Severe congestive heart failure patient on amiodarone presenting
with myxedema coma: A case report
Mazen Shaheen, MD
University of CincinnatiCincinnati, Ohio

Case Report

Swan Ganz showed the cardiac indices listed in table 1.  Two days after admission, the patient clinical condition deteriorated and the family decided to withdrew care. The patient expired and no autopsy was performed.

Table 1. Cardiac indices pre and post administration of IV thyroxine (T4).

Discussion:

Correspondence: Dr. Mazen Shaheen, university of Cincinnati, College of Medicine, Department of Internal Medicine, 231 Albert sabin Qay
E-mail : Mazenshaheen78@yahoo.com

Myxedema coma is a misnomer for usually patients are not in coma but rather have altered mental status (4).The recognition of myxedema coma is challenging and could be missed for low prevalence and absence of specific symptoms (2). Three essential elements helping to establish the diagnosis are altered mental status, hypothermia and presence of precipitating event (2,4).The common precipitating events are infection,sepsis, cold exposure, stroke, gastrointestinal bleeding and non-compliance with thyroxine replacement therapy(3). Hypothyroidism is associated with decreased Beta adrenergic response in most tissues contributing to development of cardiovascular dysfunction, altered mental status and hypothermia (5). Our patient had elevated TSH, low T4, altered mental status, and hypothermia thus meeting all criteria for myxedema coma. In this case, the patient also suffered from exacerbation in heart failure secondary to hypothyroidism, and his cardiac indices improved following T4 treatment as seen in the swan ganz parameters pre and post T4 treatment. The treatment of myxedema coma consists of intravenous loading dose of T4 or T3 (active form of T4) 300 to 500 micra, followed by daily IV maintenance dosage 50-100 micra (1).

Amiodarone, a class III antiarrythmic agent, is very effective in treating life threatening ventricular arrhythmias especially in heart failure patients (6). It has low pro-arrythmic effect and low negative ionotropic effect among patients with compromised ejection fraction (7). Nevertheless, Amiodarone has deleterious effects on thyroid function reported to range from subclinical hypothyroidism, subclinical hyperthyroidism to overt clinical hypothyroidism and hyperthyroidism (8). Amiodarone is an iodine rich compound ( 37% iodine by weight ) ,and so a normal daily dose of 200 mg po bid generates about 6-12 mg of free iodine which is about 40 folds higher than the World Health Organization (WHO) recommended daily dose of 0.15-0.30 mg per day(8). The high levels of iodine cause hypothyroidism by Wolf-Chaicoff (8). The incidence of amiodarone induced hypothyroidism is 6% in countries with low iodine intake and 13% in countries with high iodine intake (8). Unlike the pulmonary toxicity of amiodarone, which is dose dependent, the thyroid toxicity of amiodarone does not correlate with the dose (2,8). To date, 200 cases of myxedema coma have been reported with only one case secondary to long term amiodarone therapy (1,3).

  The American Association of Clinical Endocrinologists recommends that patients should have a baseline TSH measurement before initiating amiodarone, and then they should be monitored at 6-month intervals during treatment. (9). However no special note is taken for heart failure patients who  may suffer serious morbidity and mortality from hypothyroidism, and thus may deserve closer follow up for TSH levels.