Structural contributions to fibrillatory rotors in a patient-derived computational model of the atria

• Published in: Europace (London, England) England), 2014-11, Vol.16 Suppl 4 (suppl 4), p.iv3-iv10
• Main Authors: Gonzales, Matthew J, Vincent, Kevin P, Rappel, Wouter-Jan, Narayan, Sanjiv M, McCulloch, Andrew D
• Format: Article
• Language: English
• Subjects: Action Potentials; Atrial Fibrillation - diagnosis; Atrial Fibrillation - diagnostic imaging; Atrial Fibrillation - physiopathology; Atrial Fibrillation - therapy; Atrial Function, Right; Computer Simulation; Electrophysiologic Techniques, Cardiac; Fibrosis; Finite Element Analysis; Heart Atria - diagnostic imaging; Heart Atria - pathology; Heart Atria - physiopathology; Humans; Male; Models, Cardiovascular; Predictive Value of Tests; Refractory Period, Electrophysiological; Time Factors; Tomography, X-Ray Computed
• ISSN: 1099-5129; 1532-2092
• DOI: 10.1093/europace/euu251

The aim of this study was to investigate structural contributions to the maintenance of rotors in human atrial fibrillation (AF) and possible mechanisms of termination. A three-dimensional human biatrial finite element model based on patient-derived computed tomography and arrhythmia observed at electrophysiology study was used to study AF. With normal physiological electrical conductivity and effective refractory periods (ERPs), wave break failed to sustain reentrant activity or electrical rotors. With depressed excitability, decreased conduction anisotropy, and shorter ERP characteristic of AF, reentrant rotors were readily maintained. Rotors were transiently or permanently trapped by fibre discontinuities on the lateral wall of the right atrium near the tricuspid valve orifice and adjacent to the crista terminalis, both known sites of right atrial arrhythmias. Modelling inexcitable regions near the rotor tip to simulate fibrosis anchored the rotors, converting the arrhythmia to macro-reentry. Accordingly, increasing the spatial core of inexcitable tissue decreased the frequency of rotation, widened the excitable gap, and enabled an external wave to impinge on the rotor core and displace the source. These model findings highlight the importance of structural features in rotor dynamics and suggest that regions of fibrosis may anchor fibrillatory rotors. Increasing extent of fibrosis and scar may eventually convert fibrillation to excitable gap reentry. Such macro-reentry can then be eliminated by extending the obstacle or by external stimuli that penetrate the excitable gap.