Endocrinology involves the study of glands that secrete hormones into the circulation for effects at distant target sites. Classic endocrine glands include organs like the pituitary gland, thyroid and parathyroid glands, pancreatic islets, adrenal glands, ovaries, and testes. It is now clear that hormones are also secreted from nontraditional endocrine organs and play critical roles in the regulation of physiologic processes. Examples of such organs include the heart (natriuretic peptides), kidney (renin and erythropoietin), adipose tissue (leptin, adiponectin, and irisin), and gut (cholecystokinin and incretins). Once in the circulation, hormones bind to receptors on target tissues to elicit biological effects. Target tissues for some hormones (eg, glucocorticoid, thyroid hormone) can be numerous, reflecting the wide distribution of receptors, while other tissues may have a more limited distribution (eg, androgens). Because hormone receptors can be so ubiquitous throughout the body, the presence or absence of a single hormone can have multiple effects on one or more organ systems, including the cardiovascular system. This chapter considers most of the common and some uncommon endocrinopathies that can affect the heart, addressing specifically how they can be recognized and treated to best restore cardiovascular health.
The cardiovascular signs and symptoms of thyroid disease are some of the most characteristic and clinically relevant signs and symptoms seen. Both hyperthyroidism and hypothyroidism produce changes in cardiac contractility, myocardial oxygen consumption, cardiac output, blood pressure, and systemic vascular resistance. Although it is well known that hyperthyroidism can produce atrial fibrillation, it is less well recognized that hypothyroidism predisposes to ventricular dysrhythmias. The importance of the recognition of the effects of thyroid disease on the heart is highlighted by the recognition that restoration of normal thyroid function in almost all cases reverses the abnormal cardiovascular changes.
Thyroid disease is quite common, affecting approximately 9–15% of the adult female population and a smaller percentage of males. This gender-specific prevalence likely results from autoimmune causes for the most common forms of thyroid disease, such as Graves and Hashimoto disease. However, with advancing age, especially beyond the eighth decade of life, the incidence of disease in males increases to equal that of females.
Thyroid hormone regulates oxidative and metabolic processes throughout the body by directing cellular protein synthesis at the nuclear level. Nongenomic actions of thyroid hormones have also been recognized based on rapid tissue responses that take place before RNA transcription could occur and by recognition of triiodothyronine (T3) and thyroxine (T4) binding sites outside of the nucleus. Both overproduction and underproduction of thyroid hormone can disrupt normal metabolic function. Under the control of pituitary release of thyroid-stimulating hormone (TSH), the thyroid gland secretes T4 and T3, mostly bound to plasma proteins. The free, or unbound, fraction of hormone negatively feeds back at the level of the hypothalamus and pituitary to suppress further release of thyroid-releasing hormone (TRH) and TSH.
Cardiovascular Effects of Thyroid Hormones