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This version published online on March 18, 2008
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2008-0092
A more recent version of this article appeared on June 1, 2008
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Submitted on January 14, 2008
Accepted on March 7, 2008

Activation of electrical triggers of atrial fibrillation in hyperthyroidism

K. Wustmann, J. P. Kucera, A. Zanchi, A. Burow, T. Stuber, B. Chappuis, P. Diem, and E. Delacrétaz*

Department of Cardiovascular Medicine, University Hospital Bern, Switzerland; Department of Physiology, University of Bern, Switzerland; Division of Nephrology and Department of Medicine, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland; Department of Endocrinology, University Hospital Bern, Switzerland

* To whom correspondence should be addressed. E-mail: etienne.delacretaz{at}insel.ch.

Context: A shortening of the atrial refractory period has been considered as the main mechanism for the increased risk of atrial fibrillation in hyperthyroidism. However, other important factors may be involved.

Objective: Our objective was to determine the activity of abnormal supraventricular electrical depolarizations in response to elevated thyroid hormones in patients without structural heart disease.

Patients and Design: Twenty-eight patients (25 female, 3 male, mean age 43±11 years) with newly-diagnosed and untreated hyperthyroidism were enrolled in a prospective trial after exclusion of heart disease. Patients were followed for 16±6 months and were studied at baseline and 6 months after normalization of serum thyrotropin levels.

Main Outcome Measures: The incidence of abnormal premature supraventricular depolarizations (SVPD) and the number of episodes of supraventricular tachycardia was defined as primary outcome measurements before the start of the study. In addition, heart rate oscillations (turbulence) after premature depolarizations and heart rate variability were compared at baseline and follow-up.

Results: SVPD decreased from 59±29 to 21±8 per 24 hours (p=0.003), very early SVPD (so called "P on T") decreased from 36±24 to 3±1 per 24 hours (p<0.0001), respectively, and non-sustained supraventricular tachycardias decreased from 22±11 to 0.5±0.2 per 24 hours (p=0.01) after normalisation of serum thyrotropin levels. The hyperthyroid phase was characterised by an increased heart rate (93±14 versus 79±8 beats per min, p<0.0001) and a decreased turbulence slope (3.6 versus 9.2, p=0.003), consistent with decreased vagal tone. This was confirmed by a significant decrease of heart rate variability.

Conclusion: Hyperthyroidism is associated with an increased supraventricular ectopic activity in patients with normal hearts. The activation of these arrhythmogenic foci by elevated thyroid hormones may be an important causal link between hyperthyroidism and atrial fibrillation.


Key words: hyperthyroidism • atrial ectopic beats • atrial fibrillation • heart rate turbulence • heart rate variability







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