In 1786, the cardiovascular manifestations of thyrotoxicosis were recognized by Caleb Parry, who noted, “There is one malady which I have, in five cases, seen coincident with what appeared to be enlargement of the heart — the malady to which I elude is enlargement of the thyroid gland” (Figure 1).1
Thyroid hormone is an important regulator of cardiac gene expression, and many of the cardiac manifestations of thyroid dysfunction are associated with alterations in T3-mediated gene transcription. As a result, cardiac output, ejection fraction, and heart rate are all found to be increased while isovolemic relaxation time and peripheral vascular resistance are decreased in the hyperthyroid states. Furthermore, thyroid hormone increases blood volume and erythropoietin secretion with subsequent increased preload and cardiac output. However, to understand the alterations in cardiac hemodynamics that accompany hyperthyroidism, it is important to review the underlying mechanisms of thyroid hormone action at the cellular level.
How to Cite:
1. Nabbout LA, Robbins RJ. The Cardiovascular Effects of Hyperthyroidism. Methodist DeBakey Cardiovascular Journal. 2010;6(2):3-8. DOI: http://doi.org/10.14797/mdcvj.197