Thyrotoxic cardiac disease

被引：89
作者：
Dahl P. [1 ]
Danzi S. [1 ]
Klein I. [1 ]
机构：
[1] North Shore University Hospital Feinstein, Department of Medicine, Institute for Medical Research, Manhasset, NY 11030
来源：
Current Heart Failure Reports | 2008年 / 5卷 / 3期
基金：
美国国家卫生研究院;
关键词：
Thyroid Hormone; Amiodarone; Hyperthyroidism; Myosin Heavy Chain; Systemic Vascular Resistance;
D O I：
10.1007/s11897-008-0026-9
中图分类号：
学科分类号：
摘要：
The most recognizable features of hyperthyroidism are those that result from the effects of triiodothyronine (T3) on the heart and cardiovascular system: decreased systemic vascular resistance and increased resting heart rate, left ventricular contractility, blood volume, and cardiac output. Although these measures of cardiac performance are enhanced in hyperthyroidism, the finding of clinical cardiac failure can be somewhat paradoxical. About 6% of thyrotoxic individuals develop symptoms of heart failure, but less than 1% develop dilated cardiomyopathy with impaired left ventricular systolic function. Heart failure resulting from thyrotoxicosis is due to a tachycardia-mediated mechanism leading to an increased level of cytosolic calcium during diastole with reduced ventricular contractility and diastolic dysfunction, often with tricuspid regurgitation. Pulmonary artery hypertension in thyrotoxicosis is gaining awareness as a cause of isolated right-sided heart failure. In both cases, older individuals are more likely to be affected. Treatment needs to be directed at management of the acute cardiovascular complications, control of the heart rate, and thyroid-specific therapy to restore a euthyroid state that will lead to resolution of the signs and symptoms of heart failure. © Springer Science+Business Media, LLC 2008.
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收藏
页码：170 / 176
页数：6
相关论文
共 47 条
  • [1] Klein I., Endocrine disorders and cardiovascular disease, Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, pp. 2033-2047, (2008)
  • [2] Bianco A.C., Kim B.W., Deiodinases: Implications of the local control of thyroid hormone action, J Clin Invest, 116, pp. 2571-2579, (2006)
  • [3] Klein I., Danzi S., Thyroid disease and the heart, Circulation, 116, pp. 1725-1735, (2007)
  • [4] Lazar M.A., Chin W.W., Nuclear thyroid hormone receptors, J Clin Invest, 86, pp. 1777-1782, (1990)
  • [5] Klein I., Ojamaa K., Mechanisms of disease: Thyroid hormone and the cardiovascular system, N Engl J Med, 344, pp. 501-509, (2001)
  • [6] Wu Y., Koenig R.J., Gene regulation by thyroid hormone, Trends Endocrinol Metab, 11, pp. 207-211, (2000)
  • [7] Klemperer J., Klein I., Gomez M., Et al., Thyroid hormone treatment after coronary-artery bypass surgery, N Engl J Med, 333, pp. 1522-1527, (1995)
  • [8] Dillmann W.H., Cellular action of thyroid hormone on the heart, Thyroid, 12, pp. 447-452, (2002)
  • [9] Davis P.J., Davis F.B., Nongenomic actions of thyroid hormone on the heart, Thyroid, 12, pp. 459-466, (2002)
  • [10] Osman F., Franklyn J.A., Holder R.L., Et al., Cardiovascular symptoms and cardiac rate and rhythm abnormalities improve with treatment in patients with hyperthyroidism, J Am Coll Cardiol, 49, pp. 71-81, (2007)
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