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In healthy hearts myocytes are typically coupled to nearest neighboursthrough gap junctions. Under pathological conditions such as fibrosis, or inscar tissue, or across ablation lines myocytes can uncouple from theirneighbours. Electrical conduction may still occur via fibroblasts that not onlycouple proximal myocytes but can also couple otherwise unconnected regions. Wehypothesise that such coupling can alter conduction between myocytes viaintroduction of delays or by initiation of premature stimuli that canpotentially result in reentry or conduction blocks. To test this hypothesis wehave developed several $2$-cell motifs and investigated the effect offibroblast mediated electrical coupling between uncoupled myocytes. We haveidentified various regimes of myocyte behaviour that depend on the strength ofgap-junctional conductance, connection topology, and parameters of the myocyteand fibroblast models. These motifs are useful in developing a mechanisticunderstanding of long-distance coupling on myocyte dynamics and enable thecharacterisation of interaction between different features such as myocyte andfibroblast properties, coupling strengths and pacing period. They arecomputationally inexpensive and allow for incorporation of spatial effects suchas conduction velocity. They provide a framework for constructing scar tissueboundaries and enable linking of cellular level interactions with scar inducedarrhythmia.

Fibroblast mediated dynamics in diffusively uncoupled myocytes -- a simulation study using 2-cell motifs