LETTER TO THE EDITOR
Thyroid hormone and arrhythmogenic activity
Johann Auer, MDa
a Department of Cardiology and Intensive Care,General Hospital Wels,Grieskirchnerstrasse 42,A-4600 Wels,Austria
Robert Berent, MD,
Thomas Weber, MD and
Bernd Eber, MD, FESC
johann.auer{at}khwels.at
We read with great interest the study by Chen et al. (1) in a recent issue of the Journal. The investigators report that thyroid hormone changes the electrophysiologic activity of the pulmonary vein cardiomyocytes, and they suggest that increased tri-iodothyronine-induced automaticity and enhanced triggered activity may increase the arrhythmogenic activity of cardiomyocytes in hyperthyroidism. They conclude that this mechanism contributes to arrhythmogenic activity of hyperthyroidism.
Hyperthyroidism is known to be an important risk factor in the etiology of atrial fibrillation (AF)(2). In a large retrospective study investigating an unselected, community-based population of older persons (3), we could demonstrate that the prevalence of AF was 2.3% in subjects with normal values for serum thyrotropin, 13.8% in patients with overt hyperthyroidism (both low serum thyrotropin values [ 0.03 mU/l] and elevated free tri-iodothyronine and free thyroxine concentrations), and 12.7% in patients with subclinical hyperthyroidism (low values of serum thyrotropin [<0.4 mU/l], and free tri-iodothyronine and free thyroxine concentrations within the normal range). The relative risk of AF in subjects with subclinical hyperthyroidism, compared with those with normal concentrations of serum thyrotropin, was 5.2 (95% confidence interval [CI] 2.18.7, p < 0.01). Thus, a low serum thyrotropin concentration was associated with a more than five-fold higher likelihood for the presence of AF, with no significant difference between subclinical and overt hyperthyroidism.
Individuals with low serum concentrations of thyrotropin regardless of concentrations of free tri-iodothyronine and free thyroxine should be considered as a population at risk for the development of AF (4). Thus, thyroid secretion needs not increase much, if at all, and serum concentrations of free tri-iodothyronine and free thyroxine can stay within normal values for AF to occur. Moreover, when AF occurs, there is only rarely either concurrent or subsequent overt hyperthyroidism, but it is more commonly associated with subclinical hyperthyroidism (5). We consider this topic important, because subclinical hyperthyroidism is, at all, more common than overt hyperthyroidism among people over age 60 (5) and does not progress to overt hyperthyroidism in most cases (6).
We agree with Chen et al. (1) that L-tri-iodothyronine-induced increased automaticity and enhanced triggered activity may be one mechanism that could increase the arrhythmogenic activity of cardiomyocytes in overt hyperthyroidism. But it is obvious from clinical data that mechanisms, other than those triggered by free tri-iodothyronine and free thyroxine, are important in AF associated with low serum thyrotropin.
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References
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1. Chen YC, Chen SA, Chen YJ, Chang MS, Chan P, Lin CI. Effects of thyroid hormone on the arrhythmogenic activity of pulmonary vein cardiomyocytes. J Am Coll Cardiol. 2002;39:366372[Abstract/Free Full Text]
2. Woeber KA. Thyrotoxicosis and the heart. N Engl J Med. 1992;327:9498[Abstract]
3. Auer J, Scheibner P, Mische T, Langsteger W, Eber O, Eber B. Subclinical hyperthyroidism as a risk factor for atrial fibrillation. Am Heart J. 2001;142:838842[CrossRef][Medline]
4. Singer DE. Randomized trials of warfarin for atrial fibrillation. N Engl J Med. 1992;327:14511453[Medline]
5. Sawin CT, Geller A, Wolf PA, et al. Low serum thyrotropin concentration as a risk factor for atrial fibrillation in older persons. N Engl J Med. 1994;331:12491252[Abstract/Free Full Text]
6. Utiger RD. Subclinical hyperthyroidismjust a low serum thyrotropin concentration, or something more? N Engl J Med. 1994;331:13021303[Free Full Text]
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