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Am J Physiol Endocrinol Metab 281: E190-E195, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 1, E190-E195, July 2001

Sympathovagal imbalance in hyperthyroidism

J. Burggraaf1, J. H. M. Tulen3, S. Lalezari1, R. C. Schoemaker1, P. H. E. M. De Meyer2, A. E. Meinders2, A. F. Cohen1, and H. Pijl2

1 Centre for Human Drug Research and 2 Department of General Internal Medicine, Leiden University Medical Centre, 2333 CL Leiden; and 3 Department of Psychiatry, Erasmus University, 3015 GD Rotterdam, The Netherlands

We assessed sympathovagal balance in thyrotoxicosis. Fourteen patients with Graves' hyperthyroidism were studied before and after 7 days of treatment with propranolol (40 mg 3 times a day) and in the euthyroid state. Data were compared with those obtained in a group of age-, sex-, and weight-matched controls. Autonomic inputs to the heart were assessed by power spectral analysis of heart rate variability. Systemic exposure to sympathetic neurohormones was estimated on the basis of 24-h urinary catecholamine excretion. The spectral power in the high-frequency domain was considerably reduced in hyperthyroid patients, indicating diminished vagal inputs to the heart. Increased heart rate and mid-frequency/high-frequency power ratio in the presence of reduced total spectral power and increased urinary catecholamine excretion strongly suggest enhanced sympathetic inputs in thyrotoxicosis. All abnormal features of autonomic balance were completely restored to normal in the euthyroid state. beta -Adrenoceptor antagonism reduced heart rate in hyperthyroid patients but did not significantly affect heart rate variability or catecholamine excretion. This is in keeping with the concept of a joint disruption of sympathetic and vagal inputs to the heart underlying changes in heart rate variability. Thus thyrotoxicosis is characterized by profound sympathovagal imbalance, brought about by increased sympathetic activity in the presence of diminished vagal tone.

heart rate variability; catecholamines


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