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J Thorac Cardiovasc Surg 2004;128:834-840
© 2004 The American Association for Thoracic Surgery


Surgery for Congenital Heart Disease

The Contegra conduit in the right ventricular outflow tract induces supravalvular stenosis

Bart Meyns, MD, PhDa,*, Leen Van Garsse, MDa, Derize Boshoff, MDb, Benedicte Eyskens, MDb, Luc Mertens, MD, PhDb, Marc Gewillig, MD, PhDb, Steffen Fieuwsc, Erik Verbeken, MD, PhDd, Willem Daenen, MDa

a Department of Cardiac Surgery, University Hospital Leuven, Leuven, Belgium
b Department of Pediatric Cardiology, University Hospital Leuven, Leuven, Belgium
c Department of Biostatistics, University Hospital Leuven, Leuven, Belgium
d Department of Pathology, University Hospital Leuven, Leuven, Belgium

Received for publication April 22, 2004; revisions received July 23, 2004; accepted for publication August 5, 2004.

* Address for reprints: Bart Meyns, MD, PhD, Department of Cardiac Surgery, University Hospital Gasthuisberg, Herestraat 49, 3000 Leuven, Belgium (E-mail: Bart.Meyns{at}uz.kuleuven.ac.be).

OBJECTIVE: We sought to evaluate the incidence and nature of pulmonary stenosis after implantation of the bovine jugular vein graft (Contegra; Medtronic, Inc, Minneapolis, Minn) in the right ventricular outflow tract.

METHODS: Between May 2000 and September 2002, 58 Contegra conduits (8-22 mm) were implanted during primary (n = 27) or redo operations (n = 31) in 57 patients, with ages ranging from 2 days to 48 years (mean, 9 years). Indications were truncus arteriosus (n = 16), tetralogy of Fallot (n = 28), pulmonary replacement in the Ross operation (n = 10), and Rastelli-type repair for double-outlet right ventricle (n = 4). Echocardiography was prospectively performed by a fixed team of investigators during follow-up (mean, 22.7 ± 10 months). A peak gradient of greater than 50 mm Hg was considered severe stenosis.

RESULTS: Two patients died from Staphylococcus aureus–induced septicemia and enterococcal endocarditis after 12 days and 12 weeks, respectively. One patient died of heart failure caused by endocardial fibroelastosis after 1 year. Freedom from severe stenosis at the distal anastomosis was 91% ± 3% at 3 months, 68% ± 6% at 12 months, and 49% ± 8% at 24 months. The risk of development of stenosis does not change over time. Younger age and its derivatives (graft size and indication) are significantly related to the occurrence of severe stenosis (P < .0001). Seventeen (29%) conduits required an endovascular intervention (balloon dilatation or stent). Seven (12%) conduits were explanted (endocarditis, 2; stenosis, 5). Histologic analysis of the explanted conduits showed excessive proliferation of neointima at the level of the distal anastomosis. Valve regurgitation was observed in 9 (16%) conduits and was always secondary to dilatation in the presence of severe distal stenosis.

CONCLUSION: The Contegra conduit induces a neointimal proliferation at the level of the pulmonary anastomosis. This leads to a high incidence of severe stenosis at intermediate-term follow-up.





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