Matthew J Gonzales1, Kevin P Vincent1, Wouter-Jan Rappel2, Sanjiv M Narayan3, Andrew D McCulloch4. 1. Department of Bioengineering, University of California San Diego, Mail Code 0412, 9500 Gilman Drive, La Jolla, CA 92093-0412, USA. 2. Department of Physics, University of California San Diego, La Jolla, CA, USA Center for Theoretical Biological Physics, University of California San Diego, La Jolla, CA, USA. 3. Department of Medicine, University of California San Diego, La Jolla, CA, USA Cardiac Biomedical Science and Engineering Center, University of California San Diego, CA, USA VA San Diego Healthcare System, San Diego, CA, USA. 4. Department of Bioengineering, University of California San Diego, Mail Code 0412, 9500 Gilman Drive, La Jolla, CA 92093-0412, USA Department of Medicine, University of California San Diego, La Jolla, CA, USA Cardiac Biomedical Science and Engineering Center, University of California San Diego, CA, USA amcculloch@ucsd.edu.
Abstract
AIMS: 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. METHODS AND RESULTS: 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. CONCLUSION: 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. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: The aim of this study was to investigate structural contributions to the maintenance of rotors in humanatrial fibrillation (AF) and possible mechanisms of termination. METHODS AND RESULTS: 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. CONCLUSION: 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. Published on behalf of the European Society of Cardiology. All rights reserved.
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