Thyroid hormone-induced changes in cardiac function, has been recognized over the last 150 years. Specifically, Triiodothyronine-3 (T3) induced cardiovascular change has been intensively studied during the last two decades (Dillman, 1990) (American Thyroid Association (ATS) 2014). Still more than 13 million Americans are affected by thyroid disease and about 60% of them remain undiagnosed (DeRuiter, 2002). Further each year roughly about 5% of new Americans patients are diagnosed with a thyroid disease (ATA 2104).
The thyroid is situated just below the larynx. Its function is to intake Iodine, which is found in many foods and convert the iodine into thyroid hormones T3 and T4 (Endocrineweb, 2012). The thyroid gland is the only gland in the body that is able to absorb iodide. Additionally thyroid cells are the only cells in the human body that can absorb iodide and combine it with the amino acid tyrosine. Synthesis of thyroid hormone is essentially done in a two-step process. The first step in the synthesis of thyroid hormone is the incorporation of iodine into thyroglobulin – a diametric protein. This process is sometimes referred to as ‘organification’ of iodide. Once the iodide is taken up and converted to iodine, it is then condensed onto tyrosine residues on the polypeptide backbone of the protein molecule thyroglobulin. The iodinated tyrosine is then incorporated into thyroglobulin. (University of Connecticut Health Center (UCHU)) The second, simultaneous synthetic reaction is where iodotyrosine (iodinated tyrosine) molecules are coupled together by a coupling reaction to form di-iodotyrosine. When two di-iodotyrosine couple together they form Thyroxin - T4. If a di-iodotyrosine and a mono-iodotyrosine or uncoupled iodotyrosine are coupled together, then tri-iodotyronine - T3 is formed (UCHU). The normal ratio of production of T3 and T4 is about 80% T3 and 20% T4. Although these numbers seem lob sided, the potency in terms of hormone strength of T3 is about four times stronger than T4 (Endocrineweb, 2012). T3 and T4 are then released into the blood stream by proteolysis and transported throughout the body where they can control metabolism (Endocrineweb, 2012). This function is vital as every cell in the body depends on thyroid hormones for the regulation of their metabolism. The entire process of regulation of the thyroid gland is dependent upon the pituitary gland. (Lemaire 2005) When the levels of thyroid hormones drops too low, the pituitary glans produces Thyroid Stimulating Hormone (TSH), which as the name suggests stimulates production and secretion of thyroid hormones. The pituitary gland is in turn regulated by the hypothalamus, part of the brain that produces TSH Releasing Hormone (TRH), more specifically thyrotropin releasing hormone, (Endocrineweb, 2012) which instructs the pituitary gland to produce TSH.
The gland functions on a negative feedback control system. The production and secretion of T3 and T4 by the thyroid gland are stimulated by THS in turn; thyroid hormones inhibit the production of TRH, thereby inhibiting further production of THS. This feedback system plays an extremely important role in thyroid disorders. For the purposes of this paper we will look only at the overproduction of thyroid hormone, and the effects it has on cardiovascular change.
The overproduction and secretion of excessive amounts of free thyroid hormone is a condition called hyperthyroidism, or hyperthyreosis. Graves’ disease, an autoimmune disease, is the most common cause of hyperthyroidism, however, the clinical manifestations or effects of hyperthyroidism are largely independent of its specific cause. (Siengnethaler, 2007)

Recall that the thyroid gland operates on a feed back loop. In hyperthyroidism, the hypothalamus is tricked into thinking that the thyroid gland is not producing thyroid hormone and as a result produces TRH which in turn makes the pituitary gland produce TSH which stimulates the thyroid to produce