Pulmonary autograft valve explants show typical degeneration

Objectives: We sought to evaluate the microscopic characteristics of pulmonary autograft valve explants. Methods: 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. Results: 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. Conclusions: 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.

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