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Eur J Cardiothorac Surg 2002;22:802-807
© 2002 Elsevier Science NL

Structural degeneration of pulmonary homografts used as aortic valve substitute underlines early graft failure

^a Department of Cardiothoracic Surgery, Leiden University Medical Center, Leiden, The Netherlands
^b Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands

Received 17 January 2002; received in revised form 25 June 2002; accepted 3 July 2002.

* Corresponding author. Department of Cardiothoracic Surgery, Leiden University Medical Center, PO 9600, 2300 RC Leiden, The Netherlands. Tel.: +31-71-5262355; fax: +31-71-5248284
e-mail: d.r.koolbergen{at}lumc.nl

Objectives: The limited availability of donor valves and experimental evidence that pulmonary valves can withstand systemic pressure made us use cryopreserved pulmonary homografts as aortic valve substitutes. We observed a high incidence of early reoperation because of severe graft insufficiency due to cuspal tears. The mid-term results are evaluated in this study and histological analysis of explanted homografts is performed to investigate the cause of graft failure. Methods: From December 1991 to April 1994, 16 patients (13 male; mean age 37.3 years, range 21–59 years) underwent aortic valve replacement with a cryopreserved pulmonary homograft. The indication was endocarditis (n=4), bioprosthesis degeneration (n=3) or congenital aortic valve disease (n=9). All homografts were implanted freehand in the subcoronary position. All patients were contacted for follow-up and recent echo-Doppler studies were reviewed. Six explanted homografts were examined microscopically using routine histological techniques to analyze changes in cell population, collagen and elastic fiber structure. Results: Follow-up was complete in all patients. Reoperation was required in ten patients because of severe graft incompetence (mean implantation time 5.9 years, range 2.8–8.0 years). In two patients, recurrent endocarditis was the cause of graft failure. In the other eight patients the leaflets looked pliable and thin with gross tearing in one or more cusps. The histopathologic changes observed were remarkably similar in all examined grafts: the cusp tissue was almost non-cellular and the collagen fiber structure had mostly disappeared. At the site of rupture, the tissue had become thin with strongly degenerated collagen and elastic fiber structure. In the six patients with a homograft remaining in situ, echo-Doppler showed trivial to mild insufficiency in five cases and moderate to severe in one case, whereas no significant gradients were observed. Conclusions: We concluded that structural reduction of cell number and degenerative alterations in the molecular composition of the extracellular matrix in valve tissue is the main cause of early graft failure in this series. The use of cryopreserved pulmonary homografts in the systemic circulation is therefore not advised.

Key Words: Cryopreserved pulmonary homografts • Pathology • Pulmonary homograft • Pulmonary allograft

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