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 language | English |
|---|---|
| Pages (from-to) | 1317-1324 |
| Number of pages | 8 |
| Journal | Lancet |
| Volume | 380 |
| Issue number | 9850 |
| DOIs | |
| Publication status | Published - Oct 2012 |
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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 journal › Article
}
TY - JOUR
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.
PY - 2012/10
Y1 - 2012/10
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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U2 - 10.1016/S0140-6736(12)61269-0
DO - 10.1016/S0140-6736(12)61269-0
M3 - Article
C2 - 22932716
AN - SCOPUS:84867336413
VL - 380
SP - 1317
EP - 1324
JO - The Lancet
JF - The Lancet
SN - 0140-6736
IS - 9850
ER -