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Department of Medicine I, Endocrine Unit, Gutenberg-University Hospital, Mainz, Germany, and Department of Medicine, Division of Endocrinology & Metabolism, University of California, San Diego, CA, USA
* To whom correspondence should be addressed. E-mail: wdillmann{at}ucsd.edu.
The close link between the thyroid gland and the heart was clear in the earliest descriptions of hyperthyroidism. Influences of increased thyroid hormone secretion on cardiovascular function were noticed over 200 yr ago. In 1785, a British physician, C. Parry, noted for the first time an association between the swelling of the thyroid area and heart failure (1). Parry described eight cases, all women, with a thyroid enlargement, a rapid heartbeat and palpitations, and four were judged to have cardiac enlargement. From his descriptions of the pulses, it is likely that his first patient had atrial fibrillation. In his paper, published in 1825, he stated: "There is one malady which I have in five cases seen coincident with what appeared to be an enlargement of the heart. The malady to which I elude is enlargement of the thyroid gland." An Irish physician, R. Graves described 50 yearsr later: "four cases of violent and long continued palpitation in females with thyrotoxicosis" (2). On the European continent, the cardiac aspects of hyperthyroidism were also noted by C. von Basedow (3), a practitioner in Merseburg, Germany, who in 1840 reported three cases with goiter, palpitations and exophthalmos. The cardiovascular manifestations of myxedema remained essentially unrecognized until 1918, when H. Zondek of Munich (4) described what he termed ,,Das Myxödemherz", noting all of the classical clinical and electrocardiography features of far advanced myxedema except for pericardial effusions. He also noted the reversibility of these changes upon treatment with thyroid extract. The next decades following these original descriptions was characterized predominantly by clinical observations related to cardiovascular effects of excessive thyroid hormone: arrhythmias, changes in cardiac contractility, and peripheral vasodilatation (5).
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