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

Damasceno, Thayrine R.; Tanaka, Denise M.; Magnani, Enrico F.; Oliveira, Rafael D. B.; Pereira, Danielle A. G.; Vieira-Alves, Ildernandes; Lemos, Virginia S.; Cabeza, Jorge M.; Fabricio, Camila G.; Resende, Alessandra A.; Gonçalves, Dawit A. P.; Zanetti, Gustavo de Oliveira; Carvalho, Eduardo E. Vieira de; Simões, Marcus V.; Oliveira, Luciano F. L.

doi:10.36660/abc.20230707i

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Original Article • Arq. Bras. Cardiol. 121 (8) • 2024 • https://doi.org/10.36660/abc.20230707i copy

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

Authorship SCIMAGO INSTITUTIONS RANKINGS

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.

Keywords:
Chagas Cardiomyopathy; Myocarditis; Cardiorespiratory Fitness; Exercise; Myocardial Perfusion Imaging

Variables	CT-SED (n=6)	CCC-SED (n=16)	CT-APT (n=8)	CCC-APT (n=12)	p Values
LVEF (%)
Pre	52.93 ± 1.49	45.49 ± 8.84	49.86 ± 2.93	43.74 ± 9.92
Post	52.47 ± 3.59^† † p≤0.05 vs. post-treatment CCC-SED, Bonferroni test for multiple comparisons.	39.69 ± 7.80^* * p<0.05 vs. baseline of the same experimental group,	47.28 ± 5.67^† † p≤0.05 vs. post-treatment CCC-SED, Bonferroni test for multiple comparisons.	42.46 ± 4.47	0.007
LVDD (mm)
Pre	7.71 ± 0.51	7.57 ± 0.70	7.73 ± 0.34	7.71 ± 0.43
Post	7.96 ± 0.56	7.99 ± 1.00	8.22 ± 0.50	8.34 ± 0.60^* * p<0.05 vs. baseline of the same experimental group,	0.030
LVSD (mm)
Pre	5.68 ± 0.43	5.68 ± 0.94	5.99 ± 0.40	6.13 ± 0.54
Post	6.08 ± 0.53	6.06 ± 1.01	6.47 ± 0.81	6.80 ± 0.74	0.050
LV Mass (mg)
Pre	519.19 ± 89.55	549.85 ± 96.73	532.02 ± 98.15	541.89 ± 84.71
Post	667.78 ± 125.04^* * p<0.05 vs. baseline of the same experimental group,	686.99 ± 152.06^* * p<0.05 vs. baseline of the same experimental group,	735.47 ± 170.16^* * p<0.05 vs. baseline of the same experimental group,	622.15 ± 129.83	0.014
MPD (%)
Pre	2.45 ± 1.69	4.64 ± 3.45	3.08 ± 2.56	4.81 ± 3.52
Post	3.31 ± 2.44^† † p≤0.05 vs. post-treatment CCC-SED, Bonferroni test for multiple comparisons.	8.29 ± 7.06^* * p<0.05 vs. baseline of the same experimental group,	2.56 ± 3.43	6.30 ± 3.38	0.010

Variables	CT-SED (n=6)	CCC-SED (n=16)	CT-APT (n=8)	CCC-APT (n=12)	p Values
Time until exaustion (s)
Pre	464.67 ± 32.47	445.21 ± 72.19	494.00 ± 71.25	481.20 ± 76.57
Post	557.50 ± 91.24	539.64 ± 94.04^* * p<0.05 vs. baseline of the same experimental group,	686.78 ± 109.59^* * p<0.05 vs. baseline of the same experimental group, ^† † p≤0.05 vs. post-treatment CCC-SED, Bonferroni test for multiple comparisons.	687.20 ± 141.67^* * p<0.05 vs. baseline of the same experimental group, ^† † p≤0.05 vs. post-treatment CCC-SED, Bonferroni test for multiple comparisons.	0.043
VO_2peak (mL.Kg.min)
Pre	38.50 ± 3.46	42.70 ± 5.45	42.11 ± 4.40	40.32 ± 5.08
Post	43.04 ± 4.90	43.75 ± 4.42	43.33 ± 3.43	45.60 ± 5.65^* * p<0.05 vs. baseline of the same experimental group,	0.254
VO _2@AT (mL.Kg.min)
Pre	31.22 ± 6.79	33.06 ± 5.48	30.12 ± 4.54	30.56 ± 3.25
Post	30.90 ± 6.25	28.95 ± 5.86	33.44 ± 3.96	34.39 ± 4.06^† † p≤0.05 vs. post-treatment CCC-SED, Bonferroni test for multiple comparisons.	0.759

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