Ventricular repolarization pattern under heart cooling in the rabbit.
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. 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. 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. 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.