Mechanism of electrocardiographic T-wave flattening in diabetes mellitus: experimental and simulation study.

In the present study we investigated the contribution of ventricular repolarization time (RT) dispersion (the maximal difference in RT) and RT gradients (the differences in RT in apicobasal, anteroposterior and interventricular directions) to T-wave flattening in a setting of experimental diabetes mellitus. In 9 healthy and 11 diabetic (alloxan model) open-chest rabbits, we measured RT in ventricular epicardial electrograms. To specify the contributions of apicobasal, interventricular and anteroposterior RT gradients and RT dispersion to the body surface potentials we determined T-wave voltage differences between modified upper- and lower-chest precordial leads (T-wave amplitude dispersions, TWAD). Expression of RT gradients and RT dispersion in the correspondent TWAD parameters was studied by computer simulations. Diabetic rabbits demonstrated flattened T-waves in precordial leads associated with increased anteroposterior and decreased apicobasal RT gradients (P<0.05) due to RT prolongation at the apex. For diabetics, simulations predicted the preserved T-vector length and altered sagittal and longitudinal TWAD proven by experimental measurements. T-wave flattening in the diabetic rabbits was not due to changes in RT dispersion, but reflected the redistributed ventricular repolarization pattern with prolonged apical repolarization resulting in increased anteroposterior and decreased apicobasal RT gradients.

Ventricular repolarization pattern under heart cooling in the rabbit.

AIM: Prolongation of ventricular repolarization is characteristic of myocardial cooling. In the present study, we investigated whether this prolongation is uniform or not throughout ventricular epicardium and how these hypothermia-induced changes express in the body surface potential distribution. METHODS: Epicardial and body surface potential mapping from 64 unipolar leads was carried out in 18 anaesthetized adult rabbits. Mild hypothermia documented by lowering the mediastinal and rectal temperature from 38 to 32 degrees C was elicited by perfusion of the mediastinum with cooled saline. Activation times, repolarization times and activation-recovery intervals were determined in each epicardial lead. RESULTS: Baseline activation-recovery intervals distributed non-uniformly on the ventricular epicardium, increasing progressively from the apex to the base and from the left ventricular (LV) sites to the right ventricular (RV) sites (P < 0.05), governing the repolarization sequence of ventricular epicardium. Heart cooling from 38 to 32 degrees C produced the heterogeneous prolongation of activation-recovery intervals which was more pronounced at the apex than at the base, and in the LV areas compared to the RV areas (P < 0.05). These nonuniform changes in local repolarization durations resulted in the development of base-to-apex repolarization sequence and inversion of the body surface potential distribution during the T wave. CONCLUSION: Thus, under cooling the rabbit heart from 38 to 32 degrees C, the nonuniform prolongation of local repolarization durations resulted in the reversal of ventricular epicardial repolarization sequence which, in turn, was responsible for the inversion in the body surface potential distribution during the T wave.