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

Abstract

Background

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.

Case summary

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.

Discussion

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.

Introduction

The left ventricular (LV) summit, the highest point of the LV epicardium, is a triangular region near the bifurcation of the left anterior descending and the left circumflex coronary arteries.¹ Because of these anatomical limitations, the detailed mapping is difficult. Therefore, the mechanism of ventricular tachycardia (VT) originating from LV summit is not well understood. In this case, by entrainment technique, we revealed the re-entrant mechanism of the VTs with the slow conducting zone at the LV summit area.

Summary figure

Case presentation

A 70-year-old man was transferred for out-of-hospital cardiopulmonary arrest due to ventricular fibrillation and received an implantable cardioverter-defibrillator (ICD) 8 years ago. He was referred for palpitation to our hospital with a VT of left bundle branch block (LBBB) configuration and inferior axis deviation with a heart rate of 115 b.p.m., which was below the VT zone of the ICD. The VT was recurrent, so he had 1st radiofrequency catheter ablation (RFCA). Two types of VTs with right bundle branch block (RBBB) and LBBB morphologies originating from the LV summit were recognized (Figure 1; VT1 and VT2). The cycle length of two VTs was ∼500 ms. The VT1 was terminated with RFCA at the left coronary cusp (LCC). However, 9 months later, the VT recurred, so he had 2nd RFCA. The cycle length of the VT was 640 ms with some changes of the LBBB morphology (VT3) (Figure 1).

Two decapolar catheters were positioned in the right ventricular outflow tract (RVOT) and in the His bundle-Right ventricular apex (RVA), respectively. Another decapolar catheter with an inner lumen was inserted from the internal jugular vein and placed in the coronary sinus, and a 2 Fr micro-catheter was positioned in the anterior intraventricular vein (AIV) through the lumen. The electrograms in the AIV catheter showed fragmentation (Fg) that preceded the QRS onset by 47 and 30 ms during the VT3 and VT2 (Figure 2A and B). Pacing from the RVA entrained these two VTs with constant and progressive fusion (Figure 1). During the entrainment pacing with a stimulus interval of 560 ms, the fragmented potentials in the AIV catheter were activated orthodromically and those in the His bundle were activated antidromically (Figure 2A). During the VT2, a far field potential, which appeared to be intramural potential, was recorded 138 ms later than a near field potential in distal electrodes of the RVOT (Figure 2B), whereas during the VT3, the sequence of these potentials was reversed with a conduction time of 110 ms between two potentials (Figure 2A), indicating intramural VT substrate.² Moreover, a similar potential was observed during the VT1 in the distal electrodes of a catheter placed in the LCC at the 1st session (Figure 2C). These observations indicated the two VTs originated from the LV summit with a re-entrant mechanism, the exit of which was the right ventricle for VT2 and left ventricle for VT3.

Radiofrequency catheter ablation was neither effective at the LV endocardium just below the aortic sinus cusp, where the electrogram occurred 35 ms earlier from the onset of QRS complex during the VT3 (Figure 3A, left), nor at the RVOT, where a good pace-map of the VT2 was obtained (not showed). So, an irrigated ablation catheter was inserted to the AIV, where the electrogram preceded the onset of QRS by 46 ms (Figure 3A, right). At this site, RFCA with an energy of 25 W terminated the VT3. However, the VT3 was still inducible. We thus applied bipolar radiofrequency ablation between the LV endocardium and AIV. We used the T-cable to create a bipolar radiofrequency ablation circuit using the standard unipolar ablation equipment:³ A 3.5 mm tip irrigated catheter (FlexAbility™, SE, Abbott) in the LV endocardium that was connected to the ground/impedance port, and another 3.5 mm tip irrigated catheter (ThermoCool SmartTouch, Biosense-Webster, CA, USA) in AIV, which was connected to the active/ablation port. The impedance in the AIV catheter was high. Therefore, we raised the upper limit up to 250 Ω and increased an irrigation flow rate (from 15/min to 28 mL/min). We then delivered an initial energy of 15 W and gradually increased it up to 25 W with careful monitoring in case of sudden impedance drop. Decrease in the impedance during the energy delivery for 75 s was 25 Ω (Figure 3B). After three bipolar RF applications, the VTs became non-inducible.

Discussion

A non-re-entrant mechanism, such as abnormal automaticity or triggered activity, is considered to be operative in the non-sustained VT/premature ventricular contractions originating from the LV summit area. This is because the majority occurred spontaneously or was induced during isoproterenol infusion, but could not be induced by programmed stimulation.⁴ In contrast, some patients had idiopathic sustained LV summit VTs with multiple morphologies, i.e. LBBB and RBBB configurations, which could be induced by programmed stimulation.^5,6 The preferential conduction to the RVOT and LVOT from a single intramural origin might have produced the multiple VTs.⁶ However, proof of the mechanism of sustained VTs originating from the LV summit area is lacking, probably because of the intramural or subepicardial origin that is inaccessible to the mapping catheter.

In our case, during the VT2 and VT3, the fragmented potential that preceded the QRS onset was observed in the AIV catheter. By entrainment pacing from the RVA, this fragmentation and the far field potential in the RVOT were activated orthodromically, whereas the ventricular electrogram in the His bundle area were activated antidromically (Figure 2A). This phenomenon can be translated into the constant fusion and progressive fusion (Figure 1), thereby confirming a re-entrant mechanism. Interestingly, we also observed a double potential, which was a far field and near field potential, in the distal electrodes of a catheter placed in the RVOT and LCC. During the VT1 and VT3 with RBBB morphology, the far field potential was preceded to the near field potential, whereas during the VT2 with LBBB morphology, the sequence of these potentials was reversed. The conduction time between these two potentials was more than 100 ms, which indicated intramural VT substrate.^2,7 For this reason, we needed to performed a bipolar ablation to eliminate the VTs.

Lead author biography

Masahiro Toba graduated from Toyama University in 2011, and he was a senior resident in the Department of Cardiovascular Medicine at Sapporo City General Hospital from 2013–16. Currently, he is a staff cardiologist at the same hospital. His area of interest is cardiac electrophysiology including catheter ablation of ventricular arrhythmias.

Consent: The patient consented to the publication of his case in the scientific literature in accordance with COPE guidelines.

Funding: None declared.

Data availability

The data underlying this article are available in the article.

References

Author notes