Structural contributions to fibrillatory rotors in a patient-derived computational model of the atria
Year: 2014
Type: article
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.
Source: EP Europace
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: G1331081088, The Maintenance of Human Atrial Fibrillation, G1621881903, G1778270432, G214752006, G2635291395, G3396716915, Multi-Scale Modeling of the Failing Heart for Cardiac Rysynchronization Therapy, NATIONAL BIOMEDICAL COMPUTATION RESOURCE, Multi-scale Systems Model of Murine Heart Failure, G793309042, G8112278214, G8172343151, G8586407002, Medical Scientist Training Program, G9000304218, G9000318651, Training in Multi-scale Analysis of Biological Structure and Function
OpenAlex ID: W2093847362
