# Bipolar radiofrequency ablation for re-entrant ventricular tachycardia of right bundle branch block and left bundle branch block morphologies with the common slow conduction zone at the left ventricular summit: a case report

## TL;DR

A case report describes using bipolar radiofrequency ablation to treat complex ventricular tachycardia with multiple morphologies originating from the left ventricular summit.

## Contribution

Demonstrates re-entrant mechanism in ventricular tachycardia with multiple morphologies using entrainment pacing and fragmented potentials.

## Key findings

- Fragmented potentials in the anterior intraventricular vein catheter showed orthodromic activation during entrainment pacing.
- Bipolar radiofrequency ablation between the left ventricular endocardium and anterior intraventricular vein eliminated inducibility of tachycardia.
- Two components of ventricular electrogram with over 100 ms interval suggested intramural substrate and slow conduction.

## Abstract

The left ventricular (LV) summit has anatomical limitations, so the detailed mapping is difficult. Therefore, the mechanism of ventricular tachycardia (VT) originating from the LV summit is not well understood.

A 70-year-old man had VTs with right bundle branch block (VT1 and VT3) and left bundle branch block (VT2) morphologies originating from the left ventricular summit (LV summit). During the VT2 and VT3, fragmented potentials, which occurred earlier than the QRS onset, were recorded from bipolar electrodes of a catheter at the anterior intraventricular vein (AIV). By pacing from right ventricular apex, constant and progressive fusion were observed. During the entrainment pacing, the fragmented potentials in the AIV catheter were activated orthodromically and those in the His bundle were activated antidromically. In addition, there were two components of the ventricular electrogram at the LV summit area with the interval of more than 100 ms during the VTs. We performed bipolar radiofrequency ablation between the LV endocardium and AIV, and the VTs became non-inducible.

Non-sustained VT/premature ventricular contraction originating from LV summit is generally considered to occur due to abnormal automaticity or triggered activity. In contrast, using entrainment technique, we demonstrated that the VTs with multiple morphologies were sustained with a re-entrant mechanism. Fragmentated potentials recorded in the AIV catheter were activated orthodromically with the entrainment pacing, indicating the slowly conducting isthmus. The intramural VT substrate was also suggested with a prolonged conduction time between the two ventricular components during the VTs.