Degeneration of Bioprosthetic Heart Valves: Update 2020

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  • Alexander E. Kostyunin
    Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation
  • Arseniy E. Yuzhalin
    Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation
  • Maria A. Rezvova
    Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation
  • Evgeniy A. Ovcharenko
    Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation
  • Tatiana V. Glushkova
    Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation
  • Anton G. Kutikhin
    Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation

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<jats:title>Abstract</jats:title> <jats:p xml:lang="en">The implantation of bioprosthetic heart valves (BHVs) is increasingly becoming the treatment of choice in patients requiring heart valve replacement surgery. Unlike mechanical heart valves, BHVs are less thrombogenic and exhibit superior hemodynamic properties. However, BHVs are prone to structural valve degeneration (SVD), an unavoidable condition limiting graft durability. Mechanisms underlying SVD are incompletely understood, and early concepts suggesting the purely degenerative nature of this process are now considered oversimplified. Recent studies implicate the host immune response as a major modality of SVD pathogenesis, manifested by a combination of processes phenocopying the long‐term transplant rejection, atherosclerosis, and calcification of native aortic valves. In this review, we summarize and critically analyze relevant studies on (1) SVD triggers and pathogenesis, (2) current approaches to protect BHVs from calcification, (3) obtaining low immunogenic BHV tissue from genetically modified animals, and (4) potential strategies for SVD prevention in the clinical setting.</jats:p>

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