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Ascending Aortic Extension for Right Pulmonary Artery Stenosis Associated With Ventricular‐to‐Pulmonary Artery Conduit Replacement
Author(s) -
Curran Ronald D.,
Mavroudis Constantine,
Backer Carl L.
Publication year - 1997
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.1997.tb00154.x
Subject(s) - medicine , cardiology , pulmonary artery , right pulmonary artery , stenosis , ascending aorta , ventricular outflow tract , left pulmonary artery , surgery , aorta
A bstractBackground : Ventricular‐to‐pulmonary artery conduits in growing patients with congenital heart disease will require replacement from time to time due to somatic growth, neointimal hyperplasia, and pulmonary artery stenosis. The purpose of this article is to review our experience with ascending aortic extension for significant long‐segment pulmonary artery stenosis in patients undergoing reoperation for right ventricular‐to‐pulmonary artery conduit replacement. Methods : From 1989 to 1997, 8 patients had aortic transection, right pulmonary artery augmentation arterioplasty, and aortic interposition graft (Hemashield in 7 and Gore‐tex in 1) in association with right ventricular‐to‐pulmonary artery conduit replacement in 7 patients and completion Fontan operation in 1 patient. Aortic cross‐clamp time was 90 ± 34 minutes, and the cardiopulmonary bypass time was 205 ± 37 minutes. Results : All patients survived. In those 7 patients who had conduit replacement, the RV/LV ratio declined from 0.78 ± 0.15 to 0.45 ±; 0.05 postoperatively (P < 0.05). Average length of stay was 8.9 ± 7.2 days. Follow‐up range is 18 months to 8 years (mean 4 years). Two complications included cardiac transplantation for pre‐existing poor left ventricular function and accelerated conduit stenosis leading to conduit re‐replacement. Conclusion : Ascending aortic extension facilitates long‐segment pulmonary artery augmentation arterioplasty and enlarges the retroaortic space, preventing future compression restenosis.