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The adult heart is composed of a dense network of cardiomyocytes surrounded by nonmyocytes, the mostabundant of which are cardiac fibroblasts. Several cardiac diseases, such as myocardial infarction or dilatedcardiomyopathy, are associated with an increased density of fibroblasts, that is, fibrosis. Fibroblasts play asignificant role in the development of electrical and mechanical dysfunction of the heart; however the underlyingmechanisms are only partially understood. One widely studied mechanism suggests that fibroblasts produceexcess extracellular matrix, resulting in collagenous septa. These collagenous septa slow propagation, causezig-zag conduction paths, and decouple cardiomyocytes resulting in a substrate for arrhythmia. Anotheremerging mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactionswith cardiomyocytes via gap junctions. Due to the challenges of investigating fibroblast-myocyte coupling innative cardiac tissue, computational modeling and in vitro experiments have facilitated the investigation into themechanisms underlying fibroblast-mediated changes in cardiomyocyte action potential morphology, conductionvelocity, spontaneous excitability, and vulnerability to reentry. In this paper, we summarize the major findings ofthe existing computational studies investigating the implications of fibroblast-myocyte interactions in the normaland diseased heart. We then present investigations from our group into the potential role of voltage-dependentgap junctions in fibroblast-myocyte interactions.

Computational Approaches to Understanding the Role of Fibroblast-Myocyte Interactions in Cardiac Arrhythmogenesis