Thyroid hormone predisposes rabbits to atrial arrhythmias by shortening monophasic action period and effective refractory period: results from an in vivo study.

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.