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ObjectiveTo assess the long term outcome of radiofrequency (RF) catheter ablation for idiopathic ventricular tachycardia (VT) originating from the outflow tract of the right ventricle, with special reference to the morphological variation in the VT-QRS complexes.Patients13 patients whose ventricular tachycardia was treated with RF ablation were followed up more than 18 months after RF ablation.ResultsEndocardial mapping revealed the various extensions of ventricular tachycardia origin (from 0·5 × 0·5 cm to 2·0 × 2·0 cm) in which the earliest local electrogram was recorded during ventricular tachycardia. In all five tachycardias from a relatively wider origin (more than 0·5 × 0·5 cm) and in four of eight from a narrow origin (< 0·5 × 0·5 cm), subtle morphological variation in the VT-QRS complexes was observed. In tachycardias with morphological variation, the local electrogram at the tachycardia origin also showed concomitant variation in morphology and activation sequence. Ventricular tachycardia from a narrow site was eliminated by RF ablation to the confined site, but a larger number of RF applications was required in tachycardias from a wider origin. All 13 tachycardias were successfully ablated by RF current, and during the follow up period of 28·2 (SD 7·2) months, recurrence was observed in only one patient who had a wider origin.ConclusionsLong term efficacy of RF ablation was excellent in idiopathic ventricular tachycardia originating from the outflow tract of the right ventricle. Subtle morphological variations were frequently observed in this type of ventricular tachycardia, and about half of them represented a relatively wider arrhythmogenic area.

An electrophysiologic study was attempted in a patient who experienced cardiac arrest. Programmed electrical stimulation from the right ventricle, without the use of any drugs, induced ventricular fibrillation (VF) twice. Disopyramide prevented the induction of ventricular arrhythmia by rendering VF to a nonsustained polymorphic ventricular tachycardia when administered at 300 mg/day, and noninducible at 400 mg/day. However, ST-segment elevation and the rSr' pattern in leads V"1"-"3 characteristic of Brugada syndrome became exaggerated by disopyramide. Disopyramide exerted discrepant action on the electrocardiographic (ECG) abnormalities and induction of VF in this patient, suggesting the efficacy of antiarrhythmic drugs assessed by an electrophysiologic study may be unrelated to ECG abnormalities in cases of Brugada syndrome.

A 41 year old man with incomplete right bundle branch block and persistent coved-type ST elevation in the right precordial leads during sinus rhythm had an episode of syncope while driving. He had never had syncope before and there was no family history of sudden cardiac death. Ventricular fibrillation was induced during electrophysiological study (EPS) by double extrastimuli applied to the right ventricle. Disopyramide was effective in preventing ventricular fibrillation during EPS. β Adrenoceptor stimulation manifested bifid T waves and reduced ST segment elevation in right precordial leads. Simultaneously recorded monophasic action potential (MAP) duration at 90% repolarisation did not change in the right ventricular outflow tract, while it shortened in the left ventricular septum. These findings suggest that right precordial bifid T waves might result from relatively early repolarisation of the left ventricles. Moreover the gradient of action potential duration might explain the mechanism of ST segment abnormalities in a patient with Brugada syndrome.

A transvenous implantable cardioverter defibrillator (ICD) was implanted into a 58 year old woman with idiopathic dilated cardiomyopathy who had drug refractory monomorphic ventricular tachycardia (VT). Antitachycardia pacing failed to terminate the VT; termination was attempted at 24 J, which was above the defibrillation threshold. When cardioversion at 24 J was delivered, VT with a different morphology and slower rate was reproducibly initiated. At 3 J, however, the original VT was successfully terminated without initiation of the slower VT. A new VT may be induced by high energy cardioversion. This may be a manifestation of the proarrhythmic potential of ICDs.