Exercise Training Reduces Inflammation and Fibrosis and Preserves Myocardial Function and Perfusion in a Model of Chronic Chagas Cardiomyopathy

Author(s):Show less -

Thayrine R. Damasceno ^[1] ; Denise M. Tanaka ^[2] ; Enrico F. Magnani ^[3] ; Rafael D. B. Oliveira ^[4] ; Danielle A. G. Pereira ^[5] ; Ildernandes Vieira-Alves ^[6] ; Virginia S. Lemos ^[7] ; Jorge M. Cabeza ^[8] ; Camila G. Fabricio ^[9] ; Alessandra A. Resende ^[10] ; Dawit A. P. Gonçalves ^[11] ; Gustavo de Oliveira Zanetti ^[12] ; Eduardo E. Vieira de Carvalho ^[13] ; Marcus V. Simões ^[14] ; Luciano F. L. Oliveira

Affiliation:Show less -

^[1] Universidade Federal de Minas Gerais - Brasil

^[2] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto - Brasil

^[3] Universidade Federal de Minas Gerais - Brasil

^[4] Universidade Federal de Minas Gerais - Brasil

^[5] Universidade Federal de Minas Gerais - Brasil

^[6] Universidade Federal de Minas Gerais - Brasil

^[7] Universidade Federal de Minas Gerais - Brasil

^[8] Hospital Israelita Albert Einstein - Brasil

^[9] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto - Brasil

^[10] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto - Brasil

^[11] Universidade Federal de Minas Gerais - Brasil

^[12] Universidade Federal de Minas Gerais - Brasil

^[13] Universidade Federal do Triângulo Mineiro - Brasil

^[14] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto - Brasil

• Document type: Journal article
• Source: Arquivos Brasileiros de Cardiologia; v. 121, n. 8 2024-09-09.

Abstract

Abstract Background: Chronic Chagas cardiomyopathy (CCC) is caused by an inflammatory process induced by Trypanosoma cruzi, which leads to myocarditis with reactive and reparative fibrosis. CCC progresses with myocardial perfusion abnormalities and histopathological events that affect cardiorespiratory fitness (CRF). Objectives: We evaluated the effects of aerobic physical training (APT) on myocardial perfusion and on morphological and functional impairments related with inflammation and fibrosis in Syrian hamsters with CCC. As a secondary objective, we analyzed the cross-sectional areas of the skeletal muscle. Methods: Hamsters with CCC and their respective controls were divided into four groups: CCC sedentary, CCC-APT, sedentary control and APT control. Seven months after infection, the animals underwent echocardiography, myocardial perfusion scintigraphy and cardiopulmonary exercise testing. Moderate-intensity APT was performed for fifty minutes, five times a week, for eight weeks. Subsequently, the animals were reassessed. Histopathological analysis was conducted after the above-mentioned procedures. The level of significance was set at 5% in all analyses (p<0.05). Results: CCC sedentary animals presented worse myocardial perfusion defects (MPD) over time, reduced left ventricle ejection fraction (LVEF) and showed more inflammation and fibrosis when compared to other groups (mixed ANOVA analysis). Conversely, APT was able to mitigate the progression of MPD, ameliorate inflammation and fibrosis and improve CRF efficiency in CCC-APT animals. Conclusions: Our study demonstrated that APT ameliorated cardiac dysfunction, MPD, and reduced inflammation and fibrosis in CCC hamster models. Additionally, CCC-SED animals presented skeletal muscle atrophy while CCC-APT animals showed preserved skeletal muscle CSA. Understanding APT's effects on CCC's pathophysiological dimensions is crucial for future research and therapeutic interventions. (AU)

• FAPESP's process: 16/25403-9 - Investigations on the pathogenesis, pathophysiology and therapy in humans and in an experimental model with the chronic cardiomyopathy of Chagas Disease
• Grantee: José Antonio Marin-Neto
• Support Opportunities: Research Projects - Thematic Grants