Citations

Of the 614 open-heart operations performed at the Mayo Clinic for acquired aortic valvular disease, 130 were performed on patients who also required repair of other valves. Review of the remaining 484 operations resulted in the following observations. Operation for acquired aortic valvular disease may now be accomplished with a hospital mortality rate of 4%. The incidence of late death and failure of patients to improve has averaged 44% for previously employed techniques of valvular repair. Failure of the valve or prosthesis to function properly was the most common cause of late failure after operations in which these earlier methods were used. In the 138 more recent cases, in which operations employing the aortic ball valve (Starr-Edwards prosthesis) were used, the incidence of late failure has been reduced to 14%, and failure of the prosthesis to function properly has not yet occurred in the absence of infection. Late bacterial endocarditis and thromboembolism were the most serious problems associated with use of the ball-valve prosthesis. In contrast with the late results of the former techniques, use of the ball valve has resulted in improvement for 79% of the patients; in the great majority of these there has been a dramatic return to normal living. Despite the highly satisfactory results of current methods, the fact that 14% of patients have already died after an initially successful operative result, and that another 12% have suffered complications causing their late result to be less than totally satisfactory, indicates that the policy of recommending for operation only those patients who have significant and progressive cardiac disability should be continued.

Recently we have studied the role of surgical treatment of patients having occlusive cerebrovascular disease, particularly incipient stroke (or focal intermittent cerebrovascular insufficiency). This report concerns 35 pa-patients with incipient stroke in whom circulation was restored to normal by operation on an artery in an attempt to prevent transient ischemic episodes and cerebral infarction. Since all of the patients were neurologically normal at the time of the surgical procedure, we were concerned primarily with the risk of [see tablein the PDF file] the procedure, particularly in terms of cerebral infarction. The operative mortality rate was 8.5 per cent (three patients). Six patients (17 per cent) sustained cerebral infarcts. Four of these had mild neurologic deficits, usually consisting of clumsiness and mildly reduced discriminatory sensation in one hand; one had a severe neurologic deficit, and one died. Evidence shows that at least some of these infarcts resulted from emboli arising from the operative site at the time of or shortly after the operation. The results of long-term follow-up revealed that 66 per cent of the surgically treated patients were normal compared to 25 per cent of a contrast group; and 17 per cent of the treated patients had suffered cerebral infarcts compared to 40 per cent of the contrast group. The long-term results are thus similar to the immediate postoperative results. These findings simply indicate that an operated patient's prognosis was good over the long term if the cerebral ischemic episodes were relieved and if he sustained no complications from the surgical procedure.

Nineteen patients with ventricular septal defect and severe aortic valvular incompetence have been operated on at the Mayo Clinic. There were two early deaths and two late deaths. The ventricular septal defect was located high and anteriorly in the septum and was often small. Aortic valvular incompetence was due, in most cases, to a deformed, prolapsing right coronary cusp. Mild to moderate degrees of infundibular pulmonary stenosis coexisted in nine patients. Repair of the ventricular septal defect was readily accomplished in most cases by direct suture, and relief of obstruction to right ventricular outflow was effected, when required, by resection of the crista supraventricularis. Repair of the aortic incompetence was attempted by a variety of means, but the incidence of persistent significant regurgitation was high, except when prosthetic cusp replacement was used. It is currently our policy to defer operation in children unless there are significant symptoms. When the patient is past the age of about 12 to 14 years, operation is advised under proper circumstances, and it consists generally of suturing of the ventricular septal defect and replacement of the right coronary cusp of the aortic valve.

Open operation by means of extracorporeal circulation has been used on 47 patients with congenital aortic stenosis at the Mayo Clinic between April 1955 and July 1, 1960; 33 patients had valvular stenosis, 11 had subvalvular stenosis, and three had supravalvular stenosis. The over-all operative mortality rate was 13 per cent; 6 per cent of patients with valvular aortic stenosis died in the hospital. Severe aortic insufficiency did not develop in any patient operated on for valvular aortic stenosis although a diastolic murmur was present after operation in some. Rarely, however, was the transvalvular gradient completely eliminated by operation although 90 per cent of the surviving patients were either asymptomatic or had definite clinical improvement. Late follow-up hemodynamic studies suggest that a persistent transvalvular gradient may regress in time. Relief of obstruction caused by subvalvular variety of aortic stenosis is difficult whether stenosis is localized or diffuse. Even in this gruop, however, it has been possible to achieve good results with careful attention to certain technical details. Patients with congenital aortic stenosis should be operated on before the development of the sequelae of severe left ventricular hypertension.

