Myxedema Heart Disease

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Abstract
THE CLINICAL syndrome of “myxedema heart” consists of an enlarged sluggish heart with low electrical voltages and flattened or inverted T waves on the electrocardiogram, changes which are reversible with the administration of thyroid hormone. Other abnormalities of the cardiovascular system, including bradycardia, diminished cardiac output, increased circulation time, and increased arteriovenous difference, may occur in myxedematous patients without overt involvement of the heart. The exact nature of the cardiac lesion in myxedema heart disease has been the subject of considerable debate (11, 15, 16). Some authors have believed that involvement of the myocardium by the myxedematous process is the dominant abnormality (1, 4, 14). The importance of coronary artery disease in myxedema has been both stressed (1, 4, 5) and questioned (2). Others have considered pericardial effusion the dominant feature of the disease (17); indeed, Kern et al. thought this effusion “a constant, early, and major factor” in the syndrome of “myxedema heart” (12). To evaluate the occurrence of detectable pericardial effusion, carbon dioxide angiocardiography was performed in 9 patients with myxedema and apparent cardiac enlargement. In 7 of the 9 cases, significant pericardial effusion was demonstrated. Illustrative Case Reports CASE I: L. O'K., a 62-year-old white woman, was admitted to the Psychiatric Service of Detroit Receiving Hospital with a five-year history of progressive weakness and lethargy associated with a 25-pound loss in weight. Her voice had become deeper in pitch during this period. For the three years prior to admittance, the patient had not left her home and had spent virtually all of that time in bed. Physical examination showed a wizened and lethargic woman. Her blood pressure was 90/60, the pulse was 68 and regular. Upon examination of the heart the point of maximal impulse was palpated at the left sixth interspace at the anterior axillary line. The heart sounds were decreased. The thyroid was not palpable. Deep tendon reflexes showed a delayed return. Pertinent laboratory findings were an p131 uptake at two hours of 4 per cent; at twenty-four hours, 2 per cent; p131 with thyroid-stimulating hormone at two hours, 5 per cent; at twenty-four hours, 1 per cent. The blood cholesterol was 191 mg per 100 ml. Electrocardiography demonstrated very low voltages throughout and flat ST segments and flat T waves over the left ventricle. On radiographic examination of the chest, the heart shadow was grossly enlarged and the lungs were clear (Fig. 1,A). Carbon dioxide angiocardiography showed a marked increase in the right atrial-pericardial shadow indicative of a considerable accumulation of pericardial effusion (Fig. l,B). A diagnosis of primary idiopathic myxedema was made.

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