Department of Surgery Columbia University New York NY.
Division of Cardiac Surgery, Department of Surgical Sciences Città della Salute e della Scienza di Torino/University of Turin Italy.
J Am Heart Assoc. 2021 Feb 2;10(3):e018921. doi: 10.1161/JAHA.120.018921. Epub 2021 Jan 26.
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 ≈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.
生物瓣心脏瓣膜（BHVs）与机械瓣相比，在很大程度上避免了长期抗凝的需要，但随着再次手术率分别约为 10%和 30%，其恶化和耐用性降低的风险也越来越大，分别在 10 年和 15 年时。结构性瓣膜退化是 BHV 植入后的一种常见、不可预防和不可治疗的后果，通常表现为瓣叶钙化。然而，25%归因于结构性瓣膜退化的 BHV 再次手术仅伴有最小程度的瓣叶矿化。本综述讨论了 BHV 结构性瓣膜退化的非钙化机制，强调了蛋白浸润、糖基化、氧化和机械应激以及炎症之间的假定作用和病理生理关系，以及对手术和经导管 BHVs 的结构后果。
