4.6 Article

A Poroelastic Approach for Modelling Myocardial Oedema in Acute Myocarditis

期刊

FRONTIERS IN PHYSIOLOGY
卷 13, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2022.888515

关键词

myocarditis; oedema formation; computational modelling; computational immunology; large-strain poroelasticity

资金

  1. Universidade Federal de Juiz de Fora (UFJF)
  2. Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) -Brazil [001]
  3. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) -Brazil [423278/2021-5, 308745/2021-3, 310722/2021-7, 315267/2020-8]
  4. Fundacao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG) -Brazil [CEX APQ 1359 02830/17, TEC APQ 03213/17]
  5. Monash Mathematics Research Fund [S05802-3951284]
  6. Ministry of Science and Higher Education of the Russian Federation [075-15-2020-926]

向作者/读者索取更多资源

This paper investigates the formation of myocardial edema in acute infectious myocarditis and modifies a model to describe the associated dynamics. Computational methods can provide insights into the relationship between pathogens and the immune system, shedding light on the variations in myocarditis inflammation among different patients.
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.

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