Noncalcific Mechanisms of Bioprosthetic Structural Valve Degeneration.
Noncalcific Mechanisms of Bioprosthetic Structural Valve Degeneration.
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DOI：
10.1161/jaha.120.018921
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发表时间：
2021-02-02
影响因子：
5.4
通讯作者：
Ferrari G
中科院分区：
文献类型：
--
作者：
Marro M;Kossar AP;Xue Y;Frasca A;Levy RJ;Ferrari G
与机械瓣膜相比，生物人工心脏瓣膜（bhv）在很大程度上避免了长期抗凝的需要，但在10年和15年的再手术率分别约为10%和30%时，生物人工心脏瓣膜（bhv）越来越容易恶化和降低耐用性。结构性瓣膜变性是BHV植入后常见的、不可预防和无法治疗的后果，通常以小叶钙化为特征。然而，25%因结构性瓣膜退行性变导致的BHV再手术发生的小叶矿化很小。这篇综述讨论了BHV结构性瓣膜变性的非钙化机制，强调了蛋白质浸润、糖基化、氧化和机械应力、炎症以及手术和经导管BHV的结构性后果之间的假定作用和病理生理关系。
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.