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Cardiac complications in endocrine diseases

An article from the E-Journal of the ESC Council for Cardiology Practice

Cardiovascular abnormalities associated with pathologic changes of endocrine glands are due to the fact that various hormones interact with the cardiovascular system. Pituitary, adrenal, parathyroid and thyroid hormone excesses or deficiencies may produce cardiovascular disorders that usually resolve with the correction of the underlying endocrine disease.


The main glands, which are involved with the heart, are presented below. You will note that Diabetes Mellitus is not discussed in this article.

I - Pituitary gland

1) Growth hormone 

Growth hormone (GH) hypersecretion leads to acromegaly, which is associated with increased mortality due to cardiovascular disease. Risk depends on age, disease severity and duration. Hypertension, insulin resistance, diabetes mellitus and hyperlipidemia frequently occur in these patients. Additionally, right and left ventricular hypertrophy, aortic and mitral valve disease, which persist despite disease cure, are common findings. Secondary hypertension occurs in 20-40% of patients with acromegaly and it is an independent factor for mortality in these patients. ECG abnormalities including left axis deviation, septal Q-waves, ST-T wave depression, abnormal QT dispersion and conduction defects occurr in 50% of patients. Moreover, atrial, ventricular ectopy, sick sinus syndrome, supraventricular and ventricular beats may occur (1).

  • Transphenoidal surgery with the resection of pituitary adenoma is the procedure of choice. If GH levels remain elevated, long-acting somatostatin analogues, GH receptor anatagonists or radiotherapy can be used.
  • Both hypertension and left ventricular hypertrophy improve with treatment (6-12 months) and survival is significantly greater in patients achieving disease remission.

Increased cardiovascular mortality has been observed in hypopituitary patients that are GH deficient. Although the exact mechanisms have not been delineated, meticulous substitution of glucocorticoids, sex steroids and (where indicated) GH is the suggested approach in these patients.

2) Adrenocorticotropic hormone

The excess of adrenocorticotropic hormone (ACTH) in Cushing disease contributes to cortisol excess from the adrenals. The cardiac effects of glucocorticoids excess in Cushing disease rise from their direct effect on heart, liver, muscle and fat. Accelerated atherosclerosis is the result of abnormal glucose metabolism, hyperglycemia and hyperinsulinemia, hypertension and altered clotting and platelet function. The rise in serum glucose and the development of insulin resistance gives rise to activation of proinflammatory cytokines such as tumor necrosis factor-alpha and interleukin-6 which may underlie the accelerated atherosclerosis of insulin resistance. Left ventricular hypertrophy with impaired contractility was found in 40 % of patients. ECG changes in the form of PR and QT changes are common (2).

  • Transphenoidal surgery of pituitary adenoma can partially or completely reverse the increased ACTH. Treatment of ectopic ACTH requires identification and treatment of the neoplastic process (1, 2).


II - Adrenal glands

They hold two major segments: the cortex and the medulla. The cortex zona glomerulosa produces aldosterone and the zona fasciculate produces primarily cortisol and some androgenic steroids. The zona reticularis also produces cortisol and androgens. ACTH regulates synthesis of cortisol in both zona reticularis and fasciculate. The zona glomerulosa shows a much lesser degree of ACTH responsiveness and responds primarily to angiotensin II by increasing aldosterone secretion.

1) Cortisol

Excess in cortisol due to adenomatous or rarely malignant neoplastic process arising in the adrenal gland itself is described as Cushing syndrome. The clinical findings in this entity are the same as in Cushing disease and are due to the effect of cortisol on the cardiovascular system (4).

2) Hyperaldosteronism

The renin-angiotensin system controls the production of aldosterone although the major cause of increased aldosterone is the response to the activation of the renin angiotensin system, there are well-recognized aldosterone-producing benign adrenal adenomas (Conn syndrome). Hypertension is the main complication in hyperaldosteronism. However, the degree of left ventricular hypertrophy exceeds that expected from hypertension alone, because of the increase in both volume and pressure load due to high aldosterone levels (5).

  • Surgical rejection of adrenal tumor is the treatment of choice.

3) Adrenal insufficiency

Primaryadrenal insufficiency most commonly arises from bilateral loss of adrenal function due to autoimmune reasons, or infection, hemorrhage, metastatic malignancy or inborn errors of steroids metabolism and leads to dramatic reduction of both gluco- and mineralocorticoids. Secondary adrenal insufficiency is due to pituitary dependent loss of ACTH and leads to a fall in glucocorticoids, whereas mineralocorticoids remain normal. The hypovolemia, hypotension and acute cardiovascular collapse resulting from renal sodium wasting, hyperkalemia and loss of vascular tone are the main characteristics of the disease. The hyperkalemia can alter the ECG, producing low P waves and peaked T waves. Patients present with cardiac atrophy, which resolves after disease treatment.

  • Management of acute Addisonian crisis with hydrocortisone replacement, restoration of intravascular fluid deficit and treat the underlying precipitating cause are needed (6).

