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Updated: Aug 19, 2026

Isolation and Physiological Analysis of Mouse Cardiomyocytes
Published on: September 7, 2014
Myocardiocyte apoptosis in heart failure in chronic Chagas' disease
Sebastião Tostes1, Denise Bertulucci Rocha-Rodrigues, Gilberto de Araujo Pereira
1Laboratory of Immunology, Faculdade de Medicina do Triângulo Mineiro, Rua Frei Paulino, 30 Uberaba MG 38025-180, Brazil.
Insights
Chagas
Area of Science:
- Cardiology
- Infectious Diseases
- Pathology
Background:
- Chagas' disease, caused by Trypanosoma cruzi, affects millions in South America.
- Cardiac involvement is a primary cause of death in Chagas' disease patients.
- Myocarditis and fibrosis are prominent in chronic Chagas' disease, especially with heart failure.
Purpose of the Study:
- To investigate the role of apoptosis in myocardial cell loss in chronic Chagas' disease.
- To determine if apoptosis contributes to heart failure pathogenesis in Chagas' disease.
- To evaluate apoptosis in both myocardial and inflammatory cells.
Main Methods:
- Analysis of 22 left ventricle autopsy specimens (11 with heart failure, 11 without).
- TUNEL assay to detect early apoptotic events.
- Histopathological evaluation of fibrosis on HE-stained slides.
Main Results:
- Significantly higher levels of fibrosis in patients with heart failure.
- Increased numbers of apoptotic myocardial cells in heart failure patients.
- Elevated apoptotic inflammatory cells observed in heart failure cases.
Conclusions:
- Myocardial cell loss through apoptosis contributes to heart failure in chronic Chagas' disease.
- Fibrosis and apoptosis of myocardial and inflammatory cells are key factors in Chagas' disease heart failure.
- Understanding these mechanisms can inform future therapeutic strategies.
Abstract:
Chagas' disease is caused by the parasite Trypanosoma cruzi. The disease affects 16-18 million patients in South America and heart involvement is the major cause of morbidity and mortality of the disease. The myocarditis observed during the chronic phase affects patients independently of the clinical manifestation, although patients with heart failure present an intense degree of myocarditis and fibrosis. To address the pathogenesis of heart failure in Chagas' disease, we investigated the role of myocardial cell loss by apoptosis in patients in the chronic phase of Chagas' disease. Apoptosis was also evaluated in inflammatory cells. Twenty-two specimens of the left ventricle were obtained during autopsies. Eleven samples from patients with heart failure and equal number from patients without heart failure. The material was analyzed by TUNEL methods to identify early apoptotic events and fibrosis was evaluated on HE-stained slides. In patients with heart failure, the extent of fibrosis and the number of apoptotic myocardial and inflammatory cells were significantly higher than in specimens obtained from patients without heart failure. These results suggest that myocardial cell loss by apoptosis and fibrosis contribute to heart failure in the chronic phase of Chagas' disease.
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