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The Effects of Aspirin and Clopidogrel Response on Myonecrosis After Percutaneous Coronary Intervention A BRIEF-PCI (Brief Infusion of Intravenous Eptifibatide Following Successful Percutaneous Coronary Intervention) Trial Substudy. JACC. Cardiovascular interventions [JACC Cardiovasc Interv] Journal article

 
Saw J, Densem C, Walsh S, Jokhi P, Starovoytov A, Fox R, Wong G, Buller C, Ricci D, Mancini GB, Fung A 
The Effects of Aspirin and Clopidogrel Response on Myonecrosis After Percutaneous Coronary Intervention A BRIEF-PCI (Brief Infusion of Intravenous Eptifibatide Following Successful Percutaneous Coronary Intervention) Trial Substudy. [JOURNAL ARTICLE]
JACC Cardiovasc Interv 2008 Dec; 1(6):654-659.


OBJECTIVES: The purpose of this study was to evaluate the effects of aspirin and clopidogrel response on myonecrosis after percutaneous coronary intervention (PCI) with glycoprotein (GP) IIb/IIIa blockade.
BACKGROUND: Aspirin and clopidogrel resistance is increasingly recognized, but its effects on PCI outcomes with GP IIb/IIIa blockade are unknown.
METHODS: This was a prospective, pre-specified substudy of the BRIEF-PCI (Brief Infusion of Intravenous Eptifibatide Following Successful Percutaneous Coronary Intervention) trial, which randomized 624 patients to 18-h or <2-h eptifibatide infusion after uncomplicated PCI. To be eligible, patients must have been pre-treated with aspirin (>/=5 days) and clopidogrel (75 mg/day >/=5 days, 300 mg loading >/=6 h, or 600 mg loading >/=2 h) and must not have received GP IIb/IIIa inhibitors within 48 h. Verify-Now Aspirin and Clopidogrel (P2Y(12)) assays were performed at baseline before PCI. Patients with aspirin reaction unit (ARU) >/=550 were labeled as aspirin resistant. Clopidogrel low-responders were defined as those in the lowest quartile of platelet inhibition. The primary end point was the prevalence of myonecrosis within 24 h after PCI.
RESULTS: We enrolled 209 patients into our substudy, of which 185 had aspirin response assessed, 198 had clopidogrel response assessed, and 174 had both assessed. There were 4.9% who were aspirin resistant. Clopidogrel low-responders were defined as those in the lowest quartile with platelet inhibition <19%. Only 1.1% had both aspirin resistance and low clopidogrel response. There was no difference in myonecrosis prevalence among aspirin-resistant compared with aspirin-sensitive patients (11.1% vs. 27.8%, p = 0.259) or among clopidogrel low-responders compared with clopidogrel responders (23.5% vs. 29.3%, p = 0.433).
CONCLUSIONS: Aspirin and clopidogrel response did not affect myonecrosis prevalence amongst patients who received eptifibatide for PCI.



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