**7. Conclusions**

This study presents the first complete electrophysiological mechanism of COVID infected ventricle tissue with and without hypokalemia comorbidities and its responses to HCQ treatment. This model strategically allows more direct studies of ion channel perturbation from clinical observation of infected victims. This study's main conclusion is that when healthy cardiac tissue is infected by COVID, it engenders shorter QT interval, low amplitude or inverted T-waves and ST depression, which could be used as biomarkers. When treated with HCQ, in case of severe COVID-19, there is no significant adverse effect, but in mild COVID-19, QT interval prolongs and T-peak increases in ECG. Secondly, COVID-19 withal to the comorbid cardiac ventricle causes a slight QT interval elongation, notched T-waves *A High Fidelity Transmural Anisotropic Ventricular Tissue Model Function to Investigate… DOI: http://dx.doi.org/10.5772/intechopen.99873*

in hypokalemia1, inverted T-waves in the presence of all severe hypoxia. In particular, the hypokalemic ventricle is prone to arrhythmia in the presence of COVID-19 and the addition of HCQ drug has no significant effects. Increasing the dosage of HCQ has the effect of prolonging the QT interval, and QRS duration and inclusion of AZM magnifies this effect. PVCs could be detected on pacing the tissue with PBs at lower doses of HCQ, and it led to the initiation of reentrant arrhythmia in *severe* COVID-19 conditions. Further, the pacing protocol also determines the appearance of reentry. Thus, the finding of this in-silico model could be considered for HCQ management in patients with pre-existing pathologies.
