Key result
Coupling endocardial and Purkinje cells slows autorhythmic firing and stabilizes spiral-wave turbulence in modeling.
This computational model demonstrates how Purkinje-myocardium coupling parameters and junction density profoundly influence spiral-wave dynamics, a key mechanism in ventricular arrhythmias.
May guide computational arrhythmia modeling; leaves open whether Purkinje-endocardial coupling modulates clinical ventricular arrhythmias.
We present systematic numerical studies of the possible effects of the coupling of human endocardial and Purkinje cells at cellular and two-dimensional tissue levels. We find that the autorhythmic-activity frequency of the Purkinje cell in a composite decreases with an increase in the coupling strength; this can even eliminate the autorhythmicity. We observe a delay between the beginning of the action potentials of endocardial and Purkinje cells in a composite; such a delay increases as we decrease the diffusive coupling, and eventually a failure of transmission occurs. An increase in the diffusive coupling decreases the slope of the action-potential-duration-restitution curve of an endocardial cell in a composite. By using a minimal model for the Purkinje network, in which we have a two-dimensional, bilayer tissue, with a layer of Purkinje cells on top of a layer of endocardial cells, we can stabilize spiral-wave turbulence; however, for a sparse distribution of Purkinje-ventricular junctions, at which these two layers are coupled, we can also obtain additional focal activity and many complex transient regimes. We also present additional effects resulting from the coupling of Purkinje and endocardial layers and discuss the relation of our results to the studies performed in anatomically accurate models of the Purkinje network.
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Nayak et al. (2017) studied Mathematical model of cardiac arrhythmias. Endocardial and Purkinje cell coupling vs. Uncoupled endocardial and Purkinje cells was evaluated on Autorhythmic-activity frequency and spiral-wave dynamics. Coupling human endocardial and Purkinje cells in a computational model decreased the autorhythmic-activity frequency of Purkinje cells and stabilized spiral-wave turbulence.
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