Noncalcific Mechanisms of Bioprosthetic Structural Valve Degeneration

Bioprosthetic heart valves (BHVs) largely circumvent the need for long-term anticoagulation compared with mechanical valves but are increasingly susceptible to deterioration and reduced durability with reoperation rates of approximate to 10% and 30% at 10 and 15 years, respectively. Structural valve degeneration is a common, unpreventable, and untreatable consequence of BHV implantation and is frequently characterized by leaflet calcification. However, 25% of BHV reoperations attributed to structural valve degeneration occur with minimal leaflet mineralization. This review discusses the noncalcific mechanisms of BHV structural valve degeneration, highlighting the putative roles and pathophysiological relationships between protein infiltration, glycation, oxidative and mechanical stress, and inflammation and the structural consequences for surgical and transcatheter BHVs.

Automated summary

Bioprosthetic heart valves (BHVs) offer an alternative to mechanical valves with reduced long-term anticoagulation needs, but are prone to structural valve degeneration which may require reoperation. This degeneration, often characterized by leaflet calcification, can also occur with minimal mineralization in some cases, posing challenges for treatment. Various factors such as protein infiltration, glycation, oxidative and mechanical stress, and inflammation may play a role in noncalcific mechanisms of BHV structural valve degeneration.