Wen Shuyu, Zhou Ying, Yim Wai Yen, Wang Shijie, Xu Li, Shi Jiawei, Qiao Weihua, Dong Nianguo
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Front Pharmacol. 2022 Jun 3;13:909801. doi: 10.3389/fphar.2022.909801. eCollection 2022.
Valve replacement is the main therapy for valvular heart disease, in which a diseased valve is replaced by mechanical heart valve (MHV) or bioprosthetic heart valve (BHV). Since the 2000s, BHV surpassed MHV as the leading option of prosthetic valve substitute because of its excellent hemocompatible and hemodynamic properties. However, BHV is apt to structural valve degeneration (SVD), resulting in limited durability. Calcification is the most frequent presentation and the core pathophysiological process of SVD. Understanding the basic mechanisms of BHV calcification is an essential prerequisite to address the limited-durability issues. In this narrative review, we provide a comprehensive summary about the mechanisms of BHV calcification on 1) composition and site of calcifications; 2) material-associated mechanisms; 3) host-associated mechanisms, including immune response and foreign body reaction, oxidative stress, metabolic disorder, and thrombosis. Strategies that target these mechanisms may be explored for novel drug therapy to prevent or delay BHV calcification.
瓣膜置换是治疗心脏瓣膜病的主要方法，即使用机械心脏瓣膜（MHV）或生物人工心脏瓣膜（BHV）替换病变瓣膜。自21世纪以来，由于具有优异的血液相容性和血流动力学特性，BHV已超过MHV成为人工瓣膜替代的主要选择。然而，BHV易于发生结构性瓣膜退变（SVD），导致耐久性受限。钙化是SVD最常见的表现形式和核心病理生理过程。了解BHV钙化的基本机制是解决耐久性受限问题的重要前提。在这篇叙述性综述中，我们全面总结了BHV钙化的机制，包括：1）钙化的组成和部位；2）材料相关机制；3）宿主相关机制，包括免疫反应和异物反应、氧化应激、代谢紊乱和血栓形成。针对这些机制的策略可能有助于探索预防或延缓BHV钙化的新型药物治疗方法。
