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 electrical heterogeneity in experimental diabetes mellitus: effect of myocardial ischemia.

Aims of the study were to compare the development of electrocardiographic responses of the ischemia-induced heterogeneities of activation and repolarization in the ventricular myocardium of normal and diabetic animals. Body surface ECGs and unipolar electrograms in 64 epicardial leads were recorded before and during 20 min after the ligation of the left anterior descending artery in diabetic (alloxan model, 4 weeks, n=8) and control (n=8) rabbits. Activation times (ATs), end of repolarization times (RTs) and repolarization durations (activation-recovery intervals, ARIs) were determined in ischemic and periischemic zones. In contrast to the controls, the diabetic rabbits demonstrated the significant prolongation of ATs and shortening of ARIs (P<0.05) during ischemia in the affected region resulting in the development and progressive increase of the ARI and RT gradients across the ischemic zone boundary. The alterations of global and local dispersions of the RTs in diabetics correlated with the T(peak)-T(end) interval changes in the limb leads ECGs. In the ischemic conditions, the diabetic animals differed from the controls by the activation delay, significant repolarization duration shortening, and the increase of local repolarization dispersion; the latter could be assessed by the T(peak)-T(end) interval measurements in the body surface ECGs.

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.

Repolarization of epicardial ventricular surface of rabbit heart in acute stenosis of the aortic arch.

Overload of the cardiac left ventricle causes opposite local changes in repolarization duration (activation-recovery intervals) on the right- and left-ventricular epicardium, which depend on the duration of overload. The activation-recovery intervals on the right-ventricular lateral surface decrease after 1-min overload, but increase after 10-min overload. The length of activation-recovery intervals on the lateral surface of the left-ventricular apex increases after 10-min aortic stenosis more markedly in comparison with that after 1-min overload. Decrease/increase of local lengths of activation-recovery intervals results in modification of the general sequence of cardiac ventricular surface repolarization.

Repolarization of the rabbit cardiac ventricles after in increase of potassium concentration in the plasma.

The sequence of ventricular epicardium repolarization in rabbits with hypokalemia is directed from the apex of the heart to its base in accordance with distribution of local repolarization intervals. Under conditions of hyperkalemia, the propagation of excitation wave is inhibited without changes in its sequence; while the duration of repolarization decrease mainly in zones where it was initially long (the base of the right ventricle), as a result of which the distribution of local repolarization intervals becomes more uniform and a relationship between the repolarization and activation sequences is formed.

Effect of torso shape and heart location in the chest on formation of cardiac electric potentials on body surface in dogs.

Experimental and theoretical methods were employed to study the effects of torso shape and heart orientation in the thoracic cavity on peculiarities of the formation cardiac electric field on the body surface in dogs. It was found that heart orientation to a greater extent than torso shape affected projections of cardiac electric potentials from the epicardium onto the body surface.

Time correlation between initial activation of ventricular myocardium and cardiac electric potentials on body surface in dogs.

Parameters of cardioelectric field on body surface and propagation of excitation in ventricular myocardium during initial activation were studied using multichannel synchronous electrocardiotopography. It was shown that inversion of areas of negative and positive potentials of cardioelectric field on body surface at the moment of excitation propagation to the epicardium reflected changes in the main direction of excitation wavefront in ventricles.