Myocarditis refers to a series of inflammatory processes that affect the heart muscle. In 2017, more than 3 million people worldwide were affected by this condition, resulting in approximately 47.000 deaths. While some aspects of the disease's origin are well understood, many questions remain unanswered. Among them is why some patients develop localized inflammation, while others present it with more diffuse inflammation, affecting larger areas of the heart. Moreover, the specific role of the pathogen causing the inflammation and its interaction with the immune system in the disease's progression remain subjects of debate. Addressing these questions could significantly impact patient treatment. In this context, computational methods can assist specialists in the understanding of the interactions between pathogens and the immune system, contributing to clarifying the scenarios that favor the development of diffuse myocarditis. This work proposes a poroelastic approach to model myocardial edema in cases of acute infectious myocarditis. A system of partial differential equations based on the finite deformation theory is developed, representing tissue displacement, fluid pressure, porosity, and pathogen and leukocyte concentrations. The most influential model parameters were analyzed to identify conditions leading to the development of diffuse myocarditis. Additionally, several experiments were conducted to explore not only the factors impacting edema formation and evolution, but also to assess the model's robustness and limitations. The results indicate that, from a qualitative standpoint, the model can reproduce the disease, considering the dynamics between the pathogen and the immune system, as well as the mechanical response of the myocardium during inflammation in a three-dimensional poroelastic mesh representing the human left ventricle Acknowledgment: FAPEMIG (PCE-00048-25; APQ-02752-24, APQ-02445-24, APQ-02513-22); FINEP SOS Equipamentos 2021 AV02 0062/22; CNPq (423278/2021-5, 310722/2021-7); CAPES, and UFJF.