Cardiomyocyte dysfunction during the chronic phase of Chagas disease

Roman‐Campos, Danilo; Sales-Junior, Policarpo A.; Duarte, Hugo L.; Gomes, Enéas Ricardo de Morais; Guatimosim, Sílvia; Ropert, Catherine; Gazzinelli, Ricardo T.; Cruz, Jáder Santos

doi:10.1590/0074-0276108022013019

Cited by 18 publications

(39 citation statements)

References 18 publications

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“…Put in perspective, we may suggest that analogous mechanisms cause AP changes in both right and left ventricle myocytes. 9,10 We previously found increased levels of transforming growth factor beta (TGF-β) and tumor necrosis factor alpha (TNF-α) in the myocardium and bloodstream of infected mice during acute and chronic phases. 8,9 TNF-α and TGF-β were previously demonstrated as modulators of ionic currents in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

“…3,[8][9][10] In ventricular cardiomyocytes, I Ca,L is a key player, integrating electrical with mechanical properties. 27 Thus, we evaluated whether I Ca,L was modified in right Figure 8A represents recordings for I Ca,L measured in isolated right ventricular myocytes in control, at 30 dpi, and at 90 dpi.…”

Section: 3mentioning

confidence: 99%

“…2,3 Changes in heart function is connected to a set of cellular and molecular changes in cardiac tissue such as disrupted myofibrils, increased myocyte apoptosis, 4 collagen deposition, 5 oxidative stress, 6 altered cellular metabolism, 7 reduced cellular contractility, 8 and disturbance of electrical properties of the heart. 9,10 There are distinct hypotheses to explain the molecular mechanisms of altered electrical and contractility properties of the heart during Chagas disease. One of the most accepted explanations claims that chronic cytokine production in the heart is responsible for most of the observed cardiac alterations.…”

Section: Introductionmentioning

confidence: 99%

“…2,11 Clinical studies and animal models have shown that right and left ventricles are compromised during the time course of Chagas disease. 3,[8][9][10][12][13][14][15] It is already known that right ventricle function is dysregulated during Chagas disease, however, few studies have pointed out which molecular mechanisms are responsible for right ventricular myocyte dysfunction. 16,17 Herein, using a murine model of Chagas disease, we studied whether the changes in electrical properties of the isolated right ventricular myocyte in acute and chronic phases of the disease are correlated with tissue fibrosis, inflammatory infiltrate, and parasite persistence in the heart.…”

Section: Introductionmentioning

confidence: 99%

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Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Cruz¹,

Santos‐Miranda²,

Sales-Junior³

et al. 2016

The American Journal of Tropical Medicine and Hygiene

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Abstract. Chagas disease, caused by the triatominae Trypanosoma cruzi, is one of the leading causes of heart malfunctioning in Latin America. The cardiac phenotype is observed in 20-30% of infected people 10-40 years after their primary infection. The cardiac complications during Chagas disease range from cardiac arrhythmias to heart failure, with important involvement of the right ventricle. Interestingly, no studies have evaluated the electrical properties of right ventricle myocytes during Chagas disease and correlated them to parasite persistence. Taking advantage of a murine model of Chagas disease, we studied the histological and electrical properties of right ventricle in acute (30 days postinfection [dpi]) and chronic phases (90 dpi) of infected mice with the Colombian strain of T. cruzi and their correlation to parasite persistence. We observed an increase in collagen deposition and inflammatory infiltrate at both 30 and 90 dpi. Furthermore, using reverse transcriptase polymerase chain reaction, we detected parasites at 90 dpi in right and left ventricles. In addition, we observed action potential prolongation and reduced transient outward K + current and L-type Ca 2+ current at 30 and 90 dpi. Taking together, our results demonstrate that T. cruzi infection leads to important modifications in electrical properties associated with inflammatory infiltrate and parasite persistence in mice right ventricle, suggesting a causal role between inflammation, parasite persistence, and altered cardiomyocyte function in Chagas disease. Thus, arrhythmias observed in Chagas disease may be partially related to altered electrical function in right ventricle.

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Section: Discussionmentioning

confidence: 99%

Section: 3mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Cruz¹,

Santos‐Miranda²,

Sales-Junior³

et al. 2016

The American Journal of Tropical Medicine and Hygiene

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“…Rats and mice are the most common species used in experimental cardiac physiology and electrophysiology studies (Zaragoza et al 2011, Nerbonne 2014, Surikow et al 2017. Several disease models including myocardial infarction (Heywood et al 2017), diabetic cardiomyopathy (Bugger & Abel 2009), hypertrophic and dilated cardiomyopathy (Xu et al 2014, Yu et al 2014), Chagas' disease (Roman-Campos et al 2013) and QT syndrome (Drum et al 2014) are well established in such animals. Some number techniques can be used to monitor and characterize cardiovascular pathologies, specially the electrocardiogram (ECG) exam.…”

Section: Introductionmentioning

confidence: 99%

Non-invasive ECG recording and QT interval correction assessment in anesthetized rats and mice

et al. 2019

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Rats and mice are the most common species used in experimental cardiac electrophysiology studies. Electrocardiogram (ECG) recording shows paramount importance for monitoring arrhythmias and cardiac function in several disease models, including QT syndrome. However, the lack of standardized reference values and QT correction formula for different animal species and lineages represent a challenge for ECG interpretation. The aim of this study is to provide an improved method for ECG recording, establishing reference range values and determine the QT formulas with higher correlation to heart rate (HR). A total of 10 Wistar rats, 10 Swiss mice, 10 C57BL/6 mice and 10 FVB/NJ mice were used in the study. Animals were submitted to anesthesia with isoflurane and ECG recording was performed using a six-channel non-invasive electrocardiograph. QT was corrected using the following formulas: Bazzett, Fridericia, Mitchell, Hodges, Van der Water and Framingham. Normal range values for ECG parameters were established in all animals studied. Pearsons’ correlation defined Hodges formula as the most suitable for QT correction. This study demonstrated an improved method of ECG recording with reference values for Swiss, FVB/NJ, C57BL/6 mice, and Wistar rats. Hodges’ formula was the most effective formula for QT correction in rodents, whereas Bazett’s and Friderica formulas were ineffective for such animals. The present work contributes to arrhythmias investigation in experimental cardiology and may reduce misinterpretations in rodents’ ECG.

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Cardiac magnetic resonance imaging in Chagas’ disease: a parallel with electrophysiologic studies

Crane

Rojas

Cooper

et al. 2020

Int J Cardiovasc Imaging

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Cardiomyocyte dysfunction during the chronic phase of Chagas disease

Cited by 18 publications

References 18 publications

Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Non-invasive ECG recording and QT interval correction assessment in anesthetized rats and mice

Cardiac magnetic resonance imaging in Chagas’ disease: a parallel with electrophysiologic studies

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