Cardiac pathologies leading to the development of organ fibrosis typically are associated with the appearance of interstitial myofibroblasts. This cell type plays a central role in excessive extracellular matrix deposition, thereby contributing to arrhythmogenic slow and discontinuous conduction by causing disorganization of the three-dimensional network of electrically coupled cardiomyocytes. Besides this involvement in structural remodeling, myofibroblasts recently have been discovered in-vitro to promote arrhythmogenesis by direct modification of cardiomyocyte electrophysiology following establishment of heterocellular electrical coupling. In particular, myofibroblasts were found to rescue impulse conduction between disjoined cardiac tissues by acting as passive electrical conduits for excitatory current flow. Although, in principle, such recovery of blocked conduction might be beneficial, propagation across myofibroblast conduits is substantially delayed, thereby promoting arrhythmogenic slow and discontinuous conduction. Second, moderately polarized myofibroblasts were found to induce cell density-dependent depolarization of cardiomyocytes, which causes arrhythmogenic slow conduction due to the reduction of fast inward currents. Finally, critical depolarization of cardiomyocytes by myofibroblasts was discovered to lead to the appearance of ectopic activity in a model of the infarct border zone. These findings obtained in vitro suggest that electrotonic interactions following gap junctional coupling between myofibroblasts and cardiomyocytes in structurally remodeled fibrotic hearts might directly initiate the main mechanisms underlying arrhythmogenesis, that is, abnormal automaticity and abnormal impulse conduction. If, in the future, similar arrhythmogenic mechanisms can be shown to be operational in intact hearts, myofibroblasts might emerge as a novel noncardiomyocyte target for antiarrhythmic therapy.