Abstract
BACKGROUND: Human atrial fibrillation (AF) can terminate after ablating localized regions, which supports the existence of localized rotors (spiral waves) or focal drivers. However, it is unclear why ablation near a spiral wave tip would terminate AF and not anchor reentry. We addressed this question by analyzing competing mechanisms for AF termination in numeric simulations, referenced to clinical observations. METHODS AND RESULTS: Spiral wave reentry was simulated in monodomain 2-dimensional myocyte sheets using clinically realistic rate-dependent values for repolarization and conduction. Heterogeneous models were created by introduction of parameterized variations in tissue excitability. Ablation lesions were applied as nonconducting circular regions. Models confirmed that localized ablation may anchor spiral wave reentry, producing organized tachycardias. Several mechanisms referenced to clinical observations explained termination of AF to sinus rhythm. First, lesions may create an excitable gap vulnerable to invasion by fibrillatory waves. Second, ablation of rotors in regions of low-excitability (from remodeling) produced re-entry in more excitable tissue allowing collision of wavefront and back. Conversely, ablation of rotors in high-excitability regions migrated spiral waves to less excitable tissue, where they detached to collide with nonconducting boundaries. Third, ablation may connect rotors to nonconducting anatomic orifices. Fourth, reentry through slow-conducting channels may terminate if ablation closes these channels. CONCLUSIONS: Limited ablation can terminate AF by several mechanisms. These data shed light on how clinical AF may be sustained in patients' atria, emphasizing heterogeneities in tissue excitability, slow-conducting channels, and obstacles that are increasingly detectable in patients and should be the focus of future translational studies.