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Original Article Prasugrel versus Clopidogrel in Patients with Acute Coronary Syndromes Stephen Artistic Anatomy By Dr. Paul Richer Pdf. D. Wiviott, M.D., Eugene Braunwald, M.D., Carolyn H. McCabe, B.S., Gilles Montalescot, M.D., Ph.D., Witold Ruzyllo, M.D., Shmuel Gottlieb, M.D., Franz-Joseph Neumann, M.D., Diego Ardissino, M.D., Stefano De Servi, M.D., Sabina A. Murphy, M.P.H., Jeffrey Riesmeyer, M.D., Govinda Weerakkody, Ph.D., C. Michael Gibson, M.D., and Elliott M. Antman, M.D., for the TRITON–TIMI 38 Investigators N Engl J Med 2007; 357:2001-2015 DOI: 10.1056/NEJMoa0706482.

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Methods To compare prasugrel, a new thienopyridine, with clopidogrel, we randomly assigned 13,608 patients with moderate-to-high-risk acute coronary syndromes with scheduled percutaneous coronary intervention to receive prasugrel (a 60-mg loading dose and a 10-mg daily maintenance dose) or clopidogrel (a 300-mg loading dose and a 75-mg daily maintenance dose), for 6 to 15 months. The primary efficacy end point was death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke. Ghost 11.5 Add Network Drivers. The key safety end point was major bleeding.

Results The primary efficacy end point occurred in 12.1% of patients receiving clopidogrel and 9.9% of patients receiving prasugrel (hazard ratio for prasugrel vs. Clopidogrel, 0.81; 95% confidence interval [CI], 0.73 to 0.90; P. Figure 1 Cumulative Kaplan–Meier Estimates of the Rates of Key Study End Points during the Follow-up Period. Panel A shows data for the primary efficacy end point (death from cardiovascular causes, nonfatal myocardial infarction [MI], or nonfatal stroke) (top) and for the key safety end point (Thrombolysis in Myocardial Infarction [TIMI] major bleeding not related to coronary-artery bypass grafting) (bottom) during the full follow-up period. The hazard ratio for prasugrel, as compared with clopidogrel, for the primary efficacy end point at 30 days was 0.77 (95% confidence interval [CI], 0.67 to 0.88; P. Avast Free Antivirus Setup .exe.part. Figure 2 Hazard Ratios and Rates of the Primary End Point, According to Selected Subgroups of Study Patients.

The primary end point was defined as death from cardiovascular causes, nonfatal myocardial infarction (MI), or nonfatal stroke. The percentages are Kaplan–Meier estimates of the rate of the end point at 15 months.

For each subgroup, the size of the square is proportional to the number of patients in the subgroups and represents the point estimate of the treatment effect. The overall treatment effect of prasugrel as compared with clopidogrel is represented by the diamond, and the dashed vertical line represents the corresponding overall point estimate. None of the P values for interactions were significant. Glycoprotein IIb/IIIa–receptor antagonist use was that during the index hospitalization. The short-term and long-term benefits of dual-antiplatelet therapy with aspirin and clopidogrel have been established for patients with acute coronary syndromes and those undergoing percutaneous coronary intervention (PCI). Despite these benefits, many patients continue to have recurrent atherothrombotic events while receiving standard dual antiplatelet therapy.

In addition, important limitations of clopidogrel remain, such as only a modest antiplatelet effect, with substantial interpatient variability and a delayed onset of action. Small clinical studies have suggested that patients with a reduced pharmacologic response to clopidogrel may be at increased risk for adverse clinical events, including myocardial infarction and coronary-stent thrombosis. Prasugrel — a novel thienopyridine — is a prodrug that, like clopidogrel, requires conversion to an active metabolite before binding to the platelet P2Y 12 receptor to confer antiplatelet activity. At the currently studied doses, prasugrel inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI.

Phase 2 testing of prasugrel, as compared with clopidogrel, in patients undergoing elective or urgent PCI showed a trend toward fewer ischemic events, with an acceptable safety profile. Thus, we designed the Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel–Thrombolysis in Myocardial Infarction (TRITON–TIMI) 38, a phase 3 trial involving patients with acute coronary syndromes with scheduled PCI, comparing a regimen of prasugrel with the standard-dose regimen of clopidogrel approved by the Food and Drug Administration. Although our trial was designed to compare regimens of prasugrel and clopidogrel, it also tests the hypothesis that the use of an agent producing a higher level of inhibition of adenosine diphosphate–induced platelet aggregation and a less-variable response than standard-dose clopidogrel reduces ischemic events. Methods TRITON–TIMI 38 was designed as a collaboration between the TIMI Study Group, the sponsors — Daiichi Sankyo and Eli Lilly — and a steering committee of investigators (see the Appendix).