ORCID Profile
0000-0002-5559-8172
Current Organisation
Brigham and Women's Hospital
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Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 26-07-2016
DOI: 10.1161/CIRCULATIONAHA.115.019861
Abstract: Patients with stable ischemic heart disease and previous myocardial infarction (MI) vary in their risk for recurrent cardiovascular events. Atherothrombotic risk assessment may be useful to identify high-risk patients who have the greatest potential to benefit from more intensive secondary preventive therapy such as treatment with vorapaxar. We identified independent clinical indicators of atherothrombotic risk among 8598 stable, placebo-treated patients with a previous MI followed up for 2.5 years (median) in TRA 2°P-TIMI 50 [Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events–TIMI 50]. The efficacy and safety of vorapaxar (SCH 530348 MK-5348) were assessed by baseline risk among patients with previous MI without prior stroke or transient ischemic attack for whom there is a clinical indication for vorapaxar. End points were cardiovascular death, MI, or ischemic stroke and GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) severe bleeding. The 9 independent risk predictors were age, diabetes mellitus, hypertension, smoking, peripheral arterial disease, previous stroke, previous coronary bypass grafting, heart failure, and renal dysfunction. A simple integer-based scheme using these predictors showed a strong graded relationship with the rate of cardiovascular death/MI/ischemic stroke and the in idual components ( P for trend .001 for all). High-risk patients (≥3 risk indicators 20% of population) had a 3.2% absolute risk reduction in cardiovascular disease/MI/ischemic stroke with vorapaxar, and intermediate-risk patients (1–2 risk indicators 61%) had a 2.1% absolute risk reduction ( P .001 each), translating to a number needed to treat of 31 and 48. Bleeding increased across risk groups ( P for trend .01) however, net clinical outcome was increasingly favorable with vorapaxar across risk groups. Fatal bleeding or intracranial hemorrhage was 0.9% with both treatments in high-risk patients. Stratification of baseline atherothrombotic risk can assist with therapeutic decision making for vorapaxar use for secondary prevention after MI. URL: www.clinicaltrials.gov . Unique identifier: NCT00526474.
Publisher: Elsevier BV
Date: 11-2018
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 17-11-2015
DOI: 10.1161/CIRCULATIONAHA.114.015042
Abstract: Vorapaxar antagonizes protease-activated receptor 1, the primary receptor for thrombin on human platelets, and reduces recurrent thrombotic events in stable patients with a previous myocardial infarction (MI). We wished to determine whether the efficacy and safety of antiplatelet therapy with vorapaxar was modified by concurrent thienopyridine use. The Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events–Thrombolysis in Myocardial Infarction 50 (TRA 2°P-TIMI 50) was a randomized, double-blind, placebo-controlled trial of vorapaxar in 26 449 patients with previous atherothrombosis. This prespecified analysis included 16 897 patients who qualified with a MI in the preceding 2 weeks to 12 months and was restricted to patients without a history of stroke or transient ischemic attack given its contraindication in that population. Randomization was stratified on the basis of planned thienopyridine use. Thienopyridine was planned at randomization in 12 410 (73%). Vorapaxar significantly reduced the composite of cardiovascular death, MI, and stroke in comparison with placebo regardless of planned thienopyridine therapy (planned thienopyridine, hazard ratio, 0.80, 0.70–0.91, P .001 no planned thienopyridine, hazard ratio, 0.75 0.60–0.94, P =0.011 P -interaction=0.67). Findings were similar when patients were stratified by actual thienopyridine use at baseline ( P -interaction=0.82) and through 18 months ( P -interaction=0.44). Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) moderate or severe bleeding risk was increased with vorapaxar and was not significantly altered by planned thienopyridine (planned, hazard ratio, 1.50 1.18–1.89, P .001 no planned, hazard ratio, 1.90, 1.17–3.07, P =0.009 P -interaction=0.37) or actual thienopyridine use ( P -interaction=0.24). Vorapaxar reduced cardiovascular death, MI, or stroke in stable patients with a history of previous MI, whether treated concomitantly with a thienopyridine or not. The relative risk of moderate or severe bleeding was similarly increased irrespective of thienopyridine use. URL: www.clinicaltrials.gov . Unique identifier: NCT00526474.
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Erin Bohula May.