The tissue concentrations of digoxin were measured in 13 cadavers who before death had been on the maintenance digoxin therapy. Tissue samples were taken from 5 different parts of the heart, from skeletal muscle, liver and kidney. Digoxin was extracted by dichlormethane and measured by radioimmunoassay. Whole blood digoxin was measured by the same method. The appropriate recovery studies showed good extraction. The highest heart digoxin concentration was found in the septa1 muscle (mean 132 5 S . D . 65 nglg) and the lowest in the left auricle (43 & 26 ng/g). The heart concentrations were in good correlation with the whole blood concentrationthe best correlation was found with the ventricular muscle (r = 0.86). The skeletal muscle concentration was about 15 % of the heart concentration (20 t 13 ng/g) and the correlation with the whole blood was poorer (r = 0.54). The kidney concentration (123 5 65 nglg) was approximately the same as that of the heart and the liver concentration was 68 -I 51 nglg. The results indicate a linear correlation between blood and heart.

Linear correlation was demonstrated between serum digoxin and papillary muscle digoxin concentrations in patients undergoing mitral valve surgery. The mean ratio of myocardial tissue to serum digoxin concentrations was 6711. This result supports the use of serum digoxin as a guide for assessing the degree of digitalization under steady-state conditions.

To study metabolic factors in the genesis of coronary heart disease in previously healthy young adults, 24 men (aged 23 to 49 years) who had recovered from proven myocardial infarction were compared with an age-matched series of 20 healthy subjects-10 business and professional men and 10 prisoners. Both series averaged 10% above ideal body weight. The patients were shorter, were heavier smokers, and had a high familial incidence (70%) of coronary heart disease. The controls had more familial diabetes. Oral glucose tolerance tests without and with cortisone showed higher peak blood sugar levels and delayed return in the patients. Four patients were found to have fasting serum triglycerides above 300 mg% and were placed in a separate category of essential hyperlipidemia. In the remaining 20 patients, serum cholesterol and triglycerides in combination were higher than in the controls, together with elevation of pre-β-lipoproteins. α 1 -Lipoprotein was decreased. Mean postheparin lipolytic activity was slightly less in the patients-in the lower part of the normal range. In the combined series of patients and control subjects, the relative body weight showed significant correlations-directly with the 1-hour blood sugar level in the glucose tolerance test and with the fasting serum triglyceride level, and inversely with the α 1 -lipoprotein. The relative body weight did not show a significant correlation with the serum cholesterol level. A set of 10 characteristics and biochemical variables, referred to in preceding paragraphs, was found to discriminate well between the patients and their controls. The total incidence of abnormal findings was high among the patients (mean, 4.9 per man) and low among the controls (mean, 1.9 per man), but the positive items were grouped in many different ways in individuals. Analysis of the data suggests that over-nutrition and heavy smoking interact with hereditary factors in certain individuals to accelerate the progress of coronary atherosclerosis. Since individuals who exhibit many of the criteria indicative of increased risk are not uncommon in our population, their identification as candidates for coronary heart disease early in life is a significant public health problem.

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