Measuring aspirin resistance, clopidogrel responsiveness, and postprocedural markers of myonecrosis in patients undergoing percutaneous coronary intervention.
Aspirin and clopidogrel are proven to prevent thromboembolic events during percutaneous coronary intervention (PCI). Enzyme release of creatine kinase-MB (CK-MB) enzyme during PCI has been associated with an increased risk of future adverse cardiac events. This study examined the correlation between measurements of aspirin resistance and the level of inhibition of the thienopyridine-specific P2Y12 platelet receptor and CK-MB release after PCI. We prospectively studied 330 patients with elective PCI treated with drug-eluting stents. Patients were pretreated with aspirin and clopidogrel. Patients with positive CK-MB or acute coronary syndrome and those on glycoprotein IIb/IIIa inhibitors were excluded. Serum assays of aspirin resistance (Ultegra Rapid Platelet Function Assay-ASA, Accumetrics) and clopidogrel resistance (Rapid Platelet Function Assay P2Y12, Accumetrics) were performed before PCI. Serum troponinI and CK-MB levels were measured at 8, 16, and 24 hours after PCI. Aspirin resistance unit (ARU) measurement > or =550 was detected in 12 patients (3.7%). Mean platelet reactivity unit (PRU; measurement of inhibition of P2Y12 activity) was 192.2 +/- 95.4 (lower PRU, more inhibition of P2Y12 receptor). There was no correlation between level of ARU or PRU and troponin I or CK-MB release after PCI at any time point. Only multivessel coronary disease was found to be a predictor of any increase in CK-MB in a multivariate analysis (odds ratio 2.2, 95% confidence interval 1.4 to 3.3, p = 0.0003). A positive correlation was found between levels of ARU and PRU. Target vessel revascularization/major adverse cardiac event rate at 6 months was 8.2% with no correlation between ARU or PRU and release of cardiac enzymes or occurrence of adverse cardiac events. In conclusion, this study does not support routine measurements of aspirin and clopidogrel resistance in stable patients undergoing PCI.
Buch
Ashesh N
AN
Department of Medicine, Division of Cardiology, Washington Hospital Center, Washington, DC, USA.
Singh
Suman
S
Roy
Probal
P
Javaid
Aamir
A
Smith
Kimberly A
KA
George
Christopher E
CE
Pichard
Augusto D
AD
Satler
Lowell F
LF
Kent
Kenneth M
KM
Suddath
William O
WO
Waksman
Ron
R
D000368:Aged; D000369:Aged, 80 and over; D000704:Analysis of Variance; D015906:Angioplasty, Balloon, Coronary; D001241:Aspirin / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000097:blood / Q000628:therapy; D052279:Creatine Kinase, MB Form / Q000097:blood / Q000187:drug effects; D004351:Drug Resistance / Q000187:drug effects*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D009336:Necrosis; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D010979:Platelet Function Tests; D011184:Postoperative Period; D011237:Predictive Value of Tests; D016016:Proportional Hazards Models; D011446:Prospective Studies; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000494:pharmacology; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood / Q000187:drug effects
D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D000077144:Clopidogrel; D052279:Creatine Kinase, MB Form; D013988:Ticlopidine; D001241:Aspirin