Key result
In a computational model, fibroblast proliferation slowed cardiac wave propagation, induced conduction block at 40-45% proliferation, decreased strains in proliferous tissue, and increased dispersions in action potential duration.
Why the study?
Does simulated fibroblast proliferation alter cardiac excitation conduction and mechanical contraction in a computational model?
Does simulated fibroblast proliferation alter cardiac excitation conduction and mechanical contraction in a computational model?
Fibroblast proliferation significantly alters cardiac electromechanical behavior, slowing wave propagation and inducing conduction block in a computational model.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications; leaves open fibroblast roles in human arrhythmogenesis.
In this study, the effects of cardiac fibroblast proliferation on cardiac electric excitation conduction and mechanical contraction were investigated using a proposed integrated myocardial-fibroblastic electromechanical model. At the cellular level, models of the human ventricular myocyte and fibroblast were modified to incorporate a model of cardiac mechanical contraction and cooperativity mechanisms. Cellular electromechanical coupling was realized with a calcium buffer. At the tissue level, electrical excitation conduction was coupled to an elastic mechanics model in which the finite difference method (FDM) was used to solve electrical excitation equations, and the finite element method (FEM) was used to solve mechanics equations. The electromechanical properties of the proposed integrated model were investigated in one or two dimensions under normal and ischemic pathological conditions. Fibroblast proliferation slowed wave propagation, induced a conduction block, decreased strains in the fibroblast proliferous tissue, and increased dispersions in depolarization, repolarization, and action potential duration (APD). It also distorted the wave-front, leading to the initiation and maintenance of re-entry, and resulted in a sustained contraction in the proliferous areas. This study demonstrated the important role that fibroblast proliferation plays in modulating cardiac electromechanical behaviour and which should be considered in planning future heart-modeling studies.
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Zhan et al. (2014) studied Cardiac fibroblast proliferation. Fibroblast proliferation vs. Normal tissue (0% fibroblast proliferation) was evaluated on Cardiac excitation conduction and mechanical contraction (conduction velocity, action potential duration, and strain). In a computational model, fibroblast proliferation slowed cardiac wave propagation, induced conduction block at 40-45% proliferation, decreased strains in proliferous tissue, and increased dispersions in action potential duration.
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