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.