| Abstract: | Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 ± 50 msec; mean ± SEM) 13–180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 ± 4.0 msec postablation; 135.7 ± 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 ± 1.0 μV postablation; 5.9 ± 0.4 μV preablation). or in the duration of the low amplitude signal (69.2 ± 2.0 msec postablation; 62.7 ± 3.4 msec preablation). At follow-up electrophysiology study performed 14 ± 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study. |
