(376e) Effects of Thermal Stress on the Mechanical Deformation of Cardiac Tissue

The electrophysiological changes initiate mechanical contraction in the cardiac tissue via excitation contraction coupling (ECC) while changes in tissue length affect the electrical activity, via stretch-activated channels (SACs) which is known as mechanoelectrical feedback (MEF) (Kiseleva I et al., 2000). Under certain conditions of abnormal mechanical deformations of tissue, MEF induce local electrical depolarizations that can lead to cardiac arrhythmias (Nazir S A, 1996b; Kuijpers et al., 2007), which may lead to sudden cardiac death and ventricular fibrillation.

Nash-Panfilov (NP) model (Nash and Panfilov, 2004) is mostly used to represent electromechanical coupling and takes into account both electrical and mechanical properties of cardiac tissue to link the excitation with contraction. This model includes an additional variable to represent an instance of active stress responsible for mechanical deformation and is coupled to the mathematical equation describing the tissue's mechanics model. A Mooney–Rivlin type model is used to describe the passive mechanical properties of the cardiac tissue. In addition to electromechanical features within cardiac tissue one needs to consider thermal effects associated with cardiac system. In particular, the effect of temperature in electrophysiology has been studied using experimental settings (Collins and Rojas, 1982; Sitsapesan et al., 1991). However, the effect of temperature on cardiac electrocardiology has been limited to the cell mathematical models. Recent works have included the effect of temperature in FitzHugh-Nagumo (FHN) and Hodgkin–Huxley mathematical model representing the propagation of neural signal taking into account dynamical heat transfer within biological tissue.

In this study, we illustrate the role of thermal stress, induced by the effects of the temperature variations, on the mechanical deformation of the cardiac tissue, adopting a model containing all the key ingredients that account for heat, ECC and  MEF coupling. Numerical examples will be provided to illustrate the effects of the thermal stress on mechanical deformation of the cardiac tissue. This may also serve to demonstrate the influence of thermal stress on the cardiac alternans, which have been shown to be a precursor to arrhythmias.

References:

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Sitsapesan R, Montgomery RA, MacLeod K T, and Williams A J. Sheep cardiac sarcoplasmic reticulum calcium-release channels: modification of conductance and gating by temperature. J. Physiol., 434, 469–488, 1991.

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Echebarria B. Mechano-electric feedback after left ventricular infarction in rats. Cardiovascular research: 45,370 – 378, 2000.

Nazir S A, and Lab M J. Mechanoelectric feedback in the atrium of the isolated guinea-pig heart. Cardiovasc. Res., 32, 112–119, 1996b.

Kuijpers N H, ten Eikelder H M, Bovendeerd, P H, Verheule S, Arts T, and Hilbers P A. Mechanoelectric feedback leads to conduction slowing and block in acutely dilated atria: a modeling study of cardiac electromechanics. Am. J. Physiol. Heart Circ. Physiol., 292, H2832–H2853, 2007.

Nash M P, Panfilov A V. Electromechanical model of excitable tissue to study re-entrant cardiac arrhythmias. Prog. Biophys. Mol. Biol. 85, 501–522, 2004.