Conduction defects and arrhythmias in Chagas' disease: Possible role of gap junctions and humoral mechanisms

A. C C De Carvalho, M. O. Masuda, H. B. Tanowitz, M. Wittner, R. C S Goldenberg, David C. Spray

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The protozoan parasite Trypanosoma cruzi causes Chagas' disease, a major cause of cardiac dysfunction in Latin Americans. Chagas' disease exhibits both acute and chronic phases, and each may be characterized by cardiac conduction disturbances. In acutely infected cultures of rodent heart cells, synchronized spontaneous beating becomes less regular, and coupling between cells is reduced. The basis of this decreased conduction is apparently in localization of the gap junction protein (Cx43) inside infected cells. Although total Cx43 is normal in infected cells, little is recognizable at appositional membranes. Electrophysiological properties are also altered by this infection. Action potentials are shortened, resting Ca2+ levels are elevated, and response to α-adrenergic agonists was altered, compared to controls. Humoral factors may contribute to the conduction defects in chronic Chagas' disease. Sera from chronically infected rabbits produced ECG abnormalities in Langendorff-perfused rabbit hearts. These findings indicate that chagasic infection may modify ion channel function in the heart, and we suggest that these changes may be manifested in the conduction disturbances that characterize this disease.

Original languageEnglish (US)
Pages (from-to)686-698
Number of pages13
JournalJournal of Cardiovascular Electrophysiology
Volume5
Issue number8
StatePublished - 1994

Fingerprint

Chagas Disease
Gap Junctions
Cardiac Arrhythmias
Connexin 43
Rabbits
Adrenergic Agonists
Connexins
Trypanosoma cruzi
Infection
Ion Channels
Action Potentials
Rodentia
Electrocardiography
Parasites
Chronic Disease
Membranes
Serum

Keywords

  • connexin
  • heart
  • immunity
  • parasite
  • Trypanosoma cruzi

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology

Cite this

De Carvalho, A. C. C., Masuda, M. O., Tanowitz, H. B., Wittner, M., Goldenberg, R. C. S., & Spray, D. C. (1994). Conduction defects and arrhythmias in Chagas' disease: Possible role of gap junctions and humoral mechanisms. Journal of Cardiovascular Electrophysiology, 5(8), 686-698.

Conduction defects and arrhythmias in Chagas' disease : Possible role of gap junctions and humoral mechanisms. / De Carvalho, A. C C; Masuda, M. O.; Tanowitz, H. B.; Wittner, M.; Goldenberg, R. C S; Spray, David C.

In: Journal of Cardiovascular Electrophysiology, Vol. 5, No. 8, 1994, p. 686-698.

Research output: Contribution to journalArticle

De Carvalho, ACC, Masuda, MO, Tanowitz, HB, Wittner, M, Goldenberg, RCS & Spray, DC 1994, 'Conduction defects and arrhythmias in Chagas' disease: Possible role of gap junctions and humoral mechanisms', Journal of Cardiovascular Electrophysiology, vol. 5, no. 8, pp. 686-698.
De Carvalho, A. C C ; Masuda, M. O. ; Tanowitz, H. B. ; Wittner, M. ; Goldenberg, R. C S ; Spray, David C. / Conduction defects and arrhythmias in Chagas' disease : Possible role of gap junctions and humoral mechanisms. In: Journal of Cardiovascular Electrophysiology. 1994 ; Vol. 5, No. 8. pp. 686-698.
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