Key result
Sera from chronic chagasic patients with beta-1 adrenergic activity shortened the QT interval and M cell action potential duration, effects that were abolished by beta-blockers.
Why the study?
Do antibodies with beta-adrenergic activity from chronic chagasic patients modulate ventricular repolarization in isolated animal hearts and myocytes?
Do antibodies with beta-adrenergic activity from chronic chagasic patients modulate ventricular repolarization in isolated animal hearts and myocytes?
Antibodies with beta-adrenergic activity from chronic chagasic patients shorten QT interval and action potential duration by increasing IKs and ICa, providing a potential mechanism for malignant ventricular arrhythmias in Chagas cardiomyopathy.
May implicate beta-adrenergic autoantibodies in Chagas arrhythmias; animal data leaves open human relevance and practice change.
AIMS: The aim of this study was to investigate whether the sera from chronic chagasic patients (CChPs) with beta-1 adrenergic activity (Ab-beta) 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-beta perfusion. Beta-adrenergic activity was also tested in guinea pig ventricular M cells. Furthermore, the immunoglobulin fraction (IgG-beta) of the Ab-beta 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-beta) did not modulate QT interval. The M cell action potential duration (APD) was reversibly shortened by Ab-beta. Atenolol inhibited this effect of Ab-beta, and Ab- did not modulate the AP of M cells. Ito was not modulated by isoproterenol nor by IgG-beta. However, IgG-beta 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-beta contribute to repolarization changes that may trigger malignant ventricular arrhythmias observed in patients with chronic chagasic or idiopathic cardiomyopathy.
No takes yet. Share an insight, caveat, or question.
Medei et al. (2008) studied Chronic Chagas disease. Sera from chronic chagasic patients with beta-1 adrenergic activity vs. Sera without beta-adrenergic activity / beta-blockers was evaluated on QT interval and M cell action potential duration. Sera from chronic chagasic patients with beta-1 adrenergic activity shortened the QT interval and M cell action potential duration, effects that were abolished by beta-blockers.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: