Elsevier

Heart Rhythm

Volume 4, Issue 9, September 2007, Pages 1177-1182
Heart Rhythm

Original-clinical
Vagal responses induced by endocardial left atrial autonomic ganglion stimulation before and after pulmonary vein antrum isolation for atrial fibrillation

https://doi.org/10.1016/j.hrthm.2007.04.023Get rights and content

Background

Elimination of vagal inputs into the left atrium (LA) may be necessary for successful catheter ablation of atrial fibrillation (AF). These vagal inputs are clustered in autonomic ganglia (AG) that are close to the pulmonary vein antrum (PVA) borders, but whether standard intracardiac echocardiography (ICE)-guided PVA isolation (PVAI) affects these inputs is unknown.

Objective

The purpose of this study was to assess whether standard ICE-guided PVAI affects vagal responses induced by endocardial AG stimulation in the LA.

Methods

Twenty consecutive patients undergoing first-time PVAI (group 1) and 20 consecutive patients undergoing repeat PVAI for AF recurrence (group 2) were enrolled in the study. Before ablation, electrical stimulation (20 Hz, pulse duration 10 ms, voltage range 12–20 V) was performed through an 8-mm-tip ablation catheter. Based on prior data, regions around all four PVA borders were carefully mapped and stimulated to localize AG inputs. A positive stimulated vagal response was defined as atrioventricular (AV) block, asystole, or increase in mean RR interval by >50%. Locations of positive vagal responses were recorded wth biplane fluoroscopy and CARTO. All patients then underwent standard ICE-guided PVAI by an operator blinded to the locations of vagal responses. Stimulation of the AG locations was then repeated postablation.

Results

Patients (age 54 ± 11 years, 30% female, ejection fraction 54% ± 7%) had a history of paroxysmal (75%) and persistent (25%) AF. In group 1, vagal responses were induced in all 20 patients around a mean of 3.8 ± 0.4 PVAs per patient. The most common response was asystole (53%), mean RR slowing >50% (28%), and AV block (20%). Postablation, vagal responses could no longer be induced in all 20 patients. A diminished response was induced (RR slowing <50%) in 2/20 patients around one PVA each. In group 2, vagal responses were not induced in any of the 20 repeat patients. Stimulation capture postablation was confirmed because transient, nonsustained (<30 seconds) AF or atrial flutter was induced in all 40 patients with stimulation, whether vagal responses were induced or not.

Conclusions

Standard ICE-guided PVAI eliminates vagal responses induced by AG stimulation. Responses are not seen in patients presenting for repeat PVAI, despite clinical recurrence of AF.

Introduction

Ever since Armour et al1 reported on the anatomy of the intrinsic cardiac nervous system in humans, it has been suggested that autonomic inputs from ganglionated plexi that surround the heart may contribute to both the initiation and maintenance of atrial fibrillation (AF). High-frequency stimulation of epicardial autonomic plexi can induce triggered activity from the pulmonary veins (PVs)2 and also affect atrial refractory periods to provide a substrate for the conversion of PV firing into sustained AF.3, 4 More specifically, increased vagal tone has been shown to be a trigger for AF in a subset of patients.5 Enhanced vagal tone can increase the inducibility of AF,6 and elimination of vagal inputs may prevent AF recurrence in both animal and patient models of vagal AF.7, 8

Radiofrequency (RF) ablation has emerged as an effective therapy for patients with symptomatic AF. The traditional approach of ablation has been to eliminate all of the triggers for AF by isolating the PVs.9 Recent data has suggested that identification and ablation of autonomic ganglia (AG) during PV isolation may improve long-term success.10 However, it is unknown whether these regions are already modified during standard PV antrum isolation (PVAI). AG responses are also unknown in patients who have AF recurrence postablation. Thus, the purpose of this study was (1) to assess the effects of standard PVAI guided by intracardiac echocardiography (ICE) on vagal responses induced by AG stimulation and (2) to assess vagal responses induced by AG stimulation in patients with AF recurrence after failed PVAI.

Section snippets

Patient population

Twenty consecutive patients undergoing first-time PVAI for symptomatic, drug-refractory AF (group 1) and twenty consecutive patients undergoing repeat-PVAI for late AF recurrences beyond 2 months (group 2) were studied. Only patients with symptomatic paroxysmal or persistent AF were included. All patients had AF that was refractory to at least one antiarrhythmic medication. Patients with prior open-heart cardiac surgery or permanent AF were excluded from the study. All patients gave written

Baseline characteristics

Of the 40 patients studied in groups 1 and 2, most were male (n = 2, 70%) with an average age of 54 ± 11 years. AF was paroxysmal in 30 (75%) patients and persistent in 10 (25%)—14/20 (70%) of group 1 patients and 16/20 (80%) group 2 patients had paroxysmal AF. Mean AF duration preablation was 5.9 ± 4.0 years. Patients had failed 2.2 ± 0.6 antiarrhythmic medications before ablation. Structural heart disease was present in 14 (35%) patients and included hypertensive heart disease (n = 8),

Main findings

This study demonstrates that in patients undergoing a first-time, ICE-guided PVAI procedure, vagal responses can be easily and reliably induced by AG stimulation in predictable anatomical locations in the LA. More importantly, these vagal responses are always eliminated by the standard PVAI lesion set, without specifically targeting these sites. This observation suggests that the success of PVAI in curing AF may, in part, be due to the elimination of these AG inputs in the LA. Alternatively,

Conclusions

Standard ICE-guided PVAI eliminates vagal responses induced by AG stimulation. Vagal responses during ablation do not correlate with vagal responses induced by AG stimulation. Vagal responses with AG stimulation are not seen in patients presenting for repeat PVAI despite clinical recurrence of AF.

References (17)

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Atul Verma is supported by a fellowship award from the Heart and Stroke Foundation of Canada and is currently with Southlake Regional Health Centre, Newmarket, Ontario, Canada.

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