Abstract 2363: Effect Of Aspirin And Clopidogrel Resistance On Myonecrosis Following Percutaneous Coronary Intervention
Background: The presence of aspirin and clopidogrel resistance is increasingly recognized. We seek to evaluate if patients with aspirin and/or clopidogrel resistance are predisposed to myonecrosis following percutaneous coronary interventions (PCI).
Methods: This study is performed as a substudy of the Brief-PCI, which randomized 620 patients to 18hr or 2hr infusion of eptifibatide following PCI. To be eligible for our substudy, patients have to be pretreated with aspirin (≥5 days) and clopidogrel (either 75mg/d ≥5 days, or 300mg loading ≥6 hr), and have not received a glycoprotein IIb/IIIa inhibitor within the past 48hrs. Bedside point-of-care platelet aggregometry using Accumetrics VerifyNow™ Aspirin and Clopidogrel assays were performed at baseline prior to PCI. Patients with aspirin reaction unit (ARU) ≥550 were labeled as “aspirin resistant”. Patients with percent inhibition ≤20% on the VerifyNow™ Clopidogrel assays were labeled as “clopidogrel resistant”. Our primary endpoint is the prevalence of myonecrosis within 24hrs post-PCI (defined as elevation of Troponin I >1μg/L when baseline levels are negative, or peak CK-MB >3 times upper limit of normal and >50% higher than baseline value).
Results: We enrolled 203 patients, of which 181 had aspirin resistance assessed, 188 had clopidogrel resistance assessed, and 169 had both assessed. There were 5% ± 1.6% who were aspirin resistant, 29% ± 3.3% who were clopidogrel resistant, and 1% ± 0.8% who were resistant to both. The overall prevalence of myonecrosis within 24hrs of PCI was 9% ± 2%. Patients who were resistant to both aspirin and clopidogrel had a higher prevalence of myonecrosis compared to those who had normal response (50% vs. 8%, p=0.031). There was no difference in myonecrosis prevalence among aspirin resistant patients compared to those with normal aspirin response (11% vs. 8%, p=0.754), or among clopidogrel resistant patients compared to those with normal clopidogrel response (11% vs. 7%, p=0.390). The mean ARU and percent inhibition was not different between those with or without myonecrosis.
Conclusion: Our data suggests that only a small proportion of patients were resistant to both aspirin and clopidogrel, and these patients may have a higher prevalence of myonecrosis following PCI.