Bilateral cardiac sympathetic denervation of a recurrent refractory ventricular tachycardia occurring after catheter ablation of atrial fibrillation and outflow tract premature ventricular contractions.

Recent studies have demonstrated the utility of cardiac sympathetic denervation (CSD) in patients with ventricular tachycardia (VT) refractory to antiarrhythmic drugs and catheter or surgical ablation. We present our experience with bilateral CSD in a patient with a recurrent VT despite attempts at treatment with catheter ablation and antiarrhythmic drugs, and this is the first description of the successful management of an idiopathic refractory VT with a bilateral CSD and concomitant oral amiodarone, occurring after catheter ablation of persistent atrial fibrillation and idiopathic outflow tract premature ventricular contractions.

INTRODUCTION

Despite the recent advance in catheter ablation of ventricular tachycardia (VT), there remains a subset of patients with VT refractory to catheter ablation and medical therapy. An increased sympathetic tone plays a critical role in such VTs, and autonomic modulation is being employed as a strategy to treat the VTs.

CASE REPORT

A 46‐year‐old female underwent a pulmonary vein isolation (PVI) for persistent atrial fibrillation (AF) and catheter ablation of bigeminal premature ventricular contractions (PVCs) originating from the right ventricular outflow tract (RVOT). Radiofrequency (RF) applications on the septal aspect of the RVOT eliminated the PVC. However, a sustained VT with a cycle length of 320 ms causing syncope occurred 2 weeks after the procedure (Figure 1). The morphology of the VT was identical to that of the prior PVC from the RVOT. Despite RF applications at the RVOT during the second procedure on the day of readmission, the VT recurred immediately after the second procedure. The recurrent VT was refractory to medical therapies including beta blockers, sotalol, and intravenous amiodarone under continuous intravenous sedation. During the third procedure at 15 days after the second procedure, RF applications at the earliest activation site on the left coronary cusp (LCC) failed to suppress the VT, and a bipolar ablation attempted between the RVOT and LCC also failed to eliminate the VT. Since increased sympathetic nerve activity represented by an increased low‐frequency/high‐frequency (LF/HF) ratio of 4.3, a normal range of >2 on the 24‐hour Holter recording, may have been associated with the VT, and a bilateral cardiac sympathetic denervation (CSD), which removed the lower half of the stellate ganglion and T2‐T4 sympathetic ganglia, was performed 17 days after the third procedure. Although non‐sustained VTs recurred with a cycle length of 360 ms within a day after the surgery, the number of nonsustained VT episodes decreased with a suppressed activity of the LF/HF ratio of 1.0, and the resting heart rate during sinus rhythm of 80 bpm decreased to 50 bpm after the surgery. The VT completely disappeared after initiating oral amiodarone of 200 mg 10 days after the CSD (Figure 2), and the patient has been free from any VT for 7 months after the CSD without any complications.

Figure 1

A, Twelve‐lead ECG before the PVI of persistent AF and bigeminal PVCs. B, ECG tracing of the recurrent sustained VT with a cycle length of 320 ms ocurring 2 weeks after the index procedure. Note that the morphology of the VT was left bundle branch block with an inferior axis, which was identical to that of the prior PVC. C, ECG monitor recording of the recurrent VT immediately after the repeat procedure targeting the VT originating from the RVOT. The sustained VT was refractory to medical therapies including beta blockers, sotalol, and intravenous amiodarone under continuous intravenous sedation. AF, atrial fibrillation; PVCs, premature ventricular contractions; PVI, pulmonary vein isolation; RVOT, right ventricular outflow tract; VT, ventricular tachycardia

Figure 2

A, Videoscopic still frame of the video‐assisted thoracic surgical left CSD before the resection of the lower half of the stellate ganglion. B, ECG monitor recording of the recurrent non‐sustained VT within 1 day after the bilataral CSD. C, ECG monitor recording 2 weeks after the bilateral CSD. Note the absence of the VT or PVCs after initiating oral amiodarone of 200 mg 10 days after the surgery. CSD, cardiac sympathetic denervation; PVCs, premature ventricular contractions; VT, ventricular tachycardia

DISCUSSION

CSD has been an established therapy for congenital long QT syndrome and catecholaminergic polymorphic VT.1 Recent studies have demonstrated its utility in the setting of VT storms and VT refractory to antiarrhythmic drugs and catheter or surgical ablation in patients with some forms of cardiomyopathies,2 while the utility of CSD for idiopathic forms of VT has not been as well defined. To the best of our knowledge, this is the first description of the successful management of an idiopathic refractory VT with a combination therapy of bilateral CSD and concomitant oral amiodarone, occurring after catheter ablation of persistent AF and idiopathic outflow tract PVCs. Considering that the VT was refractory to multiple antiarrhythmic drugs, including intravenous amiodarone prior to the CSD, the CSD not only decreased the burden of the VT, but also improved the effect of the amiodarone in suppressing the VT.

In our case, autonomic modulation following the PVI of persistent AF may have promoted the occurrence of the VT. In the study by Patel et al., a minority of patients undergoing PVI developed outflow tract VT or PVCs associated with an increase in the mean heart rate,3 possibly due to the modulation of adjacent autonomic ganglia. Hsieh et al. demonstrated a significant increase in the mean sinus rate and LF/HF ratio of up to 2.4,4 which was much lower than that of 4.3 in our patient, indicating that the elevated sympathetic nerve activity was associated with the occurrence of the sustained refractory VT.

CONFLICT OF INTEREST

The authors declare no conflict of interests for this article.

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