Maintenance and termination of atrial fibrillation in a patient‐specific model (861.1)

Abstract

Atrial fibrillation (AF) is the most common arrhythmia in the United States and is a risk factor for stroke and cardiac dysfunction. Radiofrequency (RF) ablation has shown great promise for improving outcomes for drug‐resistant AF. However, readmission rates remain high, and improving surgical strategies for targeted RF ablation is subject of intense research. In this study a patient‐specific biatrial finite element model of cardiac electrophysiology is used to explore mechanisms of AF maintenance and termination. Results demonstrate that with normal physiological anisotropy ratios and effective refractory periods (ERPs) of atrial myocytes, free wavelets do not attach to small (~1 cm), inexcitable regions and become rotors. With the depressed excitability, depressed anisotropy, and shorter ERPs present in AF, stationary rotors form around large (>1 cm) inexcitable regions and have a small spatial excitable gap; in contrast, meandering rotors are stabilized by small (<1 cm) inexcitable regions but anchor only transiently to them, colliding with their waveback and drifting until a region of space recovers and allows them to pivot. Based on these results, simulated RF ablation scars could terminate AF by two mechanisms: One, RF lesions increase the inexcitable region size for both meandering and stationary rotors, creating or widening a spatial excitable gap and allowing impingement and extermination of the rotor by an external wave. Two, the RF lesions increase the AF cycle length by increasing the path length of a rotor, in turn both regularizing the atrial activation sequence and decreasing global fractionation, promoting spontaneous termination.Grant Funding Source: Supported by NIH grants HL96544 (ADM), HL083359 (SMN, WJR), and EB009380