Key result
Glibenclamide pretreatment reduces ischemia-induced T-wave elevation by ~63%, implicating KATP channel activation.
Why the study?
Does glibenclamide attenuate peaked T waves during early myocardial ischemia in an open-chest dog model?
Does glibenclamide attenuate peaked T waves during early myocardial ischemia in an open-chest dog model?
p-value: p=< 0.05
Glibenclamide attenuates ischemia-induced peaked T waves in a dog model, suggesting that KATP channel activation partly explains early ventricular repolarization changes during myocardial ischemia.
Glibenclamide attenuates ischemia-induced T-wave changes in dogs; leaves open whether KATP blockade alters ECG findings or outcomes in human myocardial ischemia.
OBJECTIVES: ECG peaked T wave appears during the early phase of myocardial ischemia, but the underlying mechanisms remain unknown. The purpose of this study was to elucidate the role of ATP-sensitive K+ channel (KATP) in this ECG change. METHODS: In 12 anesthetized, open-chest dogs, the sinus node was crushed and the right atrium was paced at a cycle length of 400 ms. The left anterior descending coronary artery was abruptly occluded for 60 s before (control) and 15 min after an intravenous infusion of vehicle (n = 6) or glibenclamide (1 mg/kg, n = 6), a blocker of KATP. Forty-eight epicardial electrograms were simultaneously recorded from the anterior surface of the left ventricle. The potentials at 40, 80 and 120 ms from the J point were measured, and these points corresponded to the early, middle and late phases of the T wave, respectively. RESULTS: During the control occlusion, T wave increased time-dependently and the maximal T-wave change was noted at the end of 60 s of coronary occlusion. The extents of T-wave elevation at the early, mid and late T phases were 5.5 +/- 0.5, 7.3 +/- 0.8 and 11.7 +/- 1.8 mV, respectively, and these T-wave elevations were significantly reduced by 33 +/- 21%, 59 +/- 12% and 63 +/- 13%, respectively, after the pretreatment with glibenclamide but not with its vehicle. The % reductions of mid and late T by glibenclamide were significantly larger than that of early T wave (P < 0.05). CONCLUSIONS: An abrupt coronary occlusion accompanied peaked T wave as an early ECG wave change. As the extent of this T-wave elevation was attenuated by glibenclamide, the ischemia-induced alteration of ventricular repolarization can partly (60%) be explained by the modification of KATP activation.
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Kondo et al. (1996) studied Myocardial ischemia (n=12). Glibenclamide vs. Vehicle was evaluated on Reduction in T-wave elevation at early, mid, and late T phases (p=< 0.05). Pretreatment with glibenclamide significantly reduced ischemia-induced T-wave elevation by up to 63%, suggesting the ECG change is partly explained by KATP channel activation.
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