Rastelli, G.C.

In each of 12 mongrel dogs, data for end-diastolic volume, end-systolic volume, and stroke volume of the left ventricle were obtained by two independent methods: the indicator dilution method and a radiographic method. While the values for stroke volume showed good agreement between the two methods, a significant and directionally constant difference was found between values for end-diastolic volume and end-systolic volume calculated by the two different methods. This was observed in dogs with fast heart rates (exceeding 150 beats/min), as well as in dogs with heart rates of about 100 beats/min. The findings strongly suggest that a fundamental error is present in estimations of volume based on the washout of an indicator dye.

The imposition of a chronic work load (pulmonary artery constriction) on the right ventricle increases ventricular muscle mass. This is associated with increased ventricular stroke work when the animal is standing awake, during infusions of norepinephrine, and under conditions of exercise (running on a horizontal treadmill). Studies two weeks after release of chronic pulmonary artery constriction reveal stroke volume and cardiac output are increased during standing at rest, during norepinephrine infusion, and during exercise. Studies eight weeks after removal of pulmonary artery bands show that stroke volume and cardiac output are approaching the normal range. Right ventricular hypertrophy and right ventricular stroke work decline progressively and apparently in parallel in the weeks following release of chronic pulmonary artery constriction. The stroke work capacity of the ventricle seems related to the presence of right ventricular hypertrophy. With a reduction in outflow tract resistance, the stroke volume for a given set of circumstances is markedly increased. From this standpoint, the work capacity of the right ventricle may be taken as a determinant of stroke volume and cardiac output. Decrease of systemic vascular resistance and relative insensitivity of systemic vasoreceptors to norepinephrine were observed after the release of chronic pulmonary artery constriction. These phenomena have roles in the production of the observed hyperdynamic circulatory state, but their contributions to its genesis are secondary to the major role of the hypertrophied right ventricle.

Postoperative embolism occurred in 35 of 546 patients traced for 2 to 15 years after surgical repair of uncomplicated ASD. A total of 58 embolic episodes occurred, resulting in the death of 11 of these 35 patients. The incidence of embolism was not significantly related to the technique used for surgical repair. Six of the nine patients who had had a preoperative embolism also had an embolism in the postoperative period. The most significant factors associated with an increased risk of postoperative embolism were increased age of the patient, atrial fibrillation, and pulmonary hypertension, all of which are interrelated: seventy-seven per cent (27/35) of patients having a postoperative embolism had either atrial fibrillation or pulmonary hypertension, and 77% (27/35) of patients with postoperative embolism were more than 40 years old at the time of the first embolism. Because actuarial analysis suggests that 30% of patients more than 40 years of age who have atrial fibrillation after repair of ASD may have an embolism within 10 years postoperatively, continuation of anticoagulation therapy indefinitely in these patients is suggested. The highest risk of embolism occurs in the early postoperative period, suggesting the advisability of anticoagulation therapy for all adult patients during convalescence.

Complete surgical correction of transposition of the great arteries associated with subvalvular pulmonary stenosis carries a high mortality rate. A new surgical technique that achieves redirection of the ventricular outflows and relieves pulmonary stenosis by bypassing it, was successfully used to repair complete transposition of the great arteries associated with ventricular septal defect (VSD) and valvular and subvalvular pulmonary stenosis in a 14½-year-old patient. The repair consists of (1) division of the pulmonary artery, the cardiac end of which is oversewn, (2) repair of the VSD with a patch in such a way as to connect the left ventricle with the aorta, and (3) reconstruction of the pulmonary artery with an aortic homograft, including the aortic valve, which is anastomosed between the distal end of the pulmonary artery and the right ventricle. A review of the cases in which the current techniques were used indicates that the location and nature of the obstruction in the left ventricular outflow tract defies successful repair in most instances. Localized ridges and diffuse hypoplastic outflow tracts are recognized causes of obstruction, but anomalies of the mitral valve commonly contribute to or are the primary cause of subvalvular obstruction.

At the Mayo Clinic, four patients were seen in whom a ventricular septal defect (VSD) of the atrioventricular (A-V) canal type was associated with an angle of nearly 90° between the intact atrial septum and the ventricular septum. The right atrium overrode the ventricular septum and communicated with both ventricles. A complex, straddling right A-V valve had some attachments in the left ventricle and resembled the common A-V valve of persistent common A-V canal. In three of the patients, a congenital mitral valve deformity also existed. Mild cyanosis probably is not a contraindication to surgical repair in such patients because right atrial blood may enter the left ventricle directly.

The effect of the mitral Starr-Edwards ball-valve prosthesis on cardiac function was investigated in the dog. Fifteen dogs were studied for the first 48 hours after replacement of the mitral valve (the chordae tendineae [see Figure in the PDF file] had been totally resected, partially resected, or preserved). The cardiac output and left atrial pressure were similar in these three groups of animals and in two animals subjected to sham operation. Ten dogs (five with intact chordae and five with excised chordae) were studied two months after the insertion of a Starr-Edwards prosthesis. In these animals normal hemodynamic values were obtained at rest and during infusion of acetylcholine, except for a marked (liastolic gradient across the prosthesis, which developed at high cardiac output and heart rate. Six dogs were able to complete a standard test of substantial, unrestrained, graded exercise and gave a normal heart rate response. Heart rate increased and was maintained during maximal efforts, to levels of about 300 beats/min, demonstrating that heart rate need not be a limit of cardiac performance. No evidence of left ventricular dysfunction or of a decrement in cardiac performance could be demonstrated in dogs early or late after replacement of the mitral valve with a Starr-Edwards prosthesis. The presence or absence of chordae tendineae was irrelevant to cardiac performance.

Cardiac output, stroke volume, and atrial, pulmonary arterial, left ventricular, and systemic arterial pressures were measured preoperatively, during operation, and for 48 hours thereafter in 14 patients undergoing prosthetic replacement of the mitral valve. Cardiac output was usually abnormally low after repair, being lowest 3 to 6 hours after operation. This pattern was different from that in a patient undergoing plication of the posterior leaflet and very different from that in a patient undergoing removal of a left atrial myxoma, who served as controls. Ventricular filling pressure was high, there was no significant diastolic pressure difference across the Starr-Edwards prosthesis, and there was no pressure difference across the left ventricular outflow tract. Blood gas levels and pH were within satisfactory range. The data are interpreted as indicating that impairment of ventricular performance, particularly left, usually contributes significantly to the low cardiac output in these patients. This is probably related in part to preoperative ventricular function. Possible additional contributing factors are discussed.

A total of 131 patients with the partial form of common atrioventricular canal were operated on between March, 1955 and January, 1964. The over-all hospital mortality rate was 3.8%; no deaths occurred in patients who had no or only mild incompetence of the mitral valve. Permanent heart block has not occurred in the last 93 cases. Results have been good in general, although there is evidence of residual mitral valve incompetence in many patients. In the few who had severe incompetence at the mitral valve before repair, the results have been considerably less satisfactory than in the group as a whole; therefore, further work is needed on this aspect of the problem.