OBJECTIVES: We sought to evaluate the influence of platelet reactivity after clopidogrel, as assessed by the VerifyNow point-of-care assay (Accumetrics, San Diego, California), on myonecrosis in low-to-intermediate risk patients undergoing percutaneous coronary intervention (PCI). BACKGROUND: Inadequate platelet inhibition at the time of PCI is associated with a higher risk of recurrent ischemic events. METHODS: A total of 250 consecutive biomarker-negative patients treated with clopidogrel and undergoing elective PCI were enrolled. Cardiac biomarkers (creatine kinase-myocardial band and troponin I) were measured before and 8 and 24 h after intervention. Platelet reactivity after clopidogrel was assessed immediately before PCI by the VerifyNow P2Y12 point-of-care assay. High platelet reactivity (HPR) after clopidogrel was defined as a platelet reaction unit value > or =240. RESULTS: Patients with HPR (31% of the overall population) showed more frequent myonecrosis, with statistical significance with regard to creatine kinase-myocardial band elevation (35% vs. 20%; p = 0.011), and by trend with regard to troponin-I elevation (47% vs. 35%; p = 0.059). Incidence of periprocedural myocardial infarction was higher in patients with HPR, both by creatine kinase-myocardial band (13% vs. 4%; p = 0.011) and troponin-I definition (32% vs. 19%; p = 0.019). By multivariable analysis, HPR was an independent predictor of periprocedural myocardial infarction. CONCLUSIONS: Easily assessed by a point-of-care assay, HPR after clopidogrel is a frequent finding and is associated with increased risk of myonecrosis in low-to-intermediate risk patients undergoing planned PCI. Copyright (c) 2010 American College of Cardiology Foundation.Published by Elsevier Inc. All rights reserved.
OBJECTIVES: We sought to evaluate the influence of platelet reactivity after clopidogrel, as assessed by the VerifyNow point-of-care assay (Accumetrics, San Diego, California), on myonecrosis in low-to-intermediate risk patients undergoing percutaneous coronary intervention (PCI). BACKGROUND: Inadequate platelet inhibition at the time of PCI is associated with a higher risk of recurrent ischemic events. METHODS: A total of 250 consecutive biomarker-negative patients treated with clopidogrel and undergoing elective PCI were enrolled. Cardiac biomarkers (creatine kinase-myocardial band and troponin I) were measured before and 8 and 24 h after intervention. Platelet reactivity after clopidogrel was assessed immediately before PCI by the VerifyNow P2Y12 point-of-care assay. High platelet reactivity (HPR) after clopidogrel was defined as a platelet reaction unit value > or =240. RESULTS:Patients with HPR (31% of the overall population) showed more frequent myonecrosis, with statistical significance with regard to creatine kinase-myocardial band elevation (35% vs. 20%; p = 0.011), and by trend with regard to troponin-I elevation (47% vs. 35%; p = 0.059). Incidence of periprocedural myocardial infarction was higher in patients with HPR, both by creatine kinase-myocardial band (13% vs. 4%; p = 0.011) and troponin-I definition (32% vs. 19%; p = 0.019). By multivariable analysis, HPR was an independent predictor of periprocedural myocardial infarction. CONCLUSIONS: Easily assessed by a point-of-care assay, HPR after clopidogrel is a frequent finding and is associated with increased risk of myonecrosis in low-to-intermediate risk patients undergoing planned PCI. Copyright (c) 2010 American College of Cardiology Foundation.Published by Elsevier Inc. All rights reserved.