Citations

Fifty patients underwent correction of one or two valvular lesions with concomitant insertion of one to three aortocoronary vein bypass grafts. Hospital mortality was 14% and late mortality was 10%. Factors influencing operative mortality were: (1) mitral valve replacement after myocardial infarction; (2) complete obstruction of a coronary artery preoperatively; (3) high left ventricular end-diastolic pressure at rest preoperatively in patients with mitral valve disease; and (4) use of a single aortocoronary graft in the presence of multiple-vessel disease. For patients with significant associated valvular and coronary artery disease, combined correction yields results that appear sufficiently encouraging, judged by mortality and follow-up, to warrant its continued use in selected cases.

One hundred sixty-nine patients underwent replacement of the aortic valve with an aortic valve homograft; of these patients 17 had concomitant commissurotomy or annuloplasty for an associated mitral valve lesion. Homografts were prepared by sterilization with beta-propiolactone solution and stored in Hanks' solution, or were prepared by sterilization with irradiation and stored at -70 C. Operative mortality was 5.3%. Thirty (19%) of the 160 surviving patients had an aortic diastolic murmur at the time of hospital dismissal, and five of these patients had hemodynamically significant homograft incompetence. For 156 patients, follow-up was longer than 6 months; among the 147 patients who survived operation, there were 12 late deaths. Eighty-four per cent (132) of these 156 patients were alive and well 6 to 54 months after operation. Six patients have required reoperation for valve incompetence. An aortic diastolic murmur was present in 43% of patients. Five patients had significant valve incompetence; four of these patients are markedly improved over their preoperative status. Thromboembolism has been a rare complication despite the fact that anticoagulant therapy was not used. Late calcification of the homograft valve has been noted in only one patient.

Left ventricular hemodynamics at rest and during supine exercise were studied before and 1 year after internal mammary artery implantation in 24 patients with severe coronary artery disease and angina pectoris and in five similar patients before and after 1 year of medical treatment. In the surgical group, 14 had evidence of one or more implants providing collaterals to coronary arteries, and 10 had no evidence of collaterals from the implant. Only two patients, both with functioning implants, showed a return to normal of left ventricular end-diastolic pressure at rest and during exercise. There was no correlation between clinical improvement and hemodynamics at the time of the postoperative study. It is concluded that left ventricular hemodynamics may return to normal after internal mammary artery implantation but this was uncommon in the present study.

During pregnancy, when surgically reparable heart disease can no longer be medically manged, open- or closed-heart surgery is the procedure of choice without prior therapeutic abortion. Cyanotic congenital heart disease in a pregnant patient when completely correctable surgically may be an indication for surgery in itself. Available data suggest that pregnancy per se does not increase the maternal risk of heart surgery with use of extracorporeal circulation. Fetal mortality in our series was 33%.

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.

Left ventricular (LV) performance was studied during mild exercise (100 kg-m/min for 3 minutes) in 19 cases of coronary artery disease (CAD). Each patient suffered from a severe anginal syndrome. None had ventricular aneurysm, cardiomegaly, or clinical heart failure. Mean resting values follow: LV end-diastolic pressure (LVEDP), 19 ± 7 mm Hg; LV systolic pressure (LVSP), 150 ± 16 mm Hg; stroke volume index (SVI), 48 ± 10 ml/beat/m 2 ; and LV stroke work index (LVSWI), 81 ± 19 g-m/m 2 . During exercise LVEDP rose to 30 ± 8 mm Hg ( P ≤0.001) and LVS to 160 ± 20 (not significant [NS]); SVI diminished to 46 ± 11 (NS) and LVSWI, to 76 ± 24 (NS). Patients with decreased or asynchronous areas of LV myocardium identified on cine left ventriculograms had higher mean LVEDPs during exercise than did those with normal ventriculograms (34 ± 10 versus 26 ± 4 mm Hg; P ≤0.05). The difference between responses to exercise of patients who experienced angina during the study and of those who did not was NS. Administration of nitroglycerin reduced the increase in LVEDP during exercise. An abnormality in LV performance-a significant rise in LVEDP without a significant increase in SVI or LVSWI-was observed in 13 of 19 cases of CAD.