Heart rhythm · 2025
Impact of vagal effect on atrial and ventricular refractoriness and atrial fibrillation: A comparative analysis before and after cardioneuroablation.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Pachon-M Jose Carlos, Pachon-M Enrique I, Pachon Carlos Thiene C, Santillana-P Tomas G, Lobo Tasso J, Pachon-M Juan Carlos, Pachon Maria Zelia C, Clark John
Аннотация
BACKGROUND: Extracardiac vagal stimulation (ECVS) provides a simple, reproducible method to study human vagal effects. Although vagus nerve clearly modulates atrial electrophysiology, its influence on human ventricular refractoriness remains uncertain. Likewise, the impact of cardioneuroablation (CNA) on atrial and ventricular refractoriness has not been evaluated in a paired human study OBJECTIVE: This study aimed to quantify the impact of ECVS on atrial (AERP) and ventricular effective refractory periods (VERP) before and after CNA and evaluate a practical atrial fibrillation (AF) ablation functional endpoint.
METHODS: 89 consecutive patients were enrolled (76 paroxysmal AF undergoing pulmonary vein isolation plus CNA; 13 reflex syncope undergoing CNA alone). AERP and VERP were measured at 4 stages: baseline, during ECVS, after CNA, and after CNA during ECVS. AF inducibility was tested at each stage with a single extrastimulus (vagal AF induction test).
RESULTS: ECVS produced marked AERP shortening (right atrium 213.8 ± 25 to 100.6 ± 33 ms; left atrium 235.2 ± 32 to 143.3 ± 32 ms; both P < .001). After CNA, AERP returned toward baseline and was no longer modified by ECVS. In contrast, VERP in both ventricles remained unchanged across all stages (P > .13). AF inducibility rose from 3.4% at baseline to 95.5% during ECVS, then fell to 7.9% during ECVS after CNA (Cochran's Q P < .00001; McNemar P < .00001).
CONCLUSION: Vagal activation is a potent atrial AF trigger, whereas ventricular refractoriness remains unchanged facing ECVS and/or CNA, underscoring chamber-specific autonomic effects and supporting the electrophysiological safety of ECVS and of CNA. ECVS and vagal AF induction test provide objective, reproducible functional end points to guide ablation strategy, confirm atrial vagal denervation, and potentially reduce AF recurrence.
METHODS: 89 consecutive patients were enrolled (76 paroxysmal AF undergoing pulmonary vein isolation plus CNA; 13 reflex syncope undergoing CNA alone). AERP and VERP were measured at 4 stages: baseline, during ECVS, after CNA, and after CNA during ECVS. AF inducibility was tested at each stage with a single extrastimulus (vagal AF induction test).
RESULTS: ECVS produced marked AERP shortening (right atrium 213.8 ± 25 to 100.6 ± 33 ms; left atrium 235.2 ± 32 to 143.3 ± 32 ms; both P < .001). After CNA, AERP returned toward baseline and was no longer modified by ECVS. In contrast, VERP in both ventricles remained unchanged across all stages (P > .13). AF inducibility rose from 3.4% at baseline to 95.5% during ECVS, then fell to 7.9% during ECVS after CNA (Cochran's Q P < .00001; McNemar P < .00001).
CONCLUSION: Vagal activation is a potent atrial AF trigger, whereas ventricular refractoriness remains unchanged facing ECVS and/or CNA, underscoring chamber-specific autonomic effects and supporting the electrophysiological safety of ECVS and of CNA. ECVS and vagal AF induction test provide objective, reproducible functional end points to guide ablation strategy, confirm atrial vagal denervation, and potentially reduce AF recurrence.