Dissipation of the excitation front as a mechanism of self-terminating arrhythmias

I.V. Biktasheva, V.N. Biktashev, W.N. Dawes, A.V. Holden, R.C. Saumarez, A.M. Savill

Submitted to IJBC: Nov. 12, 2002. Accepted: Dec. 11, 2002.

The dissipation of the excitation wavefronts is a specific mechanism of propagation failure if the sharp gradient of the transmembrane voltage at the wavefront smears out and spread of voltage becomes diffusive, as the main excitation current becomes inactivated. This is produced by the normal kinetics of the ionic currents underlying the action potential. Here we demonstrate that the dissipation of the excitation wavefront can cause arrhythmia as well as lead to its self-termination. We use Courtemanche et al. model of human atrial action potential to demonstrate how re-entry creates dynamic electrophysiologic inhomogeneity of the tissue. Local dissipation of the excitation front cause wave breaks and instantaneous displacement of the tip of the re-entry, and the same mechanism can lead to elimination of all wavelets, as the inhomogeneity creates conditions for simultaneous dissipation of their excitation fronts.