Fenton1998_MyocardiumVortexDynamics

This a model from the article:
Vortex dynamics in three-dimensional continuous myocardium with fiber rotation:
Filament instability and fibrillation.

Fenton F, Karma A. Chaos
1998 Mar;8(1):20-47 12779708
,
Abstract:

Wave propagation in ventricular muscle is rendered highly anisotropic by the
intramural rotation of the fiber. This rotational anisotropy is especially
important because it can produce a twist of electrical vortices, which measures
the rate of rotation (in degree/mm) of activation wavefronts in successive
planes perpendicular to a line of phase singularity, or filament. This twist can
then significantly alter the dynamics of the filament. This paper explores this
dynamics via numerical simulation. After a review of the literature, we present
modeling tools that include: (i) a simplified ionic model with three membrane
currents that approximates well the restitution properties and spiral wave
behavior of more complex ionic models of cardiac action potential (Beeler-Reuter
and others), and (ii) a semi-implicit algorithm for the fast solution of
monodomain cable equations with rotational anisotropy. We then discuss selected
results of a simulation study of vortex dynamics in a parallelepipedal slab of
ventricular muscle of varying wall thickness (S) and fiber rotation rate
(theta(z)). The main finding is that rotational anisotropy generates a
sufficiently large twist to destabilize a single transmural filament and cause a
transition to a wave turbulent state characterized by a high density of
chaotically moving filaments. This instability is manifested by the propagation
of localized disturbances along the filament and has no previously known analog
in isotropic excitable media. These disturbances correspond to highly twisted
and distorted regions of filament, or "twistons," that create vortex rings when
colliding with the natural boundaries of the ventricle. Moreover, when
sufficiently twisted, these rings expand and create additional filaments by
further colliding with boundaries. This instability mechanism is distinct from
the commonly invoked patchy failure or wave breakup that is not observed here
during the initial instability. For modified Beeler-Reuter-like kinetics with
stable reentry in two dimensions, decay into turbulence occurs in the left
ventricle in about one second above a critical wall thickness in the range of
4-6 mm that matches experiment. However this decay is suppressed by uniformly
decreasing excitability. Specific experiments to test these results, and a
method to characterize the filament density during fibrillation are discussed.
Results are contrasted with other mechanisms of fibrillation and future
prospects are summarized. (c)1998 American Institute of Physics.
This model was taken from the CellML repository
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The original model was:
Fenton F, Karma A. (1998) - version05

The original CellML model was created by:
Noble, Penny, J

[e-mail]
Oxford University
Department of Physiology, Anatomy & Genetics
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