Edwards, Jesse E.

Knowledge of the structural changes in the commissures, cusps, and chordae tendineae is important to the understanding of the pathologic physiology of mitral stenosis and its surgical correction. Study of 70 hearts with mitral stenosis disclosed that a frequent cause of the obstruction was commissural fusion or shortening of the chordae tendineae or both. In a small percentage of hearts, mitral stenosis appeared to result principally from rigidity of the valvular leaflets. Measurements of the various components of the mitral valve in normal hearts have been given in a previous paper. In this communication, comparable measurements for these structures in 50 hearts with mitral stenosis are presented.

In a necropsy study of 50 cases of ventricular septal defects, the anatomic position and relations of ventricular septal defects, the causes of and ages at death, and association of ventricular septal defects with other cardiovascular malformations were determined. The present availability of surgical closure of ventricular septal defects makes this information of practical significance.

Albuminuria may be an integral part of the picture of congestive heart failure. Of 161 patients in whom the histologic renal findings were considered to be either normal or to be of such a nature as not to be responsible in themselves for albuminuria, and in whom clinically obvious causes for albuminuria had been eliminated, 141, or 88 per cent, had albuminuria. The incidence of albuminuria was about equal among the various types of heart disease when heart failure existed. A trend existed for the grade of albuminuria to parallel the grade of heart failure. Based on a study of 21 patients, there seemed to be a correlation between the grade of albuminuria and the group of hypertension, according to funduscopic examination. No correlation was found between the grade of albuminuria on one hand and the systolic or diastolic values for blood pressure, the known duration of elevated blood pressure, the grades of hematuria or the values for blood urea on the other hand. Among the 161 patients with heart failure in our group 1 (kidneys either normal or containing lesions not judged to be causes for albuminuria), there was no predominant renal lesion associated with any one cardiac lesion.

Administration of a moderately large or large dose of cortisone to dogs having acute myocardial infarctions inhibited slightly the rate of removal of necrotic muscle fibers in these animals as compared with untreated animals. Delay was appreciable at four and six days after production of the infarct in animals receiving 2.5 mg. of cortisone per kilogram of body weight and at 4, 6, 12 and 21 days in animals receiving 10 mg. per kilogram. At all other periods up to essentially complete healing of the infarcts as defined at 60 days, no appreciable differences existed between treated and untreated animals.

Previous studies in this series demonstrated structural changes in the pulmonary vascular bed as the result of mitral valvular disease and other cardiac disorders. The present study demonstrates changes in the lungs as the result of chronic left ventricular failure; these changes were like those produced by mitral stenosis. The most pronounced disturbance was medial hypertrophy. The exact mechanism is not known, but it probably is related to increased pulmonary venous pressure.

Progressive histologic changes occur in the pulmonary arteries and arterioles, as a complication of chronically elevated pulmonary arterial blood pressure, in patients with congenital septal defects of the heart. This progression is so stereotyped as to allow a division of the structural effects into 6 grades. The histologic features of each grade are described in detail in this communication. These results afford a basis for comparing the magnitude of these changes to the clinical findings.