Many theories have been suggested to explain the development of the cardiac disorders that so frequently accompany exophthalmic goiter, but none of them are adequate. The most generally accepted belief is that toxic substances, which are related to the increased activity of the thyroid gland acting through the cardiac nerves or directly on the myocardium, are responsible for the tachycardia and the heart lesions that develop. Support for this view has been sought from the pathologic findings. At necropsy, the heart in exophthalmic goiter usually exhibits moderate hypertrophy and dilatation of both chambers, with fatty infiltration of the heart muscle cells. In some cases, small scars with interstitial or perivascular round cell infiltration are found scattered through the heart muscle. These, however, may be found as well in the hearts of patients with simple goiter.1Several observers have experimentally produced similar lesions by feeding desiccated thyroid to animals.2