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We agree with Dr. Davila that the pathogenesis and medical treatment of chronic Chagas' disease is complex and warrants further research. In our study, which included only a small number of patients with Chagas' disease, there was no significant difference in sympathetic activation between Chagas and non-Chagas etiologies of heart failure (Fig. 2A of reference 1). This finding is in agreement with some (2,3), but not all (4)prior investigations. Of note, uniquely in our study, efferent muscle sympathetic nerve activity was measured directlyutilizing microneurography, a sensitive and reproducible technique, rather than indirectly with plasma norepinephrine levels. Studies of the sympathetic activation in Chagas' disease, which include patients with and without overt systolic dysfunction, may be able to distinguish between sympathetic dysregulation attributable to T. cruziinfiltration of cardiac nerves/autonomic ganglia and that attributable to the cardiac dysfunction present late in Chagas' disease.
Although many hypotheses have been advanced to explain the sympathetic activation in heart failure, including baroreceptor dysfunction, overactivity of the arterial and/or muscle chemoreceptors, or abnormalities in the “heart failure milicu,” the exact mechanisms have not been established. It remains unknown whether the same mechanisms underlie the sympathetic activation in Chagas' heart disease. Finally, the findings in our study lend support to the concept that, regardless of the etiology of left ventricular dysfunction and heart failure, a chronic exercise regimen is sympatholytic and beneficial. Studies enrolling larger numbers of patients with Chagas' heart disease are underway in our laboratory in the hope of answering this question definitively.
- American College of Cardiology Foundation