心室肌细胞电生理-力学复合模型在心力衰竭中的仿真研究

目的:研究心力衰竭情况下快速收缩心肌和慢速收缩心肌力学特性的变化及其对心脏电生理的影响。方法:基于心衰心肌生理实验数据建立心室肌细胞电生理-力学复合模型,仿真对比正常和心衰肌细胞内钙离子浓度的变化,进而研究其对细胞收缩力学特性的影响。结果:仿真显示与正常细胞相比,心衰肌细胞电生理特性的变化导致细胞内钙离子浓度降低。进而与肌钙蛋白的钙结合亚单位(TnC)结合的钙离子比正常时大大减小,直接导致细胞收缩力减小。结论:心衰时心室肌细胞的收缩力减小,肌细胞中正常的电力学反馈作用减弱,增大了心室壁细胞动作电位的透壁梯度,从而可能诱发心律失常。仿真结果与文献报道的实验发现一致,将来在组织和器官层次上的心脏建模工作可以整合单细胞的电力学模型,有助于深入研究心力衰竭的病理机制。

Cellular Level Electromechanical Modeling and Simulation of Heart Failure

Objective:To investigate the mutation of cellular mechanical properties of both fast and slow contracting myocytes in heart failure and the effects of heart failure on the mechanical and electrophysiological function of the heart.Methods:By integrating cellular action potential model based on experimental data of heart failure with modified Hunter-McCulloch-ter Keurs(HMT) mechanical heart cell model,an electromechanical cardiac cell model was constructed.Results:The simulation results show that the differences of the electrical responses between failing cells and normal cells can cause slowing relaxation of the Ca~(2 ) transient,and the difference of the Ca~(2 )-TnC concentrations between fast and slow myocytes in failing hearts was more reduced than that in nonfailing hearts.Conclusions:Heart failure results in a decrease of ventricular contracting force,which might diminish the role of mechanoelectric feedback(MEF),then induce an increase of transmural action potential duration(APD) gradients.These might cause arrhythmia in heart failure.These results are in good accordance with experimental findings reported in the literatures and might motivate further research on modeling and simulation of heart failure at the tissue and the whole organ levels.