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Background: Premature stimuli can cause ventricular fibrillation (VF) during electrophysiological testing. The electrophysiological correlations associated with the onset of VF were evaluated in 40 patients who had this rhythm induced during programmed ventricular stimulation. These parameters were compared with those observed in 51 patients who had inducible sustained monomorphic ventricular tachycardia (VT) and 45 patients who had no inducible sustained ventricular tachyarrhythmias., Methods and Results: Shortest premature coupling intervals for S2, S3, and S4 at induction of tachycardia or before achieving refractoriness, corresponding conduction latencies (defined as the time from the premature stimulus to the upstroke of the depolarization wave front recorded 35 mm away from the stimulation site), and ventricular activation times (defined as the time from the premature stimulus to the end of the depolarization wave) were compared. The mean coupling intervals were longest in the inducible VT patients: 300 +/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively. In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/- 20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194 +/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The coupling interval of the last premature extrastimulus was above 200 msec in 70% of the patients in whom VF was induced. The largest increases in latency and activation times were recorded in patients in whom VF was induced. The cumulative increase in latency, defined as increased conduction time from baseline, summed for all the premature stimuli was also the greatest at initiation of VF. In contrast, the smallest increases in these parameters were noted in the patients with no inducible VT or VF. Measurements of total activation time yielded similar results as those recorded for latencies. The most important parameters distinguishing the VT patient population from the other two groups were the low ejection fractions and the longer coupling intervals at which VT was induced, whereas in the VF group, the most important discriminating factor was cumulative activation time. Sixty-three percent of the inducible VF patients presented with abnormal hearts (myocardial infarction or cardiomyopathy), whereas 88% of the inducible VT patients had abnormal hearts. In contrast, only 25% of the patients in whom no arrhythmia was induced presented with abnormal hearts. Mean ejection fraction was 32 +/- 15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and 51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus VT)., Conclusions: The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.

Concealed anterograde penetration of the atrioventricular (AV) node has been used to explain a wide variety of electrocardiographic findings. The effects of atrial rate acceleration on this phenomenon remain undefined. To examine the dynamic interrelations between conducted and nonconducted beats at different atrial rates, a unique atrial pacing protocol of functional 2:1 AV block was used in 10 patients. The pacing protocol involved abrupt transitions from 2:1 to 1:1 AV conduction and enabled quantification of conduction delay produced by nonpropagated impulses over extremes of atrial rate. Stable 2:1 AV conduction was maintained over a mean range of atrial paced cycle lengths of 289 +/- 29.6 to 223 +/- 33.0 msec, respectively. The mean AV conduction time during 2:1 and corresponding 1:1 drives at the longest atrial paced rates were 169 +/- 33.5 and 136.5 +/- 26.9 msec, respectively--revealing a significant effect of nonpropagated impulses on subsequent conduction. Surprisingly, at the shortest atrial paced rates, the mean AV conduction times were 191.5 +/- 31.8 and 161.0 +/- 23.3 msec, respectively. The lack of significant changes in conduction time between 2:1 and 1:1 drives at the extremes of atrial rate (32.5 vs. 30 msec, p = NS) suggests that the effect of concealed conduction is "fixed" and independent of rate. Clinical implications and postulated electrophysiologic mechanisms are discussed.