Abstract

Computational modeling of tissue-scale cardiac electrophysiology requires numerically converged solutions to avoid spurious artifacts. The steep gradients inherent to cardiac action potential propagation necessitate fine spatial scales and therefore a substantial computational burden. The use of high-order interpolation methods has previously been proposed for these simulations due to their theoretical convergence advantage. In this study, we compare the convergence behavior of linear Lagrange, cubic Hermite, and the newly proposed cubic Hermite-style serendipity interpolation methods for finite element simulations of the cardiac monodomain equation. The high-order methods reach converged solutions with fewer degrees of freedom and longer element edge lengths than traditional linear elements. Additionally, we propose a dimensionless number, the cell Thiele modulus, as a more useful metric for determining solution convergence than element size alone. Finally, we use the cell Thiele modulus to examine convergence criteria for obtaining clinically useful activation patterns for applications such as patient-specific modeling where the total activation time is known a priori.

Highlights

  • Detailed tissue-scale cardiac electrophysiology simulations are commonly used to investigate the dynamics and mechanisms of arrhythmias (Sato et al, 2009; Moreno et al, 2011; Trayanova, 2014) and drive electromechanical simulations (Campbell et al, 2009; Aguado-Sierra et al, 2011; Niederer et al, 2011; Trayanova, 2011)

  • Previous studies had suggested that discretization to a spatial scale of 0.25 mm was sufficient for converged action potential propagation (Cherry and Fenton, 2004; Xie et al, 2004; Clayton and Panfilov, 2008)

  • The “reaction” portion of the monodomain equation is a system of ordinary differential equations (ODEs) that represent the flux of ions across the myocyte membrane, and the “diffusion” portion of the monodomain equation is a partial differential equation (PDE) that represents the spread of current through gap junctions and across cardiac tissue

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Summary

Introduction

Detailed tissue-scale cardiac electrophysiology simulations are commonly used to investigate the dynamics and mechanisms of arrhythmias (Sato et al, 2009; Moreno et al, 2011; Trayanova, 2014) and drive electromechanical simulations (Campbell et al, 2009; Aguado-Sierra et al, 2011; Niederer et al, 2011; Trayanova, 2011). Insufficient spatial resolution can lead to spurious behavior including artifactual breakup of reentrant waves (Krishnamoorthi et al, 2013), a lack of wavebreak (Bueno-Orovio et al, 2008), or pinning of reentrant rotors to the computational grid (Fenton et al, 2002). Niederer et al (2011a) provided a benchmark model for cardiac monodomain electrophysiology solvers that included anisotropic propagation and realistic human ventricular action potential kinetics. Previous studies had suggested that discretization to a spatial scale of 0.25 mm was sufficient for converged action potential propagation (Cherry and Fenton, 2004; Xie et al, 2004; Clayton and Panfilov, 2008).

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