A quantitative analysis was made of the pulmonary arterial medial thickness and index of medial surface area (ratio of medial tissue to pulmonary parenchyma) in 50 cases of uncomplicated ventricular septal defect in fetuses, infants, and children. The ages of the subjects ranged from 26 weeks of fetal life to 12 years. The results were compared with those obtained from a control group of the same age. During the fetal and newborn period, both the thickness and the index of surface area of the media were generally within normal limits, although in an occasional case pulmonary arterial branches were considerably thinner than those in corresponding controls. The subjects between 1 week and 5 weeks of age had a medial thickness and an index of medial surface area that were lower than the average values at the time of birth. In this regard the pulmonary arterial tree in cases of ventricular septal defect corresponded with that in normal newborn infants. Soon after, however, and most clearly from 8 weeks on, the subjects with ventricular septal defect showed a pronounced rise both in medial thickness and in the index of medial surface area, indicating the presence of considerable medial hypertrophy. Although intimal proliferation was observed in two infants of 11 and 27 days of age, it was uncommon in children less than the age of 1 year. Above that age it was almost invariably present. Plexiform or glomeruluslike structures were found in seven cases. The youngest patient with these lesions was 2½ years of age.

The pulmonary vascular tree was studied in 12 cases of uncomplicated atrial septal defect in fetuses, infants, and children. The ages of these subjects ranged from 24 weeks of fetal life to 11 years. A quantitative analysis was made of the medial thickness and of the index of medial surface area (ratio of medial tissue to pulmonary parenchyma) of the pulmonary arterial branches. In contrast to subjects with ventricular septal defect in corresponding age groups, the three fetuses in this series had medial hypertrophy, as indicated by a high index of medial surface area. In the postnatal group, both the medial thickness and the index of medial surface area were also usually greater than in the controls of corresponding ages, notably in two patients, who, at the ages of 7 weeks and 4 months, died of cardiac failure. No satisfactory explanation for these unexpected findings can be offered. Slight to moderate intimal proliferation was observed in some muscular and elastic pulmonary arteries, in bronchial arteries, and in pulmonary veins in several subjects. Thickening of the intima in elastic arteries was observed in a fetus of 26 weeks' gestation. Pronounced obliterative intimal changes were found in only one subject, an 11-year-old girl with severe pulmonary hypertension.

Among 60 necropsy specimens of isolated ventricular septal defects and more than 300 cases of ventricular septal defect observed at operation, 15 cases demonstrating unusual anatomic positions of the defect were found. The ventricular defect differed from the ordinary ventricular septal defect in that it usually occupied the position of the ventricular component of the defect in persistent common atrioventricular canal. For this reason it was named ventricular septal defect of the persistent common atrioventricular canal type. Deformities of one or both atrioventricular valves were common (nine of 15 cases). No atrial septal defects of the ostium primum type were present. Anatomic studies of the conduction tissue revealed that this tissue skirted the posterior and inferior aspects of the ventricular septal defect and that, as in persistent common atrioventricular canal, the course taken by the conduction tissue was unusually long, as a result of the peculiar posteroinferior position of the lower edge of the defect. The electrocardiographic features were striking. In all cases the mean electrical axis of the QRS lay above the isoelectric point; the vector loop obtained in the frontal plane from the scalar electrocardiogram was directed counterclockwise, and its main mass was above the zero line. In addition, in all cases there were signs of right ventricular overload, and in some cases of left ventricular overload as well. Electrocardiographic findings of this pattern have been thought by some authors to be diagnostic of persistent common atrioventricular canal, but we observed that they also occurred in each of the cases of isolated ventricular septal defect of the variety described herein. We recognize that in the usual variety of ventricular septal defect this electrocardiographic pattern occurs, but it does so uncommonly. We have not studied its exact incidence. The anatomy, hemodynamics, and surgical considerations are different in cases with this defect from those with persistent common atrioventricular canal. The surgical risk in these cases has been higher than that in the usual type of ventricular septal defect. In the discussion of the electrophysiologic theories that seek to explain the unusual electrocardiographic patterns in this group of cases, a new theory is offered, based on studies of the conduction system. In our opinion, the different orientation of the advancing fronts of depolarization is the result of congenital displacement of the bundle of His in its relation to the ventricular septal defect.