Why the study?
Bioprosthetic heart valve lifespan is limited by structural valve degeneration, which recent data suggest is driven by immune rejection processes similar to allografts and xenografts.
Immune responses similar to allograft and xenograft rejection play a major role in structural valve degeneration of bioprosthetic heart valves, suggesting that strategies to reduce immunogenicity could delay degeneration.
Highlights shared immune pathways in valve degeneration; leaves open whether immunomodulation can delay structural failure in bioprostheses.
Highlights Immune processes and mechanisms underlying bioprosthetic heart valve degeneration and rejection of allografts and xenografts are similar. Manufacturers and surgeons can implement effective approaches to prevent immune rejection in the process of production and implantation of prosthetic heart valves in order to delay the process of structural valve degeneration. Abstract Bioprosthetic heart valves (BHV) are characterized by low thrombogenicity, thus circumventing the need for long‐term anticoagulation. However, BHV lifespan is limited to 10–15 years because its tissue components are subject to degeneration. Recent research data indicate that immune responses forming the basis of humoral and cellular rejection of allografts and xenografts play a major role in the development of structural valve degeneration (SVD). This review summarizes up-to-date data on immune processes involved in SVD pathogenesis. Moreover, the latest achievements in the development of strategies to reduce the immunogenicity of BHV, such as data on immune compatibility of allogeneic material and the process of deriving low immunogenic biomaterial from genetically modified animals, decellularization of BHV, and the ways of slowing the process of degeneration are analyzed.
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Kostyunin et al. (2023) studied this question.
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