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Sera from chronic chagasic patients depress cardiac electrogenesis and conduction

P C Costa1, F S Fortes, A B Machado

  • 1Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brasil.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|April 25, 2000
PubMed

Insights

Sera from Chagas disease patients impact heart rate and atrioventricular conduction. Some sera decrease heart rate and block conduction, potentially via muscarinic pathways, while others increase heart rate through beta-adrenergic activation.

Area of Science:

  • Cardiology
  • Immunology
  • Physiology

Background:

  • Chagas disease, caused by Trypanosoma cruzi, can lead to cardiac complications.
  • Autonomic nervous system dysfunction is a known feature of chronic Chagasic cardiomyopathy.
  • Patient-derived antibodies may play a role in the pathogenesis of cardiac dysfunction.

Purpose of the Study:

  • To investigate the effects of sera from chronic Chagasic patients on cardiac function in an isolated heart model.
  • To screen these sera for muscarinic and beta-adrenergic activity.
  • To explore the potential role of these sera in cardiac arrhythmias and intercellular communication.

Main Methods:

  • Isolated rabbit hearts were perfused with sera from 58 chronic Chagasic patients.
  • Heart rate and atrioventricular (AV) conduction were measured.
  • Muscarinic and beta-adrenergic activities were screened.
  • Atropine was used to assess the involvement of muscarinic pathways.
  • Gap junction conductance was evaluated in cardiomyocyte cultures using dye injection.

Main Results:

  • Sera from 26 patients decreased heart rate, 10 increased it, and 22 had no effect.
  • Sera from 20 patients blocked AV conduction.
  • Muscarinic pathways were implicated but not solely responsible for all observed effects.
  • Sera causing heart rate increases acted via beta-adrenergic activation.
  • Two sera blocked gap junction conductance in cardiomyocytes.

Conclusions:

  • Patient sera can directly influence cardiac electrophysiology, affecting heart rate and AV conduction.
  • Both inhibitory and stimulatory effects on cardiac function are mediated by specific serum components.
  • Further investigation is needed to elucidate the precise mechanisms of serum-induced cardiac dysfunction and uncoupling.

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