In standard models of cardiac electrophysiology, including the bidomain and
monodomain models, local perturbations can propagate at infinite speed. We
address this unrealistic property by developing a hyperbolic bidomain model
that is based on a generalization of Ohm's law with a Cattaneo-type model for
the fluxes. Further, we obtain a hyperbolic monodomain model in the case that
the intracellular and extracellular conductivity tensors have the same
anisotropy ratio. In one spatial dimension, the hyperbolic monodomain model is
equivalent to a cable model that includes axial inductances, and the relaxation
times of the Cattaneo fluxes are strictly related to these inductances. A
purely linear analysis shows that the inductances are negligible, but models of
cardiac electrophysiology are highly nonlinear, and linear predictions may not
capture the fully nonlinear dynamics. In fact, contrary to the linear analysis,
we show that for simple nonlinear ionic models, an increase in conduction
velocity is obtained for small and moderate values of the relaxation time. A
similar behavior is also demonstrated with biophysically detailed ionic models.
Using the Fenton-Karma model along with a low-order finite element spatial
discretization, we numerically analyze differences between the standard
monodomain model and the hyperbolic monodomain model. In a simple benchmark
test, we show that the propagation of the action potential is strongly
influenced by the alignment of the fibers with respect to the mesh in both the
parabolic and hyperbolic models when using relatively coarse spatial
discretizations. Accurate predictions of the conduction velocity require
computational mesh spacings on the order of a single cardiac cell. We also
compare the two formulations in the case of spiral break up and atrial
fibrillation in an anatomically detailed model of the left atrium, and [...].Comment: 20 pages, 12 figure
