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• W1969174906 abstract "ObjectivesWe sought to evaluate the microscopic characteristics of pulmonary autograft valve explants.MethodsCell density and thickness of the autograft valve ventricularis were determined and compared with those of normal aortic and pulmonary valves (n = 11). Cellular phenotype and extracellular matrix involvement were assessed with immunohistochemistry. Collagen 3-dimensional architecture was studied by means of confocal microscopy.ResultsThe autograft valve exhibited characteristic thickening of the ventricularis compared with the normal aortic and pulmonary valves (137 vs 77 [P = .058] vs 37 μm [P = .002], respectively). Its cell number was increased compared with those of the normal aortic and pulmonary valves (396 vs 230 [P = .02] vs 303 [P = .083], respectively). Myofibroblasts and stressed endothelial cells, both of which were present in pulmonary autografts, were absent in control valves. The exclusive presence of matrix metalloproteinase 1 was an additional sign of extracellular matrix turnover. Apoptosis, elastinolysis, cell proliferation, and senescence were not expressed. Dense fibrosis of the autograft ventricularis with relatively well-aligned collagen fibers was observed with confocal microscopy.ConclusionsFibrous hyperplasia of the ventricularis and cellular and extracellular matrix characteristics of active remodeling were a consistent finding in pulmonary autograft valve explants. The observations suggest a primary valve-related cause to be involved in pulmonary autograft valve failure. We sought to evaluate the microscopic characteristics of pulmonary autograft valve explants. Cell density and thickness of the autograft valve ventricularis were determined and compared with those of normal aortic and pulmonary valves (n = 11). Cellular phenotype and extracellular matrix involvement were assessed with immunohistochemistry. Collagen 3-dimensional architecture was studied by means of confocal microscopy. The autograft valve exhibited characteristic thickening of the ventricularis compared with the normal aortic and pulmonary valves (137 vs 77 [P = .058] vs 37 μm [P = .002], respectively). Its cell number was increased compared with those of the normal aortic and pulmonary valves (396 vs 230 [P = .02] vs 303 [P = .083], respectively). Myofibroblasts and stressed endothelial cells, both of which were present in pulmonary autografts, were absent in control valves. The exclusive presence of matrix metalloproteinase 1 was an additional sign of extracellular matrix turnover. Apoptosis, elastinolysis, cell proliferation, and senescence were not expressed. Dense fibrosis of the autograft ventricularis with relatively well-aligned collagen fibers was observed with confocal microscopy. Fibrous hyperplasia of the ventricularis and cellular and extracellular matrix characteristics of active remodeling were a consistent finding in pulmonary autograft valve explants. The observations suggest a primary valve-related cause to be involved in pulmonary autograft valve failure." @default.
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• W1969174906 date "2010-06-01" @default.
• W1969174906 modified "2023-10-16" @default.
• W1969174906 title "Pulmonary autograft valve explants show typical degeneration" @default.
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• W1969174906 doi "https://doi.org/10.1016/j.jtcvs.2010.01.020" @default.
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