Efficacy and Safety of Vorapaxar With and Without a Thienopyridine for Secondary Prevention in Patients With Previous Myocardial Infarction and No History of Stroke or Transient Ischemic Attack: Results from TRA 2°P-TIMI 50.

BACKGROUND: 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. METHODS AND RESULTS: 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<0.001; 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<0.001; 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). CONCLUSIONS: 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. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00526474.

[Predictors of acute coronary syndrome without ST segment elevation and risk stratification in the chest pain unit]. / Predictores de síndrome coronario agudo sin supradesnivel del ST y estratificación de riesgo en la unidad de dolor torácico. Experiencia en 1.168 pacientes.

BACKGROUND: Nearly 10% of patients with an actual acute coronary syndrome (ACS) are discharged with an inadequate diagnosis. AIM: To select clinical and laboratory predictors to identify patients with a high likelihood of ACS in the Chest Pain Unit. MATERIAL AND METHODS: Prospective evaluation of patients consulting in a Chest Pain Unit of a University Hospital. Initial assessment was standardized and included evaluation of pain characteristics, electrocardiogram and Troponin I. Independent predictors of ACS were identified with a multiple logistic regression. RESULTS: In a four years period, 1,168 patients aged 62+/-23 years (69% males), were studied. After initial evaluation, 62% of the patients were admitted to the hospital for further testing and in 71% of them, a definite diagnosis of ACS was made. No events were reported by patients directly discharged from the Chest Pain Unit. Independent predictors associated with a higher likelihood of ACS were an abnormal electrocardiogram at the initial evaluation (Odds ratio (OR) 5.37, 95% confidence intervals (CI) 3.61-7.99), two or more cardiovascular risk factors (OR 2.16, 95% CI 1.21-2.84), cervical irradiation of the pain (OR 1.84, 95% CI 1.25-2.69), age over 65 years (OR 1.73, 95% CI (1.32-2.27) and a Troponin I above the upper normal limit (OR: 5.68, 95% CI 3.72-8.29). CONCLUSIONS: Simple clinical findings allow an appropriate identification of patients with a high likelihood of ACS without specialized methods for myocardial ischemia detection.

Predictores de síndrome coronario agudo sin supradesnivel del ST y estratificación de riesgo en la unidad de dolor torácico. Experiencia en 1.168 pacientes / Predictors of acute coronary syndrome without ST segment elevation and risk stratification in the chest pain unit

Background: Nearly 10 percent of patients with an actual acute coronary syndrome (ACS) are discharged with an inadequate diagnosis. Aim To select clinical and laboratory predictors to identify patients with a high likelihood of ACS in the Chest Pain Unit. Material and methods: Prospective evaluation of patients consulting in a Chest Pain Unit of a University Hospital. Initial assessment was standardized and included evaluation of pain characteristics, electrocardiogram and Troponin I. Independent predictors of ACS were identified with a multiple logistic regression. Results: In a four years period, 1,168 patients aged 62±23 years (69 percent males), were studied. After initial evaluation, 62 percent of the patients were admitted to the hospital for further testing and in 71 percent of them, a definite diagnosis of ACS was made. No events were reported by patients directly discharged from the Chest Pain Unit. Independent predictors associated with a higher likelihood of ACS were an abnormal electrocardiogram at the initial evaluation (Odds ratio (OR) 5.37, 95 percent confidence intervals (CI) 3.61-7.99), two or more cardiovascular risk factors (OR 2.16, 95 percent CI 1.21-2.84), cervical irradiation of the pain (OR 1.84, 95 percent CI 1.25-2.69), age over 65years (OR 1.73, 95 percent CI (1.32-2.27) and a Troponin I above the upper normal limit (OR: 5.68, 95 percent CI 3.72-8.29). Conclusions: Simple clinical findings allow an appropriate identification of patients with a high likelihood of ACS without specialized methods for myocardial ischemia detection.