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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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