Model for the onset of fibrillation following coronary artery occlusion

It is the hypothesis of this article that the onset of fibrillation following a coronary artery occlusion is a direct consequence of the spatial inhomogeneity of chemical processes that occur following the occlusion. In particular, the localized increase of extracellular potassium and decrease of ATP availability lead to an increase of resting potential in the affected cells. This difference in potential between affected cells and normal cells drives a current, the "current of injury," which may drive oscillations in the border zone, a "border zone arrhythmia." The border zone arrhythmia may drive a "breakup instability" (related to the action potential duration restitution instability) in the surrounding tissue, leading to self-sustained fibrillation.

In this article, we present a mathematical model demonstrating this transition from normal to fibrillatory dynamics, describing the general conditions under which this transition occurs and showing in a simple ionic model the way in which spatial inhomogeneity alone can initiate self-sustained reentrant activity.

Using general arguments and numerical simulations with generic models of excitable media, we have demonstrated that a spatial region with an elevated resting potential surrounded by a spatial region wherein action potentials are foreshortened can drive a breakup instability, leading to the rapid initiation of a fibrillatory state.