To investigate the possible mechanisms of sudden death and the potential role of electrophysiologic testing in congestive heart failure, this study evaluated the electrophysiologic substrate in a model of heart failure induced by rapid pacing, Seventeen mongrel dogs underwent cardiac pacing at 220 to 240 beats/min for 5 weeks (paced group) and 11 other dogs served as a sham-operated control group. Rapid pacing of the right ventricle produced clinical and hemodynamic features of congestive heart failure.

Dogs in the paced group had prolonged cardiac conduction time as reflected by longer epicardial activation time (36.1± 2.4 vs. 30.8 ± 0.8 ms, p < 0.05). The ventricular effective refractory period was significantly prolonged after the development of heart failure (141 ± 4 vs. 177 ± 5 ms, p < 0.01, at a basic pacing cycle length of 300 ms), whereas no significant change was found in the control group (140 ± 4 vs. 145 ± 4 ms, p = NS). The prolongation of the ventricular effective refractory period correlated with an increase in left ventricular end-diastolic pressure (r = 0.55, p < 0.001) and the ventricular effective refractory period correlated inversely with cardiac index (r = −0.49, p < 0.025).

The rest membrane potential of ventricular muscle was less negative in the paced group compared with the control group (-80.7 ± 2.2 vs. −85.6 ± 2.2 mV, p < 0.05). Intracellularly recorded action potential duration of ventricular muscle was longer in the paced than in the control group (236 ± 9.8 vs. 198.9 ± 2.6 ms, p < 0.01, action potential duration at 90% repolarization). Eight dogs (48%) in the paced group developed ventricular fibrillation alter the occurrence of heart failure, whereas no control dog had sustained arrhythmia. There was no significant difference in the inducibility of ventricular tachycardia by programmed stimulation between the paced and control groups.

In conclusion, rapid pacing-induced cardiac dysfunction is associated with electrophysiologic changes that could contribute to sudden cardiac death. These changes are not reflected by inducibility of sustained ventricular tachycardia.