Valvular heart diseases are associated with significant cardiovascular morbidity and mortality, and often require surgical and/or percutaneous repair or replacement. Valve replacement is limited to mechanical and biological prostheses, the latter of which circumvent the need for lifelong anticoagulation but are subject to structural valve degeneration (SVD) and failure. Although calcification is heavily studied, noncalcific SVD, which represent roughly 30% of BHV failures, is relatively underinvestigated. This original work establishes 2 novel and interacting mechanisms-glycation and serum albumin incorporation-that occur in clinical valves and are sufficient to induce hallmarks of structural degeneration as well as functional deterioration.
Keywords: AGE, advanced glycation end product; BHV, bioprosthetic heart valve; BP, bovine pericardium; CML, N-carboxymethyl-lysine; EOA, effective orifice area; HSA, human serum albumin; IHC, immunohistochemistry; PBS, phosphate-buffered saline; SAVR, surgical aortic valve replacement; SHG, second harmonic generation; SVD, structural valve degeneration; TAVR, transcatheter aortic valve replacement; advanced glycation end products; aortic valve disease; biomaterial; bioprosthetic heart valve.
© 2020 The Authors.