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Thyroid Hormone Predisposes Rabbits to Atrial Arrhythmias by Shortening Monophasic Action Period and Effective Refractory Period: Results from an in Vivo Study

Overview
Publisher Springer
Specialty Endocrinology
Date 2009 Jun 23
PMID 19542744
Citations 1
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Abstract

Background: Atrial arrhythmias are common complications of hyperthyroidism, but the underlying mechanisms remain to be further clarified. Thus, in this study, we try to investigate the effects of thyroid hormone on atrial electrophysiology by using a hyperthyroidism model in vivo.

Materials And Methods: Twenty-four New Zealand white rabbits were randomized into Thyroxine group (no.=12) and Control group (no.=12). In Thyroxine group, Levo-thyroxine (L-T(4)) solution (1 mg/kg x d(-1)) was injected daily into the peritoneum for 2 weeks. In Control group, the same amount of saline was injected. On day 15, 8 rabbits in each group were chosen randomly to receive electrophysiological experiment in vivo, in which electrophysiological parameters and atrial arrhythmias induced by electrical stimulation were recorded and serum thyroid hormone levels were examined. The others were killed so as to exam the L-type calcium current of atrium.

Results: Atrial monophasic action potential at 90 repolarization (AMAP(90)) and effective refractory period (AERP) were significantly shorter in Thyroxine group than in Control group (AMAP(90): 103.21+/-1.94 vs 122.14+/-6.13, p<0.01; AERP: 82.69+/-0.99 vs 102.46+/-2.32, p<0.01). There are significant differences in the incidence of atrial arrhythmias between the two groups. The mean peak of L-type calcium current (I(Ca,L)) densities (pA/pF) at -10mV was significantly higher in Thyroxine group than in Control group (-8.59+/-0.68 vs -6.54+/-0.49, no.=8, p<0.001).

Conclusions: In our hyperthyroidism model, thyroid hormone predisposed rabbits to atrial arrhythmias by shortening AMAP and AERP, which might be associated with increased I(Ca,L) current densities in atrium.

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References
1.
Gammage M, Parle J, Holder R, Roberts L, Hobbs F, Wilson S . Association between serum free thyroxine concentration and atrial fibrillation. Arch Intern Med. 2007; 167(9):928-34. DOI: 10.1001/archinte.167.9.928. View

2.
Washizuka T, Horie M, Watanuki M, Sasayama S . Endothelin-1 inhibits the slow component of cardiac delayed rectifier K+ currents via a pertussis toxin-sensitive mechanism. Circ Res. 1997; 81(2):211-8. DOI: 10.1161/01.res.81.2.211. View

3.
Watanabe H, Ma M, Washizuka T, Komura S, Yoshida T, Hosaka Y . Thyroid hormone regulates mRNA expression and currents of ion channels in rat atrium. Biochem Biophys Res Commun. 2003; 308(3):439-44. DOI: 10.1016/s0006-291x(03)01420-7. View

4.
Sun Z, Ojamaa K, Nakamura T, ARTMAN M, Klein I, Coetzee W . Thyroid hormone increases pacemaker activity in rat neonatal atrial myocytes. J Mol Cell Cardiol. 2001; 33(4):811-24. DOI: 10.1006/jmcc.2001.1353. View

5.
Parmar M . Thyrotoxic atrial fibrillation. MedGenMed. 2005; 7(1):74. PMC: 1681414. View