Impacts of Glycoprotein IIb/IIIa Inhibition on QT Dispersion After Successful Percutaneous Coronary Intervention

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Coronary ischemia augments inhomogeneity in ventricular repolarization. Decrease in the QT dispersion (QTd) following restoration of coronary blood flow to the ischemic myocardium by successful percutaneous coronary intervention (PCI) is an expected outcome. The purpose of the study was to seek whether glycoprotein IIb/IIIa (GP IIb/IIIa) inhibition has additional beneficial effects on QT dispersion after angiographically successful PCI. The study involved 111 consecutive patients scheduled for elective coronary balloon angioplasty with or without stent implantation. Sixty patients (mean age 58 ±9) were randomized to receive standard therapy including preprocedural aspirin, ticlopidine, and IV heparin, and 51 patients (mean age 54 ±10) were randomized to receive additional IV tirofiban infusion before the lesion was crossed with the guidewire. Standard 12-lead simultaneous ECG recordings for the measurement of QTd and corrected QTd (QTcd) (calculated by using Bazett's formula) were obtained before and immediately after the procedure, and at the 6th, and 24th hours. Blood samples for detection of postprocedural myocardial damage (CK-MB and cTn-I) were taken before and immediately after the procedure, at the 6th, 12th, and 24th hours. In total, 128 stenoses were treated with PCI. Seventy of these lesions were in the standard therapy group and 58 in the tirofiban group. QTd and QTcd were not statistically different between the 2 groups before and immediately after the procedure and at the 6th hours, but at the 24th hour QTd and QTcd were significantly longer in the standard therapy group (p=0.047 and p=0.001, respectively). Postprocedural troponin-I elevation (B=0.692, p=0.037), maximum inflation pressure (B=0.182, p=0.001), and previous myocardial infarction (MI) (B=0.885, p=0.004) were defined as the predictors of the final QT dispersion at the 24th hour. QT dispersion significantly decreased after successful percutaneous coronary intervention. GP IIb/IIIa inhibition therapy was not superior by means of recovery of increased QT dispersion during the early hours of the intervention, but it prevented minor myocardial necrosis and provided more long-lasting recovery in QT dispersion as compared with heparin therapy. This impact of GP IIb/IIIa receptor inhibition on QTd may be a possible mechanism by which these drugs reduce cardiovascular events after PCI.

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