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JASPER A. SMITH, M.D.; SAMUEL A. LEVINE, M.D.

Arch Intern Med. 1947;80(2):265-270.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

ONE OF the most gratifying experiences in the care of patients suffering from cardiovascular disease is the treatment of patients with thyrocardiac disease. This is true whether the cardiac disability is entirely due to thyrotoxicosis or whether there is an additional independent cardiac lesion. Such patients respond so well to proper management and often have so few of the customary signs of thyrotoxicosis that physicians have been impelled to search carefully for these cases of masked thyrotoxicosis. The result is that on minor suspicion determinations of basal metabolism are frequently performed in order not to overlook thyrotoxicosis as a remediable burden in patients suffering from various types of cardiac disability. At times the decision is difficult, because there are numerous other causes of an elevated basal metabolism apart from hyperthyroidism. Peabody and Wentworth¹ pointed out that cardiac failure itself caused an increase in consumption of oxygen and estimated that . . . [Full Text PDF of this Article]

Author Affiliations
WATERBURY, CONN.; BOSTON

From the Medical Clinic of the Peter Bent Brigham Hospital and the Department of Medicine, Harvard Medical School, Boston.

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