Two models of anisotropic propagation of cardiac excitation wave

Propagation of the action potential in the real heart is direction-dependent (anisotropic). We propose two general physical models explaining this anisotropy on the cellular level. The first, “delay” model takes into account the frequency of the cell–cell transitions in different directions of propagation, assuming each transition requires some small time interval. The second model relies on the assumption that the action potential transmits to the next cell only from the area at the pole of the previous cell. We estimated parameters of both models by doing optical mapping and fluorescent staining of cardiac cell samples grown on polymer fiber substrate. Both models gave reasonable estimations, but predicted different behavior of anisotropy ratio (ratio of largest and smallest wave velocities) after addition of sodium channels supressor like lidocaine. The results of the experiment on lidocaine effect on anisotropy ratio was in favor of the first, “delay” model. Estimated average cell–cell transition delay was $240\pm80\,\mu$s, which is close to the characteristic values of synaptic delay.