Chronic chagasic cardiopathy: the product of a turbulent host-parasite relationship
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1Departamento de Patologia, Instituto do Coraçilo, São Paulo, Brasil.
Insights
Chronic Chagasic cardiopathy pathogenesis is debated. New evidence links Trypanosoma cruzi antigens to myocarditis, suggesting direct parasite involvement rather than solely autoimmune responses.
Area of Science:
- Cardiology
- Infectious Diseases
- Immunology
Background:
- The exact cause of chronic Chagasic cardiopathy remains unclear.
- Early theories suggested an autoimmune basis due to low parasite presence in the heart.
- Recent findings challenge this, pointing towards direct parasite involvement.
Purpose of the Study:
- To review the evolving theories on Chagasic cardiopathy pathogenesis.
- To evaluate the role of the parasite Trypanosoma cruzi in myocardial inflammation.
- To explore the influence of host immune response and other factors.
Main Methods:
- Review of existing literature and theories on Chagasic cardiopathy.
- Analysis of studies utilizing immunohistochemical techniques and PCR.
- Examination of research on cytokine production, microcirculation, and fibrosis.
Main Results:
- Evidence increasingly supports direct participation of Trypanosoma cruzi antigens in myocarditis.
- Cytokine profiles appear crucial in determining disease outcome.
- Microcirculatory changes and fibrosis are significant factors linked to the parasite.
Conclusions:
- Chronic Chagasic cardiopathy likely involves direct parasite influence, not solely autoimmunity.
- The host's immune response efficiency dictates disease progression (indeterminate vs. cardiopathy).
- Further research into parasite-host interactions is essential for understanding and treatment.
Abstract:
The pathogenesis of chronic chagasic cardiopathy is still a debated matter. In this review, the main theories raised about it since the first description of the disease in 1909 by Carlos Chagas, are considered. The scarcity of T.cruzi parasites into the myocardium and the apparent lack of correlation between their presence and the occurrence of myocardial inflammatory infiltrate, have originated many theories indicating that chronic Chagas' cardiopathy is an autoimmune disease. Recently however, papers using immunohistochemical technique or PCR have demonstrated a strong association between moderate or severe myocarditis and presence of T.cruzi Ags, indicating a direct participation of the parasite in the genesis of chronic chagasic myocarditis. Different patterns of cytokine production seem to have important role in the outcome of the disease. Participation of the microcirculatory alterations and fibrosis as well as the relationship with the parasite are also emphasized. Finally, the author suggests that the indeterminate form of the disease occurs when the host immunological response against the parasite is more efficient while the chronic cardiopathy occurs in patients with hyperergic and inefficient immune response.