Search

Radiofrequency current catheter ablation was attempted for 17 morphologies of ventricular tachycardia (VT) in 14 patients. Five patients had underlying heart disease. The site of VT origin was determined as the earliest site of ventricular activation, or by pacing within the area of slow conduction. In 15 VTs, ablation was performed during VT, and 12 VTs (80%) were terminated within an average of 5.4±4.2 seconds. After ablation, 14 VTs (14/17=82%) of 11 patients (11/14=79%) could not be induced by electrical stimulation. Radiofrequency ablation appeared to be more effective in VTs without underlying heart disease (91%), and in VTs originating from the right ventricle (100%). Successful ablation sites usually showed a normal local electrograms during VT. Ablation in the slow conduction area was attempted in 3 VTs, and 2 VTs became noninducible. The mean number of applications of radiofrequency current for each VT origin was 7.7±6.4 at 20-50 Watts. In 4 patients, application of radiofrequency current was required 10 or more times because of a possible large arrhythmogenic area, or because of reinduction of VT, even though VT was terminated by radiofrequency current. No major complication was observed except for complete right bundle branch block in 1 patient. In conclusion: (1) Radiofrequency catheter ablation was considered to be effective and safe, especially for VT without underlying heart disease or VT originating from the right ventricle. (2) Ablation during VT was considered to be useful for identifying the proper ablation site and to avoid creating an unnecessary lesion.

Electrophysiologic testing was performed in 31 patients with ventricular tachycardia (21 cases) and fibrillation (10 cases) to characterize the electrophysiologic properties of patients responding or not responding to therapy with class III antiarrhythmic drugs. At the baseline, there were no differences among the patients in the monomorphic VT cycle length (CL), block CL or the width of the zone of entrainment. Ventricular tachyarrhythmias after the administration of class III drugs (sotalol: 9, amiodarone: 15 and E-4031/MS-551: 7) were inducible (non-responders) in 17 patients and non-inducible (responders) in 14 (45%). The class III drugs prolonged the sinus cycle length (SCL), QT interval and right ventricular effective refractory period (VERP), but had little effect on ventricular conduction time in the responders and non-responders. The SCL, QT interval and VERP at the three drive cycle lengths of 600, 400 and 300 msec were significantly longer in the responders than in the non-responders, but the class III drug action on VERP showed a reverse use-dependency. Isoproterenol administered to the responder did not fully reverse the class III antiarrhythmic drug-induced prolongation of QT, QTc and VERP, which remained significantly prolonged compared to the baseline values. Furthermore, when the VERP after the administration of class III drugs were greater than 270, 250 and 240 msec at the three drive cycle lengths of 600, 400 and 300 msec, respectively, it was associated with the non-inducibility of VT/VF. Though the precise mechanism of the drug efficacy is not yet known, these observations help to clarify the ability of class III drugs to prevent the induction of ventricular tachyarrhythmia.

UNLABELLED We performed electrophysiological studies in 13 patients with idiopathic VT and attempted radiofrequency (RF) catheter ablation in 4 of them. RESULTS VT was induced by programmed stimulation in all patients and the mean cycle length was 363 +/- 58 msec. In 8 of 13 patients (62%), alternation of either the cycle length and/or morphology of VT was observed. Transient entrainment was achieved in all patients by rapid pacing from the right ventricular outflow tract so reentry was considered the underlying mechanism of VT. The site of earliest activation (EAS) during VT was located at the apicoposterior portion of the left ventricular septum and used as the target site for RF catheter ablation. Spikelike presystolic activity was detected 20-40 msec prior to the large deflection of the local electrogram in four patients. VT was terminated by a few seconds of RF current in all four patients, but subsequently new VTs with a slightly different morphology were induced in three of them and re-mapping showed a shift of the EAS. After additional RF ablation at the new EAS, VT was no longer induced. No complication was noted and VT did not recur during a follow-up period for a mean of 9.3 +/- 5.2 months. CONCLUSION RF catheter ablation seems useful and safe for idiopathic VT. The alternation of QRS morphology and the findings at the time of catheter ablation suggest that an alternative pathway or multiple exists may be present in some patients with idiopathic VT, because the change in VT morphology was associated with a shift of the EAS.

In a patient with sustained ventricular tachycardia (VT), we observed two different conduction times through the reentry circuit at the critical paced cycle length. The cycle length of the VT was 420 msec and overdrive pacing initially performed at a paced cycle length of 400 msec and repeated at decrements of 10 msec until the VT was interrupted at a paced cycle length of 320 msec. During rapid pacing, constant fusion and progressive fusion were confirmed. The first post-pacing return cycle was identical to each paced cycle length. The conduction time between the stimulus artifact and the orthodromically captured electrogram at the left ventricle was constant at 350 msec in each paced cycle length. However, only at a pacing cycle length of 360 msec two conduction times were alternatively observed, one of 350 msec and the other of 365 msec. When the conduction time changed from 350 msec to 365 msec, morphological alternation both in the surface QRS complex and in the orthodromically captured electrogram was evident. Dual slow pathways or a single slow pathway with plural exits from the reentry circuit is a likely mechanism of the alternation.

BACKGROUND Information concerning the electrophysiological characteristics of the reentrant circuit is still limited. To understand the incidence and mechanism of pacing-induced interruption of ventricular tachycardia (VT), rapid pacing was performed to entrain VT, and the local electrogram at the VT origin and the surface electrocardiogram were analyzed. METHODS AND RESULTS Among 25 patients, evidence of transient entrainment was confirmed in 20 patients, but the critical paced cycle length at which VT was interrupted was obtained in 13 patients when the paced cycle length was decreased in steps of 10 msec. During pacing at the critical cycle length (defined as block cycle length), changes in the local electrogram at VT origin were confirmed in all of the 13 patients; that is, 1) a change in morphology and 2) a change in the timing of activation: a sudden shortening in the stimulus to local electrogram time (third entrainment criterion by Waldo). The two changes mean that the exit is activated from a different direction (retrograde capture) because of an orthodromic block in the slow conduction zone. The QRS complex in the surface electrocardiogram showed a change in configuration from the fusion complex to the fully paced one at the same time when the exit was captured antidromically. CONCLUSIONS Based on our observations in these patients, ventricular tachycardia interruption is very often associated with orthodromic block in the reentrant circuit at a critical cycle length of rapid pacing.

In two patients with arrhythrnogenic right ventricular dysplasia (ARVDJ, sustained ventricular tachycardia (VT) was induced by programmed stimulations during serial drug testings. One patient had five and the other had two VT morphologies, and the sites of origin were determined by endocardial catheter mappings. When overdrive pacing was performed, constant fusion in the QflS complex was observed in the two patients. Constant fusion of a different degree was also observed at different paced cycle lengths. Both patients had dilated right ventricles and wall-motion abnormality, and the diagnosis of ARVD was further confirmed by the specimen resected at the site of origin of VT. Therefore, VT in ARVD can be entrained and reentry is the most likely mechanism of such VT.