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DOI: 10.1055/s-0036-1571591
Histology of a Degenerated Tissue Engineered Pulmonary Valve 10 Years after Ross Procedure
Objectives: Our aim was to assess the histological characteristics of a degenerated tissue engineered pulmonary valve (TE-PV) 10 years after Ross procedure. TE-PV is a novel and under development treatment option for patients with pulmonary valve (PV) disease or for PV replacement (PVR) during Ross procedure. Histological changes of Matrix P decellularized xenograft for PVR over one decade are unknown.
Methods: In a 60-year old man, TE-PV was explanted during redo PVR due to severe pulmonary regurgitation 10 years after Ross procedure. Complex histological characterization of explanted TE-PV was performed as follows: Cytoplasmic, nuclear, and extracellular matrix (ECM) features were stained with hematoxylin and eosin protocol. Collagen (COL) fibers were visualized by Picrosirius Red staining. Endothelial cell layer disruptions were observed by van Willebrand factor (vWF) and Cluster of Differentiation 31 (CD31) staining. For analyzing the calcium distribution, von Kossa staining was performed. All histological findings were compared with native not degenerated porcine PV.
Results: In contrast to the porcine PV (Fig. 1A), no cellularity has been found in deeper tissue layers and the ECM structure showed many disruptions (Fig. 1B). In the porcine PV, COL type I fibers were located in the outer regions and type III fibers in the middle of the valve section (Fig. 1D). The COL structure of the explanted TE-PV was altered and showed an irregular distribution of COL type I and III fibers (Fig. 1C). Calcium deposits caused degeneration was detected in the TE-PV (Fig. 1E), whereas the porcine PV was free from calcification (Fig. 1F). The endothelial layer of the TE-PV was disrupted and showed delamination from subjacent cell layers and a damaged protective barrier (Fig. 1G,I).
Fig. 1.
Conclusion: Histological characterization of a severe degenerated TE-PV showed irregular COL distribution and progressive calcification at pulmonary cusps as causal factor for PV regurgitation.