Key result
Computational modeling of sinoatrial node cells demonstrated that pacemaking annihilation exists due to subcritical Hopf bifurcation, and intracellular calcium cycling makes pacemaking more robust.
Why the study?
Sinus node arrest is associated with the annihilation of cardiac biological oscillators, but the dynamics of pacemaking annihilation in sinoatrial node cells and tissue required investigation.
Computational modeling reveals that pacemaking annihilation in the sinoatrial node is driven by subcritical Hopf bifurcation and mitigated by intracellular calcium cycling, providing insights into sinus arrest mechanisms.
Hypothesis-generating for sinus node dynamics; leaves open clinical translation and experimental validation.
Sinus node arrest is a dangerous disease, which is associated with the annihilation of the cardiac biological oscillators. The present work investigates in detail the pacemaking annihilation of the modeled single SAN cell and heterogeneous tissue by the conventional nonlinear dynamics approach. It is found that annihilation should generally exist in the SAN system, which is due to the subcritical Hopf bifurcation. However, the annihilation is strict with the stimulus and the physiological parameters, for which the difficulty is estimated. Intracellular calcium cycling makes the pacemaking more robust against annihilation. Furthermore, some general methods for exploring the annihilation dynamics are demonstrated, which may be helpful for the investigations of the other complex biological oscillators. The present work may provide suggestive ideas for the treatments of the sinus arrest and the relevant arrhythmogenesis.
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Li et al. (2018) studied Sinus node arrest. Computational modeling of sinoatrial node cells demonstrated that pacemaking annihilation exists due to subcritical Hopf bifurcation, and intracellular calcium cycling makes pacemaking more robust.
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