Key result
In a computational model of cardiac tissue, diffusive inexcitable regions were inherently less arrhythmogenic than zero-flux inexcitable regions for initiating re-entry.
Computational modeling demonstrates that zero-flux inexcitable regions are more arrhythmogenic than diffusive inexcitable regions in initiating re-entry.
Boundary flux influences re-entry in models; leaves open translation to clinical scar-related VT risk.
The detailed mechanisms by which re-entry and ventricular fibrillation are initiated in the heart remain poorly understood because they are difficult to investigate experimentally. We have used a simplified excitable media computational model of action potential propagation to systematically study how re-entry can be produced by diffuse regions of inexcitable tissue. Patterns of excitable and inexcitable tissue were generated using a genetic algorithm. The inexcitable tissue was modeled in two ways: (i) diffusive, electrically connected but inexcitable tissue, or (ii) zero-flux, areas of tissue electrically disconnected in the same way as zero-flux boundary conditions. We were able to evolve patterns of diffuse inexcitable tissue that favored re-entry, but no single structure or pattern emerged. Diffusive inexcitable regions were inherently less arrhythmogenic than zero-flux inexcitable ones.
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Scarle et al. (2006) studied Ventricular fibrillation and re-entry. Computational modeling of inexcitable tissue (diffusive vs zero-flux) was evaluated on Initiation of re-entry. In a computational model of cardiac tissue, diffusive inexcitable regions were inherently less arrhythmogenic than zero-flux inexcitable regions for initiating re-entry.
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