Computational modeling demonstrates that fibroblast resting potential plays a critical role in modulating spiral wave stability and arrhythmogenesis in cardiac tissue.
Does not yet inform clinical arrhythmia management; leaves open whether fibroblast resting potential modulates reentry in vivo.
We consider a three-domain model of cardiac tissue consisting of fibroblasts, myocytes, and extracellular space. We show in the one dimensional case that the fibroblasts with different resting potentials may alter restitution properties of tissue. On this basis we demonstrated that in two dimensional slice of cardiac tissue, a spiral wave break up can be caused purely by the influence of fibroblasts and, vice-versa, initially unstable spiral can be stabilized by fibroblasts depending on the value of their resting potential.
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Petrov et al. (2010) studied this question.
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