Vestnik Transplantologii i Iskusstvennyh Organov (Sep 2018)
A case report of bioprosthetic valve dysfunction after tricuspid valve replacement in a preschool patient: the contribution of pannus and calcification
Abstract
Aim. To assess the contribution of pannus and calcification to the development of bioprosthetic valve dysfunction after tricuspid valve replacement in a pediatric patient.Materials and methods. A 3-month-old patient presented with tricuspid valve dysplasia and grade 4 tricuspid insufficiency underwent tricuspid valve replacement with the bioprosthesis «PeriCor» (ZAO «NeoKor», Russian Federation). The patient at the age of 6 years required a redo tricuspid valve replacement 5 years 8 months after initial surgery. Degenerative changes of the dysfunctional bioprosthetic valve explanted from the tricuspid position were assessed using macroscopic description and light microscopy. Cellular composition, the presence of bacteria, colocalization of calcifications with recipient cells were analyzed. The distribution of calcifications and their volume in the biomaterial tissue were estimated using microcomputer tomography imaging (micro-CT).Results. Bioprosthetic valve dysfunction was mainly caused by the pannus formation which was shown to encapsulate the anterior leaflet, resulting in its total failure and severe stenosis (reduced effective orifice area). There were no signs of ruptures and perforations in the valve tissues found. All leaflets were shown to contain predominantly fibroblastic cells and single blood cells, mainly located in the surface layers of the leaflets in the regions without any signs of calcification. Bacteria staining was negative for all types of the studied biomaterials. Calcifications were present in all xeno-tissue elements of the explanted bioprosthesis (i.e. leaflets, aortic segment, and pericardium). In addition, calcifications were also found in pannus growing during a functioning bioprosthetic valve. Calcifications were predominantly located in the co-optation and commissure zones of the leaflets. Importantly, massive calcifications were observed around the bioprosthetic stent frame. The total volume of calcification accounted for 1/3 of the biological component of the bioprosthesis (729 mm3).Conclusion. According to the data obtained in this study, we may conclude that the primary cause of the bioprosthesis failure was the growth of connective tissues, resulting in pannus-related dysfunction, rather than severe calcification of all bioprosthetic components. One may assume that bioprosthetic dysfunction is related to the peculiarity of the inflammatory response of the preschool patient. However, this typeof dysfunctions requires further investigation.
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