Computational Model Based Approach to Analyze Calcium (Ca2+) Concentration Effects in Ventricular Cells for Action Potential Generation Using Euler Integration Method-A Simulation Study

Abstract

Heart Failure (HF) is one of the major causes in today's industrial world. In that arrhythmias (abnormal electrical activity) is one, which is responsible for generating life threatening arrhythmias like ventricular tachycardia and fibrillation. In this article, analyse the Calcium (Ca2+) ion con- centration effects in ventriular cells for normal and arrhythmic conditions using a computational approach. Ten Tusscher's (TT) model of the human endocardial cell was used to generate single Action Potential (AP) based on Han's experimental data. In that we modified the data to describe the properties of Ca2+tr ansient process currents and their channel dynamics in TT models. Different channel failure conditions in the same group (n= 50) samples of TT models are used to analyse by using the Euler integration method. The normal intracellular Ca2+ concentration (Ca2+i) value is 0.0002mM, which having AP mean values in the range of + 15millivolt to -85millivolt but for dif-ferent abnormal such as (10%=0.00022mM, 2S%=0.00022SmM, 50%=0.0003mM, 100%=0.0004mM) having AP of mean values like (10%=17mV to -82mV, 25%=18mV to -82mV, 50%=19mV to -81mV, 100%=20mV to -80mV) Similarly, extracellular Ca2+ Concentration (Ca2+o) value is 2mM, which having AP mean values in the range of + 15millivolt to -85millivolt but for different abnormal such as (1 0 %=2.02mM., 25%=2.5mM, 50%=3mM, 5100%=4mM) having AP of mean values like (10%=17mV to - 80mV, 25%=20mV to -77mV, 50%=25mV to -75mV, 100%=35mV to -70m V). Excitation-Contraction (EC) coupling (electrical dis-turbances) can occur when a cardiac myocyte's Ca2+ homeostasis is disrupted. This type of Ca2+ homeostasis failure will cause abnormal Ca2+Induced and Ca2+ Release Process (CICR) and Ca2+transient processes. Ventricular myocyte electrical instabil-ity to intracellular Ca2+ handling disorders to inherited and acquired arrhythmias.