Abstract

Simulation of Cellular Remodeling: from Cardiac Myofiber to Whole Heart

Highlights

  • Despite substantial progress in experimental and modeling tools, the understanding of the underlying pathophysiological processes in cardiac tissue is still limited due to the difficulty in direct measurements of the mechanical and electrical processes within the contracting heart

  • One of the most common heart disease conditions is heart failure (HF), which reduces the ability of the heart to pump blood[1]

  • The electrophysiological remodeling under HF condition is associated with action potential (AP) prolongation and altered calcium (Ca2+) handling in animal models and humans[15]

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Summary

Simulation of Cellular Remodeling in the Failing Myocyte

The electrophysiological remodeling under HF condition is associated with action potential (AP) prolongation and altered calcium (Ca2+) handling in animal models and humans[15]. Several human electrophysiological models are capable of simulating these events by changing the maximal conductances or scaling factors of particular ion currents[4,5,6,7]. In these models, the density of the transient outward potassium current (Ito), which contributes significantly to AP prolongation[16], is reduced by 33-60%. Chronic elevation in intracellular Ca2+ resulting from AP prolongation may lead to the maladaptive expression of genes encoding Ca2+-handling proteins [e.g., SERCA, ryanodine receptor (RyR2)]19 In both cases, the muscle contractile process, which involves the interaction of myofilaments (actin and myosin) in the presence of Ca2+, is compromised by impaired Ca2+ handling. There are several multiscale electromechanical models aimed at investigating the effects of HF-induced intracellular remodeling on global ventricular function

Experimental data basis
Conclusions

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