BACKGROUND: Chagas' heart disease presents an interesting model of cardiac autonomic nerve dysfunction associated with morphologic lesions. A lack of quantitative evaluation of the latter suggested this study in which hearts from 34 subjects who were serum-positive for Chagas' disease but had no clinical evidence of it and who died suddenly and unexpectedly, out-of-hospital, were examined. METHODS AND RESULTS: By systematic myocardial sampling the histologic area was measured to establish: (a) the number of focal lymphocytic infiltrates x 100 mm2 and average number of lymphocytes per focus; (b) number of foci of, and myocells with, coagulative myocytolysis (contraction band necrosis) x 100 mm2; and (c) the percentage of substitutive myocardial fibrosis. In all cases findings were: (a) intermyocellular lymphocytic infiltrates (6 +/- 6 foci x 100 mm2); (b) coagulative myocytolysis (3 +/- 5 foci and 26 +/- 56 myocells x 100 mm2). CONCLUSIONS: In all 34 subjects quantitative analysis showed extensive lymphocytic infiltrates and myocardial damage typical of catecholamine cardiotoxicity. These two acute or active histological changes may explain their sudden demise produced by focal denervation with regional asynergy and consequent compensatory adrenergic stimulus with myotoxicity and malignant arrhythmia.
BACKGROUND: Chagas' heart disease presents an interesting model of cardiac autonomic nerve dysfunction associated with morphologic lesions. A lack of quantitative evaluation of the latter suggested this study in which hearts from 34 subjects who were serum-positive for Chagas' disease but had no clinical evidence of it and who died suddenly and unexpectedly, out-of-hospital, were examined. METHODS AND RESULTS: By systematic myocardial sampling the histologic area was measured to establish: (a) the number of focal lymphocytic infiltrates x 100 mm2 and average number of lymphocytes per focus; (b) number of foci of, and myocells with, coagulative myocytolysis (contraction band necrosis) x 100 mm2; and (c) the percentage of substitutive myocardial fibrosis. In all cases findings were: (a) intermyocellular lymphocytic infiltrates (6 +/- 6 foci x 100 mm2); (b) coagulative myocytolysis (3 +/- 5 foci and 26 +/- 56 myocells x 100 mm2). CONCLUSIONS: In all 34 subjects quantitative analysis showed extensive lymphocytic infiltrates and myocardial damage typical of catecholaminecardiotoxicity. These two acute or active histological changes may explain their sudden demise produced by focal denervation with regional asynergy and consequent compensatory adrenergic stimulus with myotoxicity and malignant arrhythmia.