.gov (NCT00526474). Findings 17 779 of 26 449 patients had a qualifying myocardial infarction and were assigned treatment (8898 to vorapaxar and 8881 to placebo). Median follow-up was 2 5 years (IQR 2 0-2 9). Cardiovascular death, myocardial infarction, or stroke occurred in 610 of 8898 patients in the vorapaxar group and 750 of 8881 in the placebo group ( 3-year Kaplan-Meier estimates 8 1% vs 9 7%, HR 0 80, 95% CI 0 72-0 89; p

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