Aims: Neurally meditated reflex or neurocardiogenic or vasovagal syncope (NMS) is usually mediated by a massive vagal reflex. This study reports the long-term outcome of NMS therapy based on endocardial radiofrequency (RF) catheter ablation of the cardiac vagal nervous system aiming permanent attenuation or elimination of the cardioinhibitory reflex (cardioneuroablation).
Methods and results: A total of 43 patients (18F/25M, 32.9 ± 15 years) without apparent cardiopathy (left ventricular ejection fraction=68.6 ± 5%) were included. All had recurrent NMS (4.7 ± 2 syncope/patient) with important cardioinhibition (pauses=13.5 ± 13 s) at head-up tilt test (HUT), normal electrocardiogram (ECG), and normal atropine test (AT). The patients underwent atrial endocardial RF ablation using spectral mapping to track the neurocardiac interface (AF Nest Mapping). The follow-up (FU) consisted of clinical evaluation, ECG (1 month/every 6 months/or symptoms), Holter (every 6 months/or symptoms), HUT (≥ 4 months/or symptoms), and AT (end of ablation and ≥ 6 months). A total of 44 ablations (48 ± 9 points/patient) were performed. Merely three cases of spontaneous syncope occurred in 45.1 ± 22 months (two vasodepressor, one undefined). Only four partial cardioinhibitory responses occurred in post-ablation HUT without pauses or asystole (sinus bradycardia). Long-term AT (21.7 ± 11 months post) was negative in 33 (76.7%, P < 0.01), partially positive in 7(16.3%), and normal in three patients only (6.9%) reflecting long-term vagal denervation (AT-Δ%HR pre 79.4% × 23.2% post). The post-ablation stress test and Holter showed no abnormalities. No major complications occurred.
Conclusion: Endocardial RF catheter ablation of severe neurally meditated reflex syncope prevented pacemaker implantation and showed excellent long-term results in well selected patients. Despite no action in vasodepression it seems to cause enough long-term vagal reflex attenuation, eliminating the cardioinhibition, and keeping most patients asymptomatic. Indication was based on clinical symptoms, reproduction of severe cardioinhibitory syncope, and normal atropine response.