Electrocardiographic abnormalities have been studied after administration of chloroquine in 25 patients, of emetine in 28 patients, and of emetine and chloroquine in 28 patients.Abnormalities after chloroquine were less in severity and of shorter duration than after emetine. They were more severe, became maximum later after cessation of emetine therapy, and were much longer in duration after emetine and chloroquine than after emetine. These differences are attributed to combined effects of the two drugs.Serum potassium levels showed some decrease after antiamebic therapy, the decrease being more after emetine than after chloroquine.A case is reported in which severe abnormalities and muscular paralysis occurring after emetine and chloroquine were rapidly reversed by oral potassium administration.Administration of potassium simultaneously with emetine and chloroquine often prevented or delayed the appearance or decreased the severity of abnormalities. Subsequent potassium administration usually reversed the abnormalities except in cases in which they were present before emetine therapy. It is concluded that the abnormalities are functional in nature and not due to organic myocardial damage.It is suggested that some disturbance of potassium metabolism in the myocardium and skeletal muscles may be the cause of electrocardiographic abnormalities and emetine neuritis, respectively.

One hundred and fifty patients with chronic severe anemia were studied to determine the nature of cardiac enlargement and its relation to various factors. Enlargement was present in 120 patients. It showed no consistent relation to the hemoglobin level on admission. A significant increase in the cardiac size and incidence of failure was observed with increased severity of anemia, and in female as compared to male patients. The incidence of enlargement showed no relation to the age and sex of the patient and the duration or the etiologic factor of anemia. With correction of the anemia, enlargement disappeared rapidly in 92 patients, indicating that it was due to dilatation alone. Some enlargement persisted in 28 patients, and it is believed to be associated with cardiac hypertrophy. Pericardial effusion due to heart failure in 2 patients contributed to a small extent to the enlargement of the cardiac shadow.

Cardiovascular adjustments that develop in chronic anaemia have been studied by many investigators. Studies of renal circulation in anmmia, however, are few (Bradley and Bradley, 1947;Whitaker, 1956). A characteristic reversible renal functional abnormality has been described in chronic anxmia. It has been suggested that cedema, which occurs in a large number of cases of anemia on some basis other than decreased plasma osmotic pressure or increased venous pressure, may be secondary to renal retention of salt and water, possibly attributable to glomerulotubular imbalance (Bradley and Bradley, 1947) or abnormal tubular reabsorption (Whitaker, 1956).Abnormalities of renal function in chronic anemia in patients with cedema have, however, not been reported. The present investigation of circulatory abnormalities, particularly of renal circulation, was undertaken to determine the etiological factor of cedema in patients with chronic severe anemia. SUBJECTS AND METHODSForty-five patients, 36 men and 9 women, admitted to the hospital for treatment of chronic anemia of not less than three months' duration and with hematocrit values of less than 30 per cent were selected for this study. Their ages ranged between 14 to 50 years with an average of 30 years. (Edema was present in 25 patients, 17 men and 8 women, in 8 of whom congestive heart failure was considered to be present. Dyspnoea, cedema of feet, and hepatic enlargement, which are usual manifestations of congestive heart failure, also occur in uncomplicated chronic aneemia. Heart failure was, therefore, considered to be present after careful consideration of these factors, and of elevated venous pressure, clinical and radiological evidence of pulmonary congestion, and rapid regression in size of the enlarged tender liver with improvement of the anwmia. The duration of symptoms of anmmia varied between four months and three years with an average of 15 months. The duration of anemia was presumably much longer, and was due to hookworm infestation in 21 cases, chronic dysentery in 13, bleeding hkmorrhoids in 4, and chronic malaria in 2 cases, and was of undetermined etiology in 5 cases. The hxematocrit values ranged between 8 and 28 per cent with an average of 14-4 per cent: they were up to 10 per cent in 18, between 11 and 19 per cent in 16, and 20 and 28 per cent in 11 cases. Care was taken to exclude patients with hypertension or any renal or cardiovascular disorder apart from anemia, which might interfere with the circulatory abnormalities. The laboratory data were obtained on admission in each patient, but could be obtained after treatment in only 14 patients as it was found difficult to persuade patients for follow-up study after they were cured. The data were also obtained in 20 others to serve as normal controls.

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