# Nonlinear diffusion & thermo-electric coupling in a two-variable model of cardiac action potential

## TL;DR

This study investigates how nonlinear diffusion and thermo-electric coupling influence cardiac action potential dynamics, spiral wave breakup, and arrhythmogenesis through numerical simulations of a generalized two-variable model.

## Contribution

It introduces a nonlinear Fickian diffusion formulation and analyzes their combined effects on cardiac wave behavior and fibrillation susceptibility.

## Key findings

- Temperature and nonlinear diffusion affect repolarization patterns.
- Thermo-electric coupling increases arrhythmogenesis risk.
- Spiral wave breakup is influenced by thermal and diffusion nonlinearities.

## Abstract

This work reports the results of the theoretical investigation of nonlinear dynamics and spiral wave breakup in a generalized two-variable model of cardiac action potential accounting for thermo-electric coupling and diffusion nonlinearities. As customary in excitable media, the common Q10 and Moore factors are used to describe thermo-electric feedback in a 10-degrees range. Motivated by the porous nature of the cardiac tissue, in this study we also propose a nonlinear Fickian flux formulated by Taylor expanding the voltage dependent diffusion coefficient up to quadratic terms. A fine tuning of the diffusive parameters is performed a priori to match the conduction velocity of the equivalent cable model. The resulting combined effects are then studied by numerically simulating different stimulation protocols on a one-dimensional cable. Model features are compared in terms of action potential morphology, restitution curves, frequency spectra and spatio-temporal phase differences. Two-dimensional long-run simulations are finally performed to characterize spiral breakup during sustained fibrillation at different thermal states. Temperature and nonlinear diffusion effects are found to impact the repolarization phase of the action potential wave with non-monotone patterns and to increase the propensity of arrhythmogenesis.