Long-Term Changes in Atrial Arrhythmia Burden After Renal Denervation Combined With Pulmonary Vein Isolation: SYMPLICITY-AF.

BACKGROUND

The autonomic nervous system plays an important role in atrial fibrillation (AF) and hypertension. Renal denervation (RDN) lowers blood pressure (BP), but its role in AF is poorly understood.

OBJECTIVES

The purpose of this study was to investigate whether RDN reduces AF recurrence after pulmonary vein isolation (PVI).

METHODS

This study randomized patients from 8 centers (United States, Germany) with drug-refractory AF for treatment with PVI+RDN vs PVI alone. A multielectrode radiofrequency Spyral catheter system was used for RDN. Insertable cardiac monitors were used for continuous rhythm monitoring. The primary efficacy endpoint was ≥2 minutes of AF recurrence or repeat ablation during all follow-up. The secondary endpoints included atrial arrhythmia (AA) burden, discontinuation of class I/III antiarrhythmic drugs, and BP changes from baseline.

RESULTS

A total of 70 patients with AF (52 paroxysmal, 18 persistent) and uncontrolled hypertension were randomized (RDN+PVI, n = 34; PVI, n = 36). At 3.5 years, 26.2% and 21.4% of patients in RDN+PVI and PVI groups, respectively, were free from the primary efficacy endpoint (log rank P = 0.73). Patients with mean ≥1 h/d AA had less daily AA burden after RDN+PVI vs PVI (4.1 hours vs 9.2 hours; P = 0.016). More patients discontinued class I/III antiarrhythmic drugs after RDN+PVI vs PVI (45% vs 14%; P = 0.040). At 1 year, systolic BP changed by -17.8 ± 12.8 mm Hg and -13.7 ± 18.8 mm Hg after RDN+PVI and PVI, respectively (P = 0.43). The composite safety endpoint was not significantly different between groups.

CONCLUSIONS

In patients with AF and uncontrolled BP, RDN+PVI did not prevent AF recurrence more than PVI alone. However, RDN+PVI may reduce AF burden and antiarrhythmic drug usage, but this needs further prospective validation.

Informations de copyright

Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This study was funded by Medtronic. Dr Chinitz has received honoraria from/served as a speaker for Medtronic, Abbott, and Biotronik. Dr Böhm is supported by the Deutsche Forschungsgemeinschaft (German Research Foundation; TTR 219, project number 322900939); and has received personal fees from Abbott, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cytokinetics, Edwards, Medtronic, Novartis, Recor, Servier, and Vifor during the conduct of the study. Dr Saba has received research support from Abbott, Boston Scientific, and Medtronic; and has served on the Advisory board of Boston Scientific and Medtronic. Dr Augostini has served on the Advisory Board of Huxley Medical; and has served as a speaker for Medtronic Corporation and Zoll Respicardia. Dr Kim, Hettrick, and Viktorova are employees at Medtronic. Dr Ukena has received honoraria for lectures and scientific advice from Aurigen Medical, Bayer, Biosense Webster, Boehringer Ingelheim, Medtronic, Pfizer, and ReCor Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.