# Preoperative transcutaneous vagus nerve stimulation as a novel strategy to prevent postoperative atrial fibrillation in calcific aortic valve disease: mechanistic insights and translational perspectives

## TL;DR

Preoperative vagus nerve stimulation may prevent postoperative atrial fibrillation in heart valve patients by balancing the nervous system and reducing inflammation.

## Contribution

This paper proposes preoperative transcutaneous vagus nerve stimulation as a novel preventive strategy for postoperative atrial fibrillation.

## Key findings

- Preoperative tVNS may regulate autonomic nervous system activity and limit perioperative inflammation.
- Mechanistic insights could be obtained through tissue analysis and biomechanical assessments in stimulated versus control groups.

## Abstract

Postoperative atrial fibrillation (POAF) affects 38%–63% of patients undergoing surgical replacement for calcific aortic valve stenosis (CAVS), increasing morbidity, stroke risk, and hospital stay. POAF results from an interplay between pre-existing arrhythmogenic substrates, acute surgical triggers, unresolved inflammation, and autonomic nervous system (ANS) imbalance. Specialized pro-resolving mediators (SPMs) orchestrate inflammation resolution and tissue homeostasis; their deficiency may sustain valvular inflammation and promote arrhythmogenesis. Transcutaneous vagus nerve stimulation (tVNS) is a non-invasive approach that enhances parasympathetic tone, restores sympathovagal balance, and modulates inflammatory pathways. While tVNS has been applied postoperatively, its preoperative, preventive use in POAF has not been explored, representing a novel therapeutic strategy. In patients with CAVS, preoperative tVNS could reduce POAF by regulating ANS activity and limiting perioperative inflammation. Mechanistic insights may be gained through perioperative sampling, analysis of excised valvular and atrial tissue, and biomechanical assessments comparing stimulated and control groups. Preoperative tVNS thus offers a promising strategy to prevent POAF while addressing valvular inflammation, bridging translational physiology with clinical cardiology and potentially opening new avenues for the management of CAVS.