Healthy ventricular myocardium behaves much like a continuous uniform excitable medium, despite its evident discontinuities of structure and function on sub-mm and sub-msec scales. On the basis of this analogy and the corresponding numerical models it has been predicted that myocardium should be vulnerable to a stimulus of certain phase and size which induces reentry in the form of paired vortices in 2 dimensions and vortex filaments in 3 dimensions, independent of the discontinuities and heterogeneity that apparently make diseased tissue more vulnerable. This and related consequences have now been confirmed by electrical stimulation and high-resolution myocardial mapping. The purposes for the next support interval are (1) to explore the implications for 3- dimensional vorticity, both numerically and in collaboration with experimental physiologists, as before; (2) to examine these phenomena through the interpretive lens of the best available electrophysiological model of ventricular myocardial membrane; (3) to understand the development of reentrant tachycardias into fibrillation in terms of the nonlinear dynamics of excitable media, using those electrophysiological membrane models; and (4) to examine possible mechanisms of defibrillation from the theoretical perspective thus consolidated. By computational modelling of specific ionic mechanisms of the particular excitable medium of interest, it should be possible to understand these mechanisms in quantitative detail for the first time. This will allow an understanding and control of membrane properties via altered electric fields.
