Pharmacological cardioversion as a predictor of left atrial scarring in patients undergoing catheter ablation for persistent atrial fibrillation
M Keseru, K Janosi, D Debreceni, A Ferencz, B Bocz, D Torma, P KupoAbstract
Introduction
Structural remodeling and fibrosis of the left atrium play a pivotal role in the progression of persistent atrial fibrillation (AF) and may influence the response to rhythm-control strategies. Pharmacological cardioversion (PCV) with amiodarone is widely used to restore sinus rhythm before catheter ablation, yet its relationship to the underlying fibrotic substrate remains unclear.
Purpose
We aimed to evaluate the association between left atrial scarring and the success of PCV, and to identify clinical predictors of atrial fibrosis in patients undergoing catheter ablation for persistent AF.
Methods
In this prospective single-center study, 83 patients with persistent AF underwent amiodarone loading followed by PCV; in non-responders, sinus rhythm was restored by electrical cardioversion (ECV). Prior to ablation, high-density electroanatomical mapping was performed to assess left atrial scarring. Patients were classified into a PCV group (successful pharmacological cardioversion) and an ECV group (failed PCV). Clinical variables, mapping characteristics, and 12-month AF recurrence rates were compared.
Results
Left atrial scarring was significantly less common in the PCV group than in the ECV group (56% vs. 78%; p=0.036). In multivariate analysis, successful amiodarone-induced cardioversion was an independent negative predictor of scarring (OR=0.28; 95% CI 0.09–0.87; p=0.027). The presence of atrial scarring was independently associated with older age (OR=1.09; p=0.001) and hypertension (OR=4.50; p=0.012). Procedural parameters and 12-month AF recurrence did not differ significantly between the groups.
Conclusion
Successful PCV with amiodarone, older age, and hypertension independently predict the presence of left atrial scarring. Failure of PCV may serve as a simple clinical marker of an underlying fibrotic substrate in persistent AF.