Why the study?
Spatially and temporally varying excitability is increasingly recognized as an important source of conduction instability in excitable media, but the effects of localized intermittent cellular inactivation on wave propagation remain unclear.
Dynamic functional heterogeneity through intermittent cellular inactivation can independently act as a potent arrhythmogenic substrate for reentrant activity, even without fixed structural obstacles.
May promote reentry via dynamic heterogeneity in models; hypothesis-generating and leaves open clinical translation.
Spatially and temporally varying excitability is increasingly recognized as an important source of conduction instability in excitable media. In this study, we investigate the effects of localized intermittent cellular inactivation on wave propagation using a two-dimensional continuous FitzHugh-Nagumo reaction-diffusion model. A designated region of the medium was subjected to stochastic switching between excitable and weakly excitable states, thereby representing dynamic functional heterogeneity in otherwise homogeneous tissue. Systematic simulations revealed three distinct propagation regimes as a function of the density of intermittently inactive cells within the affected region. At low densities (<4%), planar waves traversed the heterogeneous zone with only minor local distortions and recovered global coherence. At intermediate densities (approximately 4%-18%), localized wave breaks promoted the initiation of persistent spiral activity. At higher densities (>18%), conduction through the heterogeneous region was severely disrupted, leading to wavefront fragmentation and failure of coherent propagation. These results show that temporally fluctuating local inactivation, even in the absence of fixed anatomical obstacles or deterministic ectopic drivers, is sufficient in this model to generate threshold-dependent transitions from stable propagation to reentrant-like dynamics. The findings support the idea that dynamic functional heterogeneity may provide a plausible mechanistic substrate for arrhythmogenic wave instability in cardiac-like excitable media, such as atrial fibrillation (AF), and motivate further investigation in more physiologically detailed models.
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Biton et al. (2026) studied Cardiac arrhythmias (computational model). Localized intermittent cellular inactivation vs. Varying densities of inactive cells and homogeneous tissue was evaluated on Wave propagation regimes as a function of intermittently inactive cell density.
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