Key result
Distributed conduction inhomogeneities at ~10% to 20% reduce scroll wavelength and trigger wave breakup.
Why the study?
Technical limitations prevent in situ visualization of abnormal electrical scroll waves associated with VT and VF, necessitating in silico simulations to understand their dynamics.
In silico simulations demonstrate that localized conduction and ionic inhomogeneities in canine ventricular tissue models can suppress scroll-wave break up, suggesting they are less arrhythmogenic than in porcine models.
Localized inhomogeneities may suppress reentry in ventricular models; leaves open translation to human arrhythmia mechanisms.
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 (≃ 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 localized, 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 (Majumder et al., 2016) has shown that the inhomogeneity-induced suppression of scroll waves is a rare occurrence.
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Rajany et al. (2021) studied Ventricular tachycardia and ventricular fibrillation (in silico canine ventricular model). Conduction and ionic inhomogeneities (localized spherical or distributed at 5%, 10%, and 20% concentrations) vs. Homogeneous canine ventricular tissue simulation without inhomogeneities was evaluated on Scroll-wave dynamics and wave break-up. Distributed conduction inhomogeneities at 10%-20% concentrations significantly reduced scroll wavelength and induced wave breakup, whereas localized and ionic inhomogeneities suppressed breakup.
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