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J Thorac Cardiovasc Surg 1998;116:670-671
© 1998 Mosby, Inc.
LETTERS TO THE EDITOR |
Genolier, Switzerland
Pediatric Cardiac Surgery, University LausanneClinique de Genolier, Genolier CH-1272, Switzerland
To the Editor:
In August of 1969, an 8-year-old girl underwent surgery for pulmonary atresia with a ventricular septal defect. The operation was performed by Christian Barnard in South Africa. The surgical repair consisted of closure of a patent ductus arteriosus and of 2 major aortopulmonary collateral arteries to the left lung, patch closure of the ventricular septal defect, and aortic homograft interposition between the right ventricle and the pulmonary artery bifurcation.
The patient remained free of symptoms for about 21 years, with 3 uncomplicated pregnancies. On October 1990 she came to us with signs of right ventricular hypertension. Routine clinical investigations (electrocardiography, chest radiography, echocardiography), magnetic resonance imaging, and cardiac catheterization confirmed an increase in systolic right ventricular pressure (80 mm Hg) caused by an obstruction at the level of the distal anastomosis of a completely calcified conduit. The investigations also showed the presence of a residual (or recurrent) large atrial septal defect. In April 1991, 21 years 8 months after the first surgical procedure, she underwent closure of the atrial septal defect and replacement of the right ventriclepulmonary artery conduit with a 23 mm pulmonary homograft. At the end of the procedure systolic pressures of 25 mm Hg in the right ventricle and 105 mm Hg in the left ventricle were recorded. The postoperative course and the follow-up have been uneventful. Radiology (Fig 1) of the explanted conduit (Fig 2), as well as histologic study, confirmed the extensive calcification of the aortic homograft, in situ for 21 years 8 months.
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