Endocrinology involves the study of glands that secrete hormones into the circulation for effects at distant target sites. At present,
more than 100 hormones are known to be released into the circulation,
with more than 200 types of receptors on target cells in the human
body. Many of these cells contain literally thousands of receptors
on their surfaces. Because these hormone receptors are 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
Thyroid hormone has profound effects on the cardiovascular system, regulating vascular tone and contractility and the metabolic demands of the body. Thyroid disease often presents solely with cardiovascular
manifestations, necessitating a thorough search for this potentially reversible cause of heart disease.
Thyroid hormone regulates oxidative and metabolic processes throughout the body by directing cellular protein synthesis at the nuclear level. Both overproduction or underproduction of thyroid hormone
can disrupt normal metabolic function. Under the control of pituitary release of thyroid-stimulating hormone (TSH), the thyroid gland secretes tetraiodothyronine (T4) and triiodothyronine (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. One step necessary in the production of thyroid hormone is the trapping of iodine by the gland.
- Suppressed TSH below the lower normal limits.
- High free T4, total T4, and free thyroxine index, or high free T3 or total T3 radioimmunoassay in T3 toxicosis.
- High 24-hour radioactive iodine uptake in Graves disease or toxic multinodular goiter; low uptake in thyroiditis or exogenous cause.
- Symmetric goiter (often with bruit) and exophthalmos in Graves disease.
In hyperthyroidism, increased levels of thyroid hormone result in a hyperdynamic cardiovascular system. The enhanced diastolic and systolic performance is due to the effect of T3 on the regulation of specific cardiac genes. These genes promote the expression of structural proteins of the contractile apparatus of the cardiac myocyte. In addition, thyroid hormone increases calcium-activated adenosine triphosphatase (ATPase), which increases intracellular calcium concentration and inotropism.
In general, the hyperdynamic activity of the hyperthyroid cardiovascular system is similar to that of other conditions in which the sympathetic
nervous system is activated with the release of catecholamines. There is enhanced cardiac output, increased stroke volume, enhanced left ventricular contractility, decreased systemic vascular resistance, tachycardia with a wide pulse pressure, a hyperdynamic precordium, increased myocardial oxygen consumption, and increased coronary flow. Although systolic contraction and diastolic relaxation are augmented, the heart is functioning near capacity, with little cardiac reserve.
Surprisingly, catecholamine levels are low or normal in hyperthyroidism, and these catecholamine-like effects are believed to be due in part to a demonstrable increase in the responsiveness of β-catecholamine receptors. The causes of hyperthyroidism are listed in Table 32–1.
Table 32–1. Causes of Hyperthyroidism.
| Save Table
Table 32–1. Causes of Hyperthyroidism.
|Graves disease||Symmetric smooth goiter, ophthalmopathy, elevated/131I uptake, homogeneous uptake on thyroid scan, TSH-receptor antibodies|
|Toxic multinodular goiter||Nodular goiter, nonhomogeneous uptake on thyroid scan|
|Autonomous thyroid nodule||Single large “hot” nodule on thyroid scan, suppressing rest of thyroid tissue|
|Subacute||Tender firm goiter, low 131I uptake, transient high ESR|
|Radiation||Tender goiter, low 131I uptake, high ESR; occurs after 131I therapy|
|Painless (silent)||Nontender goiter, low 131I uptake, normal ESR|
|Postpartum||Nontender goiter, low 131I uptake, antithyroid antibodies, transient; tends to recur with each pregnancy|
|Amiodarone||Low or normal 131I uptake|
|Iatrogenic||Absent goiter, low serum thyroglobulin, low 131I uptake|
|Factitious||Absent goiter, low serum thyroglobulin, low 131I uptake|
|Iodine induced||Low 131I uptake, high 24-h urinary iodide excretion; history of iodine ingestion or exposure (contrast agents)|
|Struma ovarii||Low 131I uptake; may have palpable ovary|
|Trophoblastic tumor||Very high HCG|
|Metastatic follicular carcinoma||Usually obvious metastases on 131I scan|
|TSH-producing adenoma||TSH not suppressed, tumor on CT or MRI of pituitary; consider if gland regrows post thyroidectomy or 131I treatment|
Systemic Symptoms and Signs
Patients with hyperthyroidism often complain of weight loss despite an increased appetite; this helps distinguish this condition from other wasting conditions such as cancer or AIDS. Occasionally, the appetite
may be so great as to result in weight gain. A fine resting tremor of the hands is noticed, along with nervousness, anxiety, insomnia, mood swings, and irritability. Heat intolerance and sweaty skin are seen. Proximal muscle weakness and muscle wasting may be prominent. An increased number of bowel movements or diarrhea is due to decreased transit time in the gut. Diplopia on lateral gaze is seen in Graves ophthalmopathy as a result of extraocular muscle hypertrophy.
Cardiovascular Symptoms and Signs
Frequently, the patient has cardiovascular symptoms, including palpitations, dyspnea, and atypical chest pain. Cardiac arrhythmias are common, especially atrial premature contractions and atrial fibrillation. In the elderly, atrial fibrillation may be the only manifestation of thyrotoxicosis, a condition known as apathetic hyperthyroidism. Approximately 10–20% of patients with atrial fibrillation are thyrotoxic, and 10–20% of thyrotoxic patients have atrial fibrillation. ...