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Europace Advance Access originally published online on May 30, 2008
Europace 2008 10(7):868-876; doi:10.1093/europace/eun138
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Repolarization

Antibodies with beta-adrenergic activity from chronic chagasic patients modulate the QT interval and M cell action potential duration

Emiliano Horacio Medei1,*, José H.M. Nascimento1, Roberto C. Pedrosa2, Luciane Barcellos1, Masako O. Masuda1,3, Serge Sicouri4, Marcelo V. Elizari5 and Antonio C. Campos de Carvalho1

1 Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Bloco G—CCS, Cidade Universitária, Ilha do Fundão, Rio de Janeiro, RJ 21949-900, Brasil; 2 Hospital Universitário Clementino Fraga Filho, Universidade do Brasil, Rio de Janeiro, Brasil; 3 Fundação CECIERJ, Rio de Janeiro, Brasil; 4 Masonic Medical Research Laboratory, Utica, NY, USA; 5 Hospital Ramos Mejia, Cardiac Division, Buenos Aires, Argentina

Aims: The aim of this study was to investigate whether the sera from chronic chagasic patients (CChPs) with beta-1 adrenergic activity (Ab-β) can modulate ventricular repolarization. Beta-adrenergic activity has been described in CChP. It increases the L-type calcium current and heart rate in isolated hearts, but its effects on ventricular repolarization has not been described.

Methods and results: In isolated rabbit hearts, under pacing condition, QT interval was measured under Ab-β perfusion. Beta-adrenergic activity was also tested in guinea pig ventricular M cells. Furthermore, the immunoglobulin fraction (IgG-β) of the Ab-β was tested on Ito, ICa, and Iks currents in rat, rabbit, and guinea pig myocytes, respectively. Beta-adrenergic activity shortened the QT interval. This effect was abolished in the presence of propranolol. In addition, sera from CChP without beta-adrenergic activity (Ab-β) did not modulate QT interval. The M cell action potential duration (APD) was reversibly shortened by Ab-β. Atenolol inhibited this effect of Ab-β, and Ab- did not modulate the AP of M cells. Ito was not modulated by isoproterenol nor by IgG-β. However, IgG-β increased ICa and IKs.

Conclusion: The shortening of the QT interval and APD in M cells and the increase of IKs and ICa induced by IgG-β contribute to repolarization changes that may trigger malignant ventricular arrhythmias observed in patients with chronic chagasic or idiopathic cardiomyopathy.

Key Words: Antibodies, Chagas' disease, Electrophysiology, M cells, QT interval

* Corresponding author. Tel: +55 21 25626558; fax: +55 21 22808193. E-mail address: emedei70{at}biof.ufrj.br/emedei70{at}hotmail.com

Manuscript submitted 4 March 2008. Accepted after revision 6 May 2008.


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