Chagas disease, caused by Trypanosoma cruzi, affects around 10 million people, primarily in Latin America. Its acute and chronic phases are unpredictable and may result in fatal myocarditis, with sudden death due to ventricular arrhythmias in up to 60% of cases. The underlying electrophysiological remodeling remains poorly understood, and current treatment relies on non-specific guidelines without disease-specific validation. Studies on cardiomyocytes during acute and chronic stages indicate reduced calcium influx due to attenuated L-type calcium channels, compromising calcium release from the sarcoplasmic reticulum via ryanodine receptors. During diastole, impaired calcium reuptake leads to cytosolic calcium overload. The transient outward potassium current is markedly reduced, while the slow delayed rectifier potassium current is increased. Electrical coupling is also disrupted by decreased connexin-43 expression. In this study, we used a computational model of human ventricular myocytes (O'Hara) and a 2D tissue model to analyze the individual and combined effects of these alterations on cardiac electrophysiology and conduction. Based on experimental data on T. cruzi invasion, simulations were conducted to represent the acute (25% effect), intermediate (50%), and chronic (75%) stages of Chagas disease, corresponding to increasing degrees of remodeling. Preliminary results suggest that T. cruzi induces electrophysiological modifications closely associated with arrhythmogenic processes. These include a 22% action potential duration reduction under combined chronic-stage effects, flattening of the restitution curves, and a 20.4% conduction velocity decrease under the same conditions. The most pronounced effects occur in the chronic stage under combined alterations, with L-type calcium current changes contributing most significantly. This in-silico approach enhances understanding of the electrophysiological impact of Chagas disease across its different stages and supports efforts to improve diagnosis and monitoring.