• Ademir Batista da Cunha.
• Universidade Federal Fluminense, Instituto Nacional de Cardiología, Rio de Janeiro, Brasil. adanton@uol.com.br
• Rev Port Cardiol. 2003 Jun 1; 22 (6): 813-24.

AbstractChagas' disease is a major endemic disease in Latin America and a great cause for concern due to its high incidence: it afflicts 16 to 18 million individuals and places over 90 million people at risk of infection. At present, five mechanisms can be proposed to explain the pathogenesis of chronic Chagas cardiopathy: 1. direct lesion of the tissue by Trypanosoma cruzi; 2. dysfunction of the autonomic nervous system (neurogenic concept); 3. microvascular disease; 4. immunologic reaction; 5. alterations in the extracellular matrix. The neurogenic concept is the most attractive explanation for the pathogenesis of chronic Chagas cardiopathy through the involvement of the autonomic nervous system, an issue that has been prominent ever since Chagas first initiated research in the field. Köberle, in his pioneering studies on the role of the autonomic nervous system in Chagas patients in the 1950s, adopted the technique of neuron counts, whereby he registered a reduction in parasympathetic nerve cells, and thus considered Chagas cardiopathy a "parasympathetic reduction" with predominance of the sympathetic. In the 1960s, systematic studies on autonomic function, organized by Professor Dalmo Amorim, were initiated in the School of Medicine in Ribeirão Preto. Several aspects of cardiac autonomic control were later described independently by teams in Brazil (Ribeirão Preto and Brasília), Argentina (Cordoba) and Venezuela (Mérida). In general, the studies performed in Ribeirăo Preto by Amorim and Marin Neto and in Brasília by Junqueira Jr. reflected the functional involvement of the parasympathetic system, while the studies performed in Córdoba were linked with the view of cardiovascular sympathetic dysfunction. In Brazil, the involvement of the sympathetic system, with relation to the functional aspect of sympathetic denervation, is well characterized by Marin Neto through the assessment of heart rate using the tilt test in both Chagas and control groups. Further evidence of autonomic nervous system dysfunction in Chagas' disease as a factor modulating complex ventricular arrhythmias was demonstrated by Pedrosa (RJ), who reported on a specific group of chronic Chagas patients with complex ventricular arrhythmias and dilated cardiopathy. In this study, when serum from chronic Chagas patients showing neither complex ventricular arrhythmias nor ventricular dilation was inoculated in isolated rabbit hearts, it produced no harmful effect in the conduction system, in contrast to what was observed in the conduction system of rabbits inoculated with serum from the Chagas patients group with complex ventricular arrhythmias and ventricular dilatation. These facts confirm Carlos Chagas as the pioneer in postulating involvement of the autonomic nervous system in Chagas' disease, and provide an important opportunity to understand ventricular involvement in chronic Chagas cardiopathy.

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