J Interv Card Electrophysiol. 2026 May 6. doi: 10.1007/s10840-026-02346-2. Online ahead of print.
ABSTRACT
Persistent atrial fibrillation (PsAF) has a complex and multi-factorial disease substrate. Catheter ablation is a standard treatment but often fails to maintain long-term sinus rhythm. One reason for this failure involves epicardial muscle bundles. Structures like the Marshall bundle, Bachmann bundle, and septopulmonary bundle are usually bypassed during initial endocardial ablation. Current evidence highlights how these epicardial structures modulate the atrial substrate and contribute to arrhythmia recurrence. Animal and human mapping studies indicate that these muscle bundles interact with atrial fibrosis to increase conduction heterogeneity. Their role in maintaining PsAF is modulatory rather than primarily causal. Clinical evidence currently supports targeting the Marshall bundle through ethanol infusion during initial procedures. In contrast, the Bachmann and septopulmonary bundles lack strong evidence as primary targets for PsAF. They mainly act as epicardial bypasses that allow electrical signals to cross incomplete endocardial lesions. This mechanism frequently leads to macro-reentrant atrial tachycardias after the first ablation. Current electroanatomical mapping systems cannot directly visualize these epicardial bundles. Therefore, any ablation targeting them relies on anatomy rather than direct electrical guidance. Recognizing these bundles as contributory factors in the disease process and key pathways in post-ablation recurrence is necessary to guide future transmural ablation strategies.
PMID:42089936 | DOI:10.1007/s10840-026-02346-2

