Muscle sympathetic nerve activity in patients with Chagas' disease

The progression of heart failure in Chagas' disease has been explained by remodeling, leading to neurohumoral activation, or by the direct parasite damage to parasympathetic neurons during acute phase, leading to early sympathetic activation and progressive heart failure. To help distinguish between these hypotheses we studied muscle sympathetic nerve activity (MSNA) at rest and during handgrip exercise (30% of maximal voluntary contraction) in patients with Chagas' disease and normal ejection fraction vs. patients with heart failure.

A consecutive study of 72 eligible out-patients/subjects was conducted between July 1998 and November 2004. The participants were classified in three advanced heart failure groups (New York Heart Association Functional Classes II-III): Chagas' disease (n=15), ischemic (n=15) and idiopathic cardiomyopathy (n=15). Twelve Chagas' disease patients without heart failure and normal ejection fraction, and 15 normal controls were also studied. MSNA was recorded directly from the peroneal nerve by microneurography technique.

MSNA was greater in heart failure patients when compared with Chagas' disease patients without heart failure (51+/-3 vs. 20+/-2 bursts/min P=0.0001). MSNA in Chagas' patients with normal ejection fraction and normal controls was not different. During exercise, MSNA was similar in all 3 heart failure groups. And, was lower in the Chagas' patients with normal ejection fraction than in patients with Chagas' disease and heart failure (28+/-1 vs. 63+/-5 bursts/min, respectively).

MSNA is not elevated in patients with Chagas' disease with normal ejection fraction. These findings support the concept of remodeling and neurohumoral activation as a common pathway following significant cardiac injury.