Epicardial-limited electrophysiological heterogeneities do not facilitate ventricular arrhythmia induction. An experimental study

The electrophysiological heterogeneities of the myocardium are associated with vulnerability to arrhythmias. This study presents an experimental heterogeneity model based on local epicardial cooling/warming. The ventricular activation-recovery interval (ARl), conduction velocity (CV) and arrhythmogenic response to electrical pacing were determined. Electrical mapping was carried out on isolated rabbit hearts (n=8), using a specific electrode device for epicardial temperature control. With respect to baseline, ARl in the modified zone was prolonged (137 ± 22 ms vs 111 ± 13 ms, p<;0.05) under maximum hypothermia (22.3 ± 0.6 °C vs 36.7 ± 0.8 DC), and was shortened (98 ± 13 ms vs 107 ± 16 ms, p<;0.05) under conditions of hyperthermia (41.8 ± 0.3 °C vs 37.3 ± 0.4 DC). CV decreased (70 ± 17 cm/s vs 76 ± 17 cm/s, p<;0.05) under hypothermia and increased (79 ± 20 cm/s vs 75 ± 21 cm/s, p<;0.05) under hyperthermia. There were no changes in the unmodified zone. Repetitive responses were observed in four hearts, with no dependency between the appearance of responses and the induced modifications. Thermally induced dispersion of ARl and CV did not favor the induction of ventricular arrhythmias, probably because only a limited zone of the ventricular epicardium was affected.