Targeted epicardial pulsed field ablation of atrial ganglionated plexi: Electrophysiological and histologic analysis in pigs.

Background: Modulation of autonomic nervous system activation by ganglionated plexi (GP) ablation is considered a key component of atrial fibrillation (AF) treatment. Endocardial pulsed field ablation (PFA) has limited impact on epicardially located GPs owing to their significant distance from the endocardium, whereas epicardial PFA delivery directly to GP sites may display antiarrhythmic effects by effective ablation of GPs with minimal collateral myocardial damage.

Objective: This study aimed to determine antiarrhythmic and structural effects of epicardial PFA delivery to atrial GP sites.

Methods: In an open-chest pig model, 5 epicardial GP sites were carefully identified (anatomic landmarks and response to high-frequency stimulation) and targeted by saline-irrigated bipolar PFA (PFA group, n = 6, and sham-operated pigs, n = 2). Atrial epicardial electrogram amplitude, atrial effective refractory period (aERP), AF inducibility, and AF duration were investigated. Immunohistochemical staining was performed on treatment-adjacent structures.

Results: In the PFA group, PFA was successfully delivered to each GP site. Local epicardial electrogram amplitudes did not change after PFA delivery. After PFA treatment, the aERP at the higher and lower lateral right atrium increased by 49 ± 42 ms (P = .036) and 99 ± 42 ms (P = .006), respectively. AF inducibility decreased from 100% to 33% (P = .046), and AF duration decreased from 4.4 ± 0.6 minutes to 1.3 ± 2.1 minutes (P = .007). PFA treatment resulted in a lower S100-protein intensity within GP cytoplasm (-44.8%; P = .003) and GP membrane (-34.9%; P = .004), indicating acute GP damage. The surrounding atrial structures including the neuronal sympathetic network and arteries were spared.

Conclusion: Targeted anatomically and high-frequency stimulation-guided epicardial PFA delivery to GP sites induces acute GP damage, prolongs aERP, and reduces AF inducibility and AF duration while preserving surrounding neuronal, myocardial, and vascular structures.