Complete elimination of slow pathway conduction is feasible in the majority of patients. Elimination of slow pathway conduction is highly predictive of long-term success after AV node modification using an anatomically guided approach.

A 55-year-old woman with frequent problematic supraventricular tachycardia is presented. The tachycardia was irregular with predominantly normal QRS morphology and was refractory to multiple antiarrhythmic drugs. At electrophysiology study, the tachycardia was inducible with atrial or ventricular extrastimuli and dual pathways were observed. In contrast to the situation usually seen with dual atrioventricular node physiology, the slow pathway had a longer effective refractory period than the fast pathway and reentrant tachycardia was not induced. Simultaneous conduction over the fast and slow pathways during sinus rhythm was shown to be the mechanism for clinical tachycardia. The tachycardia was successfully treated using radiofrequency ablation of the slow pathway.

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 less than 0.05). The ventricular effective refractory period was significantly prolonged after the development of heart failure (141 +/- 4 vs. 177 +/- 5 ms, p less than 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 less than 0.001) and the ventricular effective refractory period correlated inversely with cardiac index (r = -0.49, p less than 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 less than 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 less than 0.01), action potential duration at 90% repolarization).(ABSTRACT TRUNCATED AT 250 WORDS)

These results indicate that high voltage shocks induce different responses in Purkinje fibers and ventricular muscle. The shock-induced rapid firing in the Purkinje fiber may contribute to postshock arrhythmias and possibly refibrillation in some cases. The shock-induced transient refractory state in the ventricular muscle may prevent the ventricle from responding to the rapid firing and thus may decrease the incidence of postshock arrhythmias.