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Thyrotoxic cardiac disease

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Abstract

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.

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Authors and Affiliations

  1. Department of Medicine and the Feinstein Institute for Medical Research, North Shore University Hospital, 350 Community Drive, Manhasset, NY, 11030, USA

    Irwin Klein

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  1. Peter Dahl
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  2. Sara Danzi
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  3. Irwin Klein
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Correspondence to Irwin Klein.

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Dahl, P., Danzi, S. & Klein, I. Thyrotoxic cardiac disease. Curr Heart Fail Rep 5, 170–176 (2008). https://doi.org/10.1007/s11897-008-0026-9

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  • DOI: https://doi.org/10.1007/s11897-008-0026-9

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