Key result
Macroscopic, insulating heterogeneities such as blood vessels can cause the spontaneous formation of pinned scroll waves that suppress electrical scroll wave turbulence in a cardiac model.
Computational simulations suggest that macroscopic anatomical heterogeneities, such as blood vessels, may play a role in suppressing ventricular fibrillation by pinning scroll waves.
Model results suggest vascular pinning may stabilize reentry; leaves open in vivo relevance and any therapeutic implications.
Electrical scroll wave turbulence in human ventricles is associated with ventricular fibrillation and sudden cardiac death. We perform three-dimensional simulations on the basis of the anisotropic Fenton-Karma model and show that macroscopic, insulating heterogeneities (e.g., blood vessels) can cause the spontaneous formation of pinned scroll waves. The wave field of these vortices is periodic, and their frequencies are sufficiently high to push the free, turbulent vortices into the system boundaries where they annihilate. Our study considers cylindrical heterogeneities with radii in the range of 0.1 to 2 cm that extend either in the transmural or a perpendicular direction. Thick cylinders cause the spontaneous formation of multi-armed rotors according to a radius-dependence that is explained in terms of two-dimensional dynamics. For long cylinders, local pinning contacts spread along the heterogeneity by fast and complex self-wrapping.
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Zhang et al. (2017) studied Ventricular fibrillation. Macroscopic, insulating heterogeneities (e.g., blood vessels) was evaluated on Spontaneous formation of pinned scroll waves and suppression of turbulence. Macroscopic, insulating heterogeneities such as blood vessels can cause the spontaneous formation of pinned scroll waves that suppress electrical scroll wave turbulence in a cardiac model.
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