Pathology of valved venous homografts used as right ventricle-to-pulmonary artery conduits in congenital heart disease surgery |
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Authors: | Chrystalle Katte Carreon Annachiara Benini Christopher Baird David Hoganson Michele Borisuk Sitaram Emani Sophie Hofferberth Robert F. Padera Stephen P. Sanders |
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Affiliation: | 1. Department of Pathology, Boston Children''s Hospital, Boston, Mass;2. Department of Cardiology, Boston Children''s Hospital, Boston, Mass;3. Department of Cardiac Surgery, Boston Children''s Hospital, Boston, Mass;4. Department of Pathology, Brigham and Women''s Hospital, Boston, Mass;5. Department of Pathology, Harvard Medical School, Boston, Mass;6. Department of Pediatrics, Harvard Medical School, Boston, Mass;7. Department of Surgery, Harvard Medical School, Boston, Mass |
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Abstract: | ObjectivesAlthough valved venous homografts (VVHs) are used for establishing right ventricle-to-pulmonary artery continuity in some complex heart defects, the tissue changes that occur in situ have not been described. We review the gross and microscopic changes observed in explanted VVH conduits and their effects on functionality.MethodsIn total, 20 explanted VVH conduits were evaluated for valve integrity, presence of thrombus, and stenosis. Hematoxylin and eosin– and trichrome-stained sections were reviewed for neointima formation, wall remodeling, inflammation, and calcification. Regurgitation and narrowing were assessed on pre-explant echocardiogram, and angiographic video clips were correlated with tissue findings. The source of the proliferating cells within the conduits was investigated by fluorescent in situ hybridization.ResultsThirteen male and 7 female infants underwent VVH implantation either as part of a composite Sano shunt (65%) or to establish right ventricle-to-pulmonary artery continuity in biventricular hearts (35%). The median duration of conduits in situ was 140 days (range: 98-340 days). Conduits were predominantly explanted for staged conversion to bidirectional Glenn (60%) and conduit upsizing (20%). The valves remained intact and functional in 75% of cases. Occlusive thrombosis was absent in all. Wall thickening due to neointima formation and wall remodeling was uniformly present and appeared to be driven by smooth muscle actin–expressing cells, which by fluorescent in situ hybridization are predominantly of recipient origin. Minimal calcification and mild adventitial chronic inflammation were present.ConclusionsVein wall thickening is a uniform finding and can cause stenosis. The valves remain functional in most, and vein walls undergo remodeling with only minimal inflammation and calcification. |
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Keywords: | Valved venous homografts composite Sano shunt wall remodeling neointima formation flourescent in situ hybridization FISH fluorescent in situ hybridization FVH femoral vein homograft PA pulmonary artery RV right ventricle SMA smooth muscle actin SVH saphenous vein homograft VVH valved venous homograft |
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