title: Representing cardiac bidomain bath-loading effects by an augmented monodomain approach: application to complex ventricular models.
abstract: Although the cardiac bidomain model has been widely used in the simulation of electrical activation, its relatively computationally expensive nature means that monodomain approaches are generally required for long-duration simulations (for example, investigations of arrhythmia mechanisms). However, the presence of a conducting bath surrounding the tissue is known to induce wavefront curvature (surface leading bulk), a phenomena absent in standard monodomain approaches. Here, we investigate the biophysical origin of the bidomain bath-loading induced wavefront curvature and present a novel augmented monodomain-equivalent bidomain approach faithfully replicating all aspects of bidomain wavefront morphology and conduction velocity, but with a fraction of the computational cost. Bath-loading effects are shown to be highly dependent upon specific conductivity parameters, but less dependent upon the thickness or conductivity of the surrounding bath, with even relatively thin surrounding fluid layers (~ 0.1 mm) producing significant wavefront curvature in bidomain simulations. We demonstrate that our augmented monodomain approach can be easily adapted for different conductivity sets and applied to anatomically complex models, thus facilitating fast and accurate simulation of cardiac wavefront dynamics during long-duration simulations, further aiding the faithful comparison of simulations with experiments.
authors.affiliation: Computing Laboratory, University of Oxford, Oxford OX1 3QD, UK. martin.bishop@comlab.ox.ac.uk
authors.forename: Martin J
authors.initials: MJ
authors.lastname: Bishop
authors.forename: Gernot
authors.initials: G
authors.lastname: Plank
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D018780:Body Surface Potential Mapping / Q000379:methods*; D003198:Computer Simulation; D020342:Finite Element Analysis; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008955:Models, Cardiovascular; D016277:Ventricular Function, Left / Q000502:physiology*