4) Pheochromocytoma

It is a usually benign tumor arising from the adrenal medulla, but that may arise anywhere within the sympathetic adrenergic nerves. Prevalence is 1 per 2000 cases of diastolic hypertension. When it coexists with medullary thyroid carcinoma or occasionally with hyperparathyroidism, it is called multiple endocrine neoplasia (MEN) syndrome type II. Pheochromocytoma presents with headache, palpitations, excessive sweating, tremulousness, chest pain, weight loss and hypertension associated with orthostatic hypotension on arising in the morning. The ECG can show left ventricular hypertrophy and inverted T due to ventricular strain. Impaired LV function due to hypertension and high catecholamines is a common finding. The primary catecholamine released is norepinephrine, but increased epinephrine can be also found. The first step for diagnosis is established by demonstrating an increase in norepinephrine or epinephrine or its metabolites in blood. Quantitative 24-hour urinary metanephrines are the most reliable screening procedures and plasma catecholamines are also fairly sensitive. Demonstration of elevated serum dopamine is a sign of possible malignant transformation, suggesting tumor in an extra-adrenal site.

  • Definitive treatment requires tumor removal (7). Preoperative pharmacological management includes 7-14 days of alpha-adrenergic blockade usually with prazocin or phenoxybenzamine. Beta-adrenergic blocker therapy is considered contraindicated before establishing sufficient alpha blockade. If supraventricular arrhythmias or tachycardia (heart rate >120 bs/min) are present, beta1-selective agents, such as atenolol, are preferred.

III - Parathyroid glands

They can produce cardiovascular disease through changes of parathyroid hormone (PTH), or through changes in serum calcium. Serum calcium regulates the synthesis and secretion of PTH through a feedback mechanism.

1) Hyperparathyroidism

Primary hyperparathyroidism produces hypercalcemia. The cardiovascular effects of hypercalcemia include an increase in myocardial contractility. ECG findings are short QT, PR, blunting of T waves and ST changes occasionally suggesting of ischaemia. Hypercalcemia provokes calcium deposits in the heart (myocardium, valve cusps-annuli and conduction system). Although systolic function is normal, diastolic function can be disturbed. Treatment is the surgical removal of parathyroid adenoma (8).

2) Hypoparathyroidism

Primary hypoparathyroidism is rare and can be seen after surgical removal of parathyroid glands or in during polyglandular syndromes. Low serum calcium prolongs QT and impairs cardiac cardiac contractility (8).

IV - Thyroid gland

The thyroid gland and the heart have an embryologic relationship and a close interaction.

1) Hyperthyroidism

Cardiovascular symptoms are predominant in the clinical presentation of hyperthyroidism. Palpitations, increase in heart rate both at rest and during sleep, exercise intolerance and dyspnea are the main manifestations. A subset of patients can experience angina like chest pain or true myocardial ischemia, even with normal coronaries, coronary vasospasm, although myocardial infarction is rare. The most common rhythm disturbance is sinus tachycardia that is usually overshadowed by atrial fibrillation. A minority of patients could present high output heart failure due to increased resting cardiac output and enhanced contractility. Treatment should include b-blocker to lower heart rate by 10-15%. Definite therapy can be accomplished by iodine-131 alone or in combination with antithyroid drugs (9).

2) Hypothyroidism

In contrast to hyperthyroidism, hypothyroidism presents with subtle cardiovascular symptoms. Mild bradycardia, diastolic hypertension, low apical impulse, an increase in low-density lipoprotein and cholesterol and increased frequency of pericardial effusions are the main findings. Echocardiography demonstrates small to moderate effusions in 30% of hypothyroid patients, which resolves weeks to months after replacement therapy (9).


1. Clayton RN: Cardiovascular function in acromegaly. Endocr Rev 2003;24:272

2. Whitworth JA, Mangos GJ, Kelly JJ. Cushing, cortisol and cardiovascular disease. Hypertension 2000;36:912

3. Giustina A, Barkan A, Chanson P et al. Guidelines for the treatment of growth hormone excess and growth hormone deficiency in adults. J Endocrinol Invest. 2008; 31: 820

4. Muiesan ML, Lupia M, Salvetti M et al. Left ventricular structural and functional characteristics in Cushing’s syndrome. J Am Coll Cardiol 2003;41:2275

5. White PC. Aldosterone: Direct effects on and production by the heart. J Clin Endocrinol Metab 2003;88:2376

6. Cooper MS, Stewart PM. Corticosteroid insufficiency in acutely ill patients. N Engl J Med 2003;348:727

7. Bravo EL. Pheochromocytoma. Cardiol Rev 2002;10: 44

8. Shluter K, Piper HM: Cardiovascular actions of parathyroid hormone and parathyroid hormone-related peptide. Cardiovasc Res 1998;37: 34
9. Ojamaa K, Ascheim D, Hryniewic K, et al. Thyroid hormone therapy of cardiovascular disease. Cardiovasc Rev Rep 2002;23: 20


Vol7 N°27

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.