Computational Model based Approach to Analyse Calcium (Ca2+) Channel in Ventricular Cells for Normal and Cardiac Arrhythmias Using Euler Integration Method – A Simulation Study

Sarvepalli Sailesh Babu, G. Gulothungan
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Abstract

Aim: In this paper, analysis of ventricular arrhythmias are made with respect to the Calcium (Ca2+) ion channel dysfunction (generating improper electrical activity). Many cases can make arrhythmias and most of them are related to generation or conduction of Action Potential (AP) in cardiac myocardium. Materials and method: Human ventricular cell based on the model of the human endocardial cell by Ten Tusscher (TT). The TT model data is modified based on the experimental data of Han, describing the properties of Ca2+ currents and its channel dynamics in human ventricular cells. Euler integration method is used to analyse the human ventricular model for different channel failure conditions in the same group of 50 samples. Results: Our research findings focus with respect to normal and deviant Ca2+ conductance (GCaL). The normal GCaL 0.000175nS and deviant GCaL increase like (10%=0.000218nS, 25%=0.000182nS, 50%=0.000262nS and 100%=0.000350nS) having the normal AP average value ranges between 26.0mV to -74.0mV and 12.0mV to -88.0mV for 10% GCaL, 18.0mV to -78.0mV for 25% GCaL, 18.0mV to -78.0mV for 50% GCaL and 21.0mV to -75.0mV for 100% GCaL deviants. Similarly, deviant GCaL decrease like (10%=0.000158nS, 25%=0.000131nS, 50%=0.000088nS and 100%=0.000001nS) having the deviant AP mean values ranges between 10.0mV to -90.0mV for 10% GCaL, 7.0mV to -92.0mV for 25% GCaL, -9.0mV to -96.0mV for 50% GCaL and -51.0mV to 100.0mV for 100% GCaL. Simultaneously its membrane Ca2+ currents are having significant variations. Conclusion: The results show clearly for the affirmation for Excitation and Coupling (EC) failures. EC failures lead to a systole phase that is more prolonged, that in turns to produce QT syndrome and hypertrophic cardiomyopathy.
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基于计算模型的欧拉积分法分析正常和心律失常心室细胞钙离子通道的模拟研究
目的:分析室性心律失常与钙离子通道功能障碍(产生不正常的电活动)的关系。许多病例可发生心律失常,多数与心肌动作电位的产生或传导有关。材料与方法:以Ten Tusscher (TT)的人心内膜细胞模型为基础的人心室细胞。TT模型数据在Han实验数据的基础上进行了修改,描述了Ca2+电流在人心室细胞中的特性及其通道动力学。采用欧拉积分法对同一组50个样本不同通道失效条件下的人体心室模型进行了分析。结果:我们的研究结果集中在正常和异常Ca2+电导(GCaL)方面。正常GCaL值为0.000175nS,异常GCaL值为(10%=0.000218nS, 25%=0.000182nS, 50%=0.000262nS和100%=0.000350nS),正常AP平均值为26.0mV至-74.0mV, 10% GCaL值为12.0mV至-88.0mV, 25% GCaL值为18.0mV至-78.0mV, 50% GCaL值为18.0mV至-78.0mV, 100% GCaL值为21.0mV至-75.0mV。同样地,偏差GCaL的下降幅度为(10%=0.000158nS, 25%=0.000131nS, 50%=0.000088nS和100%=0.000001nS),其中10% GCaL的偏差AP平均值为10.0mV至-90.0mV, 25% GCaL为7.0mV至-92.0mV, 50% GCaL为-9.0mV至-96.0mV, 100% GCaL为-51.0mV至100.0mV。同时,其膜Ca2+电流也有显著的变化。结论:研究结果为激振耦合(EC)失效提供了明确的依据。心电衰竭导致收缩期延长,进而产生QT综合征和肥厚性心肌病。
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Alinteri Journal of Agriculture Sciences
Alinteri Journal of Agriculture Sciences AGRICULTURE, MULTIDISCIPLINARY-
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