Effects of glycoprotein IIB/IIIA inhibition on QT dispersion in patients with unstable angina and non-Q-wave myocardial infarction

Acute coronary ischemia augments inhomogeneity in ventricular repolarization, which significantly correlates with ventricular fibrillation. The effects of glycoprotein IIb/IIIa receptor inhibition on QT interval dispersion (QTd), and the effects of QTd changes on in-hospital, 30 day, and long-term cardiac events in patients with unstable angina (UA) and non-Q-wave myocardial infarction (MI) have not been investigated previously. Eighty-three patients presenting with Braunwald class IIIB UA or non-Q-wave MI were randomized to standard therapy (aspirin and unfractionated heparin, 42 patients) or tirofiban therapy: addition to standard therapy (41 patients). QT interval dispersion (QTd) and corrected QTd (QTcd) were measured prior to therapy, and 6, 24, 48, 72, and 96 hours after the initiation of the treatment. In both groups QTd and QTcd were higher than normal limits during the admission, prior to therapy. The first QTd and QTcd were not different between two groups; the remaining values were significantly lower in tirofiban group except the first and last QTd (p values for QTd at 6, 24, 48, 72, and 96 hours are 0.057, 0.045, 0.0006, 0.04, and NS, respectively, and for QTcd, they are 0.017, 0.046, 0.0004, 0.012, and 0.01, respectively). When the first QTd and QTcd compared to the following measurements in each group, the first significant decrease occurred at 6th hour (p = 0.004 for QTd, and 0.004 for QTcd) in tirofiban group, whereas in standard therapy group it was occurred at 48th hour (p = 0.02) for QTd, and 72nd hour (p = 0.019) for QTcd. While the incidence of in-hospital acute MI, recurrent refractory angina, and total major cardiac events were significantly lower in the tirofiban group (p = 0.03, 0.04, and 0.01, respectively) that early QTd recovery observed, the 30 day and long-term incidence of major cardiac events were not different between the two groups. GP IIb/IIIa receptor inhibition in addition to heparin treatment causes a faster recovery of increased QT dispersion, and the early recovery of QTd is associated with a reduction in in-hospital major cardiac events.