The understanding of cardiac arrhythmia under genetic mutations has grown in interest among researchers. Previous studies focused on the effect of the D172N mutation on electrophysiological behavior. In this study, we analyzed not only the electrophysiological activity but also the mechanical responses during normal sinus rhythm and reentry conditions by using computational modeling. We simulated four different ventricular conditions including normal case of ten Tusscher model 2006 (TTM), wild-type (WT), heterozygous (WT/D172N), and homozygous D172N mutation. The 2D simulation result (in wire-shaped mesh) showed the WT/D172N and D172N mutation shortened the action potential duration by 14%, and by 23%, respectively. The 3D electrophysiological simulation results showed that the electrical wavelength between TTM and WT conditions were identical. Under sinus rhythm condition, the WT/D172N and D172N reduced the pumping efficacy with a lower left ventricle (LV) and aortic pressures, stroke volume, ejection fraction, and cardiac output. Under the reentry conditions, the WT condition has a small probability of reentry. However, in the event of reentry, WT has shown the most severe condition. Furthermore, we found that the position of the rotor or the scroll wave substantially influenced the ventricular pumping efficacy during arrhythmia. If the rotor stays in the LV, it will cause very poor pumping performance. Graphical Abstract A model of a ventricular electromechanical system. This whole model was established to observe the effect of D172N KCNJ2 mutation on ventricular pumping behavior during sinus rhythm and reentry conditions. The model consists of two components; electrical component and mechanical component. The electrophysiological model based on ten Tusscher et al. with the IK1 D172N KCNJ2 mutation, and the myofilament dynamic (cross-bridge) model based on Rice et al. study. The 3D electrical component is a ventricular geometry based on MRI which composed of nodes representing single-cell with electrophysiological activation. The 3D ventricular mechanic is a finite element mesh composed of single-cells myofilament dynamic model. Both components were coupled with Ca2+ concentration. We used Gaussian points for the calcium interpolation from the electrical mesh to the mechanical mesh.

中文翻译：

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D172N KCNJ2突变对窦性心律和折返过程中心室泵的影响的计算预测。

研究人员对遗传突变下的心律不齐的理解越来越感兴趣。先前的研究集中于D172N突变对电生理行为的影响。在这项研究中，我们不仅通过计算模型分析了正常窦性心律和折返条件下的电生理活动，还分析了机械反应。我们模拟了四种不同的心室情况，包括正常情况下的十个Tusscher模型2006（TTM），野生型（WT），杂合子（WT / D172N）和纯合子D172N突变。二维模拟结果（在金属丝网中）显示WT / D172N和D172N突变分别使动作电位持续时间缩短了14％和23％。3D电生理模拟结果表明，TTM和WT条件之间的电波长相同。在窦性心律情况下，WT / D172N和D172N通过降低左心室（LV）和主动脉压力，中风量​​，射血分数和心输出量降低了泵送功效。在再入条件下，WT条件再入的可能性很小。但是，在折返的情况下，WT已显示出最严重的状况。此外，我们发现心律失常期间转子的位置或涡旋波的位置实质上影响了心室的泵送功效。如果转子停留在LV中，将导致非常差的泵送性能。图形摘要心室机电系统的模型。建立整个模型以观察窦性心律和折返条件下D172N KCNJ2突变对心室抽动行为的影响。该模型包括两个部分：电气部件和机械部件。基于十Tusscher等人的电生理模型。IK1 D172N KCNJ2突变，以及基于Rice等人的肌丝动态（跨桥）模型。研究。3D电组件是基于MRI的心室几何结构，由代表具有电生理激活作用的单细胞的节点组成。3D心室力学是由单细胞肌丝动力学模型组成的有限元网格。两种成分都与Ca2 +浓度相关。我们将高斯点用于从电气网格到机械网格的钙插值。3D电组件是基于MRI的心室几何结构，由代表具有电生理激活作用的单细胞的节点组成。3D心室力学是由单细胞肌丝动力学模型组成的有限元网格。两种成分都与Ca2 +浓度相关。我们将高斯点用于从电气网格到机械网格的钙插值。3D电组件是基于MRI的心室几何结构，由代表具有电生理激活作用的单细胞的节点组成。3D心室力学是由单细胞肌丝动力学模型组成的有限元网格。两种成分都与Ca2 +浓度相关。我们将高斯点用于从电气网格到机械网格的钙插值。