Lourenço Wesley de Jesus, Reis Ruy Freitas, Ruiz-Baier Ricardo, Rocha Bernardo Martins, Dos Santos Rodrigo Weber, Lobosco Marcelo
Graduate Program on Computational Modelling, Federal University of Juiz de Fora, Juiz de Fora, Brazil.
Department of Computer Science, Institute of Exact Sciences, Federal University of Juiz de Fora, Juiz de Fora, Brazil.
Front Physiol. 2022 Jul 4;13:888515. doi: 10.3389/fphys.2022.888515. eCollection 2022.
Myocarditis is a general set of mechanisms that manifest themselves into the inflammation of the heart muscle. In 2017, more than 3 million people were affected by this disease worldwide, causing about 47,000 deaths. Many aspects of the origin of this disease are well known, but several important questions regarding the disease remain open. One of them is why some patients develop a significantly localised inflammation while others develop a much more diffuse inflammation, reaching across large portions of the heart. Furthermore, the specific role of the pathogenic agent that causes inflammation as well as the interaction with the immune system in the progression of the disease are still under discussion. Providing answers to these crucial questions can have an important impact on patient treatment. In this scenario, computational methods can aid specialists to understand better the relationships between pathogens and the immune system and elucidate why some patients develop diffuse myocarditis. This paper alters a recently developed model to study the myocardial oedema formation in acute infectious myocarditis. The model describes the finite deformation regime using partial differential equations to represent tissue displacement, fluid pressure, fluid phase, and the concentrations of pathogens and leukocytes. A sensitivity analysis was performed to understand better the influence of the most relevant model parameters on the disease dynamics. The results showed that the poroelastic model could reproduce local and diffuse myocarditis dynamics in simplified and complex geometrical domains.
心肌炎是一组通常表现为心肌炎症的机制。2017年，全球超过300万人受此病影响，导致约47000人死亡。这种疾病起源的许多方面已为人熟知，但关于该疾病仍有几个重要问题悬而未决。其中之一是为什么一些患者会出现明显的局部炎症，而另一些患者则会出现更为弥漫的炎症，累及心脏的大部分区域。此外，引发炎症的病原体的具体作用以及在疾病进展过程中与免疫系统的相互作用仍在讨论之中。回答这些关键问题可能会对患者治疗产生重要影响。在这种情况下，计算方法可以帮助专家更好地理解病原体与免疫系统之间的关系，并阐明为什么一些患者会患上弥漫性心肌炎。本文修改了最近开发的一个模型，以研究急性感染性心肌炎中的心源性水肿形成。该模型使用偏微分方程来描述有限变形状态，以表示组织位移、流体压力、液相以及病原体和白细胞的浓度。进行了敏感性分析，以更好地了解最相关的模型参数对疾病动态的影响。结果表明，多孔弹性模型可以在简化和复杂的几何域中重现局部和弥漫性心肌炎的动态。
