Key result
In a 1D computational model, conduction delay at the Purkinje fibre-ventricular muscle junction increased markedly at the smallest diffusion coefficients and highest loads, risking conduction block.
Computational modeling reveals that conduction delay and failure at the Purkinje fibre-ventricular muscle junction are highly sensitive to intercellular coupling and ventricular muscle load.
Model results flag parameter-sensitive conduction risk at Purkinje-muscle junctions; hypothesis-generating and requires experimental validation before any clinical consideration.
Normally, there is little conduction delay (<0.2 ms) between cells in the heart. However, at the Purkinje fibreventricular muscle junction (PVJ), long conduction delays (5-25 ms) are reported. The PVJ therefore has special conduction properties. In support of this, transitional cells are reported at the PVJ. A 1D model was developed consisting of a string of 49 Purkinje cells, connected to one or two transitional cell, connected to one or more strings of 40 ventricular myocytes (a Purkinje fibre is expected to activate a block of ventricular muscle). Rabbit Purkinje cell and left ventricular myocyte action potential models were used; the Purkinje cell model was also used for the transitional cell. The 1D mono-domain model was used to solve conduction. The diffusion coefficient (D) was set to 0.6 and 0.12 mm 2 /ms for the Purkinje fibre and ventricular muscle to give expected conduction velocities. The effects of (i) the diffusion coefficients between the terminal Purkinje cell and the transitional cell (D1) and between the transitional cell and the first ventricular myocyte (D2) and (ii) the 'load' on the Purkinje fibre (i.e. number of strings of ventricular myocytes) were investigated. The greater D1 (up to ~0.4 mm 2 /ms), the larger the load that could be supported, although further increase in D1 resulted in little further increase. Also the greater D2 (up to ~0.04 mm 2 /ms), the larger the load that could be supported, but in this case a further increase in D2 resulted in a decrease in the load that could be supported. The delay in conduction at the PVJ was dependent on D1, D2 and load and increased markedly at the smallest values of D1 and D2 and the highest loads. At a certain point, a small change could lead to large increase in the delay or even conduction failure.
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Li et al. (2016) studied Conduction delay at the Purkinje fibre-ventricular muscle junction. Variation of diffusion coefficients and load was evaluated on Conduction delay and load supported. In a 1D computational model, conduction delay at the Purkinje fibre-ventricular muscle junction increased markedly at the smallest diffusion coefficients and highest loads, risking conduction block.
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