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Histopathologic links in this canine model warrant human studies; leaves open any change to Chagas conduction management.
Atrioventricular (A-V) conduction and the functional refractory period (FRP) of the A-V system were studied in 13 dogs chronically infected by T. cruzi that had ECG disturbances indicative of myocarditis. Histopathologic findings at the A-V node and the bundle of His were correlated with the FRP and with conduction times of the A-V propagation system. Retarded conduction was related to inflammatory and fibrotic processes localized at the bundle of His. At relatively slow rates of stimulation, conduction time was prolonged, but the ventricle was capable of following high atrial rates. With augmented FRP, mononuclear cell infiltrates were observed in the A-V node or in the septal muscle around the node. This suggests that the node was included in the inflammatory process. No correlation was found between inflammatory infiltrates of the bundle of His and changes in the FRP. At relatively slow rates of stimulation, normal A-V conduction time corresponded to prolonged FRP. A-V conduction became slow as the atrial rate increased. A point was reached when the ventricle could not follow the moderately increased atrial rates. Excitability of cardiac tissues was so markedly altered in 5 dogs with severe inflammatory infiltrates that a similar study of the A-V system could not be made.
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Anselmi et al. (1967) studied this question.
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