The Production of Cardiac Lesions by Repeated Injections of Desoxycorticosterone Acetate.

Desoxycorticosterone acetate prolongs the lives and restores many of the functions of patients suffering from Addison's disease and of adrenalectomized animals (1 to 5). The beneficial effects are related to the action on the kidneys which leads to excretion of potassium and retention of sodium (1, 5). Clinical observations have suggested that injurious results due to the steroid may appear along with the beneficial effects. While receiving desoxycorticosterone acetate, certain patients develop edema which has been attributed to excessive nephrogenic retention of sodium chloride and water (3, 5). Furthermore, a number of these patients have developed cardiac symptoms, including advanced congestive failure and enlargement of the heart by roentgenogram (2 to 8). In some cases the cardiac decompensation was regarded as a manifestation of previously existing disease of the heart which was aggravated by a return of the blood pressure to normal or high values (3). Certain authors have attributed cardiac failure to the added burden brought about by the increased volume of circulating fluids which retention of sodium chloride by the kidneys has caused (5). McGavack (6) pointed out that continued treatment leads to low concentration of potassium in serum and that this abnormality may account for the heart failure. Since it is recognized that desoxycorticosterone acetate exerts little or none of the glycogenic function of the adrenal cortex, disturbances in carbohydrate metabolism might be anticipated in Addisonian patients treated with the synthetic hormone (9). Hypoglycemia has been observed but does not seem to be an important factor except during pro-