Rheumatic fever.

The time of onset of the first heart sound is related to the simultaneous electrocardiogram in subjects with mitral stenosis, mitral insufficiency, and heart disease without mitral valve disease. A delay in the first heart sound occurred in patients with only mitral stenosis and proved of diagnostic value. The degree of delay paralleled the severity of the mitral stenosis. The mechanism by which the first sound is delayed in mitral stenosis can be readily explained by the hypothesis that the first heart sound is caused by sudden tensing of the atrioventricular valves and chordae tendineae when the atrioventricular septum is pushed in the direc- tion of the atrium. In mitral stenosis, the left atrial pressure is high, while the end diastolic pressure in the left ventricle is low. The mitral valve does not close until the left ventricular pressure exceeds that of the left atrium. This disparity of pressures in the atrium and ventricle is found consistently in mitral stenosis. Significant shortening of the Q-first sound interval occurs with successful enlargement of the mitral orifice. Ventricular contraction does not contribute to the audible portion of the first sound. Moreover, this sound probably arises chiefly in the mitral rather than in the tricuspid valve. The length of the interval between the second sound and the opening snap of the mitral valve is generally in- versely related to the severity of the mitral stenosis. This interval lengthens with successful mitral surgery. The presence of an opening snap is of great diagnostic significance. It is a more frequent finding in severe mitral stenosis than is a diastolic murmur. Dehydro- genase Activity in Blood. (Oct.), The observation that during experimental and clinical myocardial infarction glutamic oxaloacetic transaminase is released from cardiac muscle resulting in increased enzyme activity in the serum suggested that other cardiac tissue enzymes behave similarly during myocardial infarction. Although present in other tissues in greater activity, lactic dehydrogenase, the enzyme concerned primarily with the reduction of pyruvic acid to lactic acid, is present in appreciable activity in cardiac muscula-ture. In order to ascertain whether lactic dehydro-genase (LD) activity is increased in the serum during myocardial infarction, it was necessary to first demonstrate its presence inhuman and animal blood, and to delineate variations in LD activity in the blood of normal and diseased man. LD activity is present in the venous serum of normal human adults. Normal activity ranges from 260 to 850 units/ml. with a mean value of 470 ± 130 units/ml. Venous whole blood hemolysates of normal adults have LD activity varying between 16,000 to 67,000 units/ml. with a mean value of 34,000 i 12,000 units/ml. Alterations in serum LD have been studied in a selected group of disease states. Experimental and clinical myocardial infarc- tion are associated with a rise in serum LD activity. rises a characteristic fashion