The effects of inhomogeneities on scroll-wave dynamics in an anatomically realistic mathematical model for canine ventricular tissue

TL;DR

This study uses detailed simulations of canine heart tissue to explore how electrical and ionic inhomogeneities influence scroll-wave behavior, revealing conditions that promote or suppress arrhythmogenic wave dynamics.

Contribution

It provides new insights into how specific inhomogeneities affect scroll-wave stability and breakup in realistic canine ventricular models, advancing understanding of arrhythmia mechanisms.

Findings

Distributed conduction inhomogeneities decrease scroll wavelength and promote wave breaks.

Localized medium-sized conduction inhomogeneities can suppress wave breaks or stabilize scrolls.

Ionic inhomogeneities generally suppress scroll-wave breakup, with high concentrations causing partial breakup.

Abstract

Ventricular tachycardia (VT) and ventricular fibrillation (VF) are lethal rhythm disorders, which are associated with the occurrence of abnormal electrical scroll waves in the heart. Given the technical limitations of imaging and probing, the in situ visualization of these waves inside cardiac tissue remains a challenge. Therefore, we must, perforce, rely on in-silico simulations of scroll waves in mathematical models for cardiac tissue to develop an understanding of the dynamics of these waves in mammalian hearts. We use direct numerical simulations of the Hund-Rudy-Dynamic (HRD) model, for canine ventricular tissue, to examine the interplay between electrical scroll-waves and conduction and ionic inhomogeneities, in anatomically realistic canine ventricular geometries with muscle-fiber architecture. We find that millimeter-sized, distributed, conduction inhomogeneities cause a substantial decrease in the scroll wavelength, thereby increasing the probability for wave breaks; by contrast, single, localized, medium-sized ($\simeq $ cm) conduction inhomogeneities, exhibit the potential to suppress wave breaks or enable the self-organization of wave fragments into stable, intact scrolls. We show that ionic inhomogeneities, both distributed or localised, suppress scroll-wave break up. The dynamics of a stable rotating wave is not affected significantly by such inhomogeneities, except at high concentrations of distributed inhomogeneities, which can cause a partial break up of scroll waves. Our results indicate that inhomogeneities in the canine ventricular tissue are less arrhythmogenic than inhomogeneities in porcine ventricular tissue, for which an earlier in silico study has shown that the inhomogeneity-induced suppression of scroll waves is a rare occurrence.