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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.T HE present availability of surgical closure of ventricular septal defects renders a number of questions particularly pertinent. Some of these may be answered by pathologic studies and clinicopathologic correlations. Such studies are proper even though there is inherent selection of cases among those included in a pathologic series. These studies provide information concerning the anatomic position and relations of ventricular septal defects, the causes of and ages at death, and the association of ventricular septal defects with other cardiovascular malformations. The present report is a necropsy study of 50 cases of ventricular septal defect.Surgical procedures designed to close the defects had not been done in any of the patients. An attempt is made to throw additional light on these problems. The diameter of the defect and the diameter of the aorta at the level of the valve were measured in each specimen. The ratio of their relative sizes was useful in defining the size of a given ventricular septal defect irrespective of the age of the patient and the size of the heart.The cause of death in each case was designated as either related or unrelated to the congenital malformation of the heart. The immediate causes of death in the former group were heart failure and bacterial endocarditis. Although heart failure was considered to have affected both ventricles, the cases with this complication could be subdivided further according to the predominant picture: predominantly left ventricular failure was considered to be manifested in the cases showing pulmonary congestion and edema, whereas predominantly right ventricular failure was considered to exist in cases having peripheral edema, serous effusion, and chronic passive congestion of the liver.The results of the pathologic studies are presented in 2 sections. The first involves those cases in which the ventricular septal defect was not associated with other cardiovascular anomalies (group A). The second section deals with those cases in which the ventricular septal defect was associated with other coincidental, congenital malformations of the heart or great vessels (group B).

Serial histologic sections of the atrioventricular (A-V) conduction system were studied in four hearts with persistent common A-V canal, and the anatomic findings were related to the abnormal ECG patterns. Two hearts were examples of the partial form and two of the complete form of A-V canal. The major anatomic abnormalities were: (1) postero-inferior displacement of the A-V node; (2) relatively short distances between the A-V node and the origin of the left bundle branching; (3) marked posteroinferior displacement of the left bundle branching system; and (4) relative hypoplasia of the anterior (superior) left bundle branches. The anatomic configuration of the A-V conduction system in A-V canal could result in relatively early impulse propagation to the posterior aspect of the ventricular septum as suggested by reported electrophysiologica studies. The anatomic findings are considered to be related closely to the known ECG patterns of A-V canal.