Targeting the ectopy‐triggering ganglionated plexuses without pulmonary vein isolation prevents atrial fibrillation

• Published in: Journal of cardiovascular electrophysiology Vol. 32; no. 2; pp. 235 - 244
• Main Authors: Sandler, Belinda, Kim, Min‐Young, Sikkel, Markus B., Malcolme‐Lawes, Louisa, Koa‐Wing, Michael, Whinnett, Zachary I., Coyle, Clare, Linton, Nick W. F., Lim, Phang B., Kanagaratnam, Prapa
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.02.2021; John Wiley and Sons Inc
• Subjects: Ablation; Arrhythmia; atrial fibrillation; Atrial Fibrillation - diagnosis; Atrial Fibrillation - surgery; Atrium; autonomic nervous system; Cardiac arrhythmia; Catheter Ablation; Electrocardiography, Ambulatory; Fibrillation; ganglionated plexus; Heart Atria; Humans; Mapping; Original; Patients; pulmonary vein ectopy; Pulmonary Veins - diagnostic imaging; Pulmonary Veins - surgery; Recurrence; Tachycardia; Treatment Outcome; pulmonary vein ectopy; atrial fibrillation; catheter ablation; autonomic nervous system; ganglionated plexus
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1111/jce.14870

Background Ganglionated plexuses (GPs) are implicated in atrial fibrillation (AF). Endocardial high‐frequency stimulation (HFS) delivered within the local atrial refractory period can trigger ectopy and AF from specific GP sites (ET‐GP). The aim of this study was to understand the role of ET‐GP ablation in the treatment of AF. Methods Patients with paroxysmal AF indicated for ablation were recruited. HFS mapping was performed globally around the left atrium to identify ET‐GP. ET‐GP was defined as atrial ectopy or atrial arrhythmia triggered by HFS. All ET‐GP were ablated, and PVs were left electrically connected. Outcomes were compared with a control group receiving pulmonary vein isolation (PVI). Patients were followed‐up for 12 months with multiple 48‐h Holter ECGs. Primary endpoint was ≥30 s AF/atrial tachycardia in ECGs. Results In total, 67 patients were recruited and randomized to ET‐GP ablation (n = 39) or PVI (n = 28). In the ET‐GP ablation group, 103 ± 28 HFS sites were tested per patient, identifying 21 ± 10 (20%) GPs. ET‐GP ablation used 23.3 ± 4.1 kWs total radiofrequency (RF) energy per patient, compared with 55.7 ± 22.7 kWs in PVI (p = <.0001). Duration of procedure was 3.7 ± 1.0 and 3.3 ± 0.7 h in ET‐GP ablation group and PVI, respectively (p = .07). Follow‐up at 12 months showed that 61% and 49% were free from ≥30 s of AF/AT with PVI and ET‐GP ablation respectively (log‐rank p = .27). Conclusions It is feasible to perform detailed global functional mapping with HFS and ablate ET‐GP to prevent AF. This provides direct evidence that ET‐GPs are part of the AF mechanism. The lower RF requirement implies that ET‐GP targets the AF pathway more specifically.