Modeling and simulation of transmural cellular electromechanical properties in heart failure

Yu Zhang, Guo-fa Shou, Rui Huang, L. Xia
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Abstract

In this paper, we present a simulation study of transmural cellular electromechanical properties in heart failure based on a integrated and refined heart cell model of Luo-Rudy II model and modified Hunter-McCullochter Keurs mechanical model. The results show that prolonged action potential duration (APD) and APD rate-adaptation are more obviously transmurally heterogeneous in heart failure than those in control hearts. The results suggest that the differences of the electrical responses between failing cells and normal cells can cause slowing relaxation of the Ca2+ transient, and the difference of the Ca2+-TnC concentrations between fast and slow myocytes in failing hearts is smaller than in nonfailing hearts. It results in a decrease of force, which might diminish the role of mechanoelectric feedback, and then induce an increase of transmural APD gradient that might cause arrhythmia in heart failure. These results are in good accordance with experimental findings reported in the literatures and this electromechanical cardiac cell model might be very useful for further modeling and simulation of heart failure at both the tissue and the whole organ levels
心力衰竭跨壁细胞机电特性的建模与仿真
在本文中,我们基于一个集成和改进的心脏细胞模型(Luo-Rudy II模型)和改进的Hunter-McCullochter Keurs力学模型,对心力衰竭的跨壁细胞机电特性进行了模拟研究。结果表明,与对照组相比,心衰患者的动作电位持续时间延长(APD)和APD速率适应具有更明显的跨壁异质性。结果表明,衰竭细胞与正常细胞之间的电反应差异可导致Ca2+瞬态松弛减慢,衰竭心脏中快、慢肌细胞Ca2+-TnC浓度的差异小于非衰竭心脏。其结果是力的减小,使机电反馈作用减弱,从而引起跨壁APD梯度增大,引起心力衰竭时心律失常。这些结果与文献报道的实验结果吻合较好,该机电心脏细胞模型可用于进一步在组织和全器官水平上对心力衰竭进行建模和模拟
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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