Department of Experimental Medicine Research Institute for Complex Issues of Cardiovascular Diseases Kemerovo Russian Federation.
Department of Molecular and Cellular Oncology The University of Texas MD Anderson Cancer Center Houston TX.
J Am Heart Assoc. 2020 Oct 20;9(19):e018506. doi: 10.1161/JAHA.120.018506. Epub 2020 Sep 21.
The implantation of bioprosthetic heart valves (BHVs) is increasingly becoming the treatment of choice in patients requiring heart valve replacement surgery. Unlike mechanical heart valves, BHVs are less thrombogenic and exhibit superior hemodynamic properties. However, BHVs are prone to structural valve degeneration (SVD), an unavoidable condition limiting graft durability. Mechanisms underlying SVD are incompletely understood, and early concepts suggesting the purely degenerative nature of this process are now considered oversimplified. Recent studies implicate the host immune response as a major modality of SVD pathogenesis, manifested by a combination of processes phenocopying the long-term transplant rejection, atherosclerosis, and calcification of native aortic valves. In this review, we summarize and critically analyze relevant studies on (1) SVD triggers and pathogenesis, (2) current approaches to protect BHVs from calcification, (3) obtaining low immunogenic BHV tissue from genetically modified animals, and (4) potential strategies for SVD prevention in the clinical setting.
生物瓣心脏瓣膜(BHVs)的植入越来越成为需要心脏瓣膜置换手术的患者的首选治疗方法。与机械心脏瓣膜不同,BHVs 的血栓形成倾向较低,表现出更好的血液动力学特性。然而,BHVs 容易发生结构性瓣膜退化(SVD),这是一种不可避免的限制移植物耐久性的情况。SVD 的发病机制尚不完全清楚,早期的概念认为这种过程纯粹是退行性的,现在被认为过于简单化。最近的研究表明,宿主免疫反应是 SVD 发病机制的主要方式,表现为一系列过程,这些过程模拟了长期移植排斥、动脉粥样硬化和天然主动脉瓣的钙化。在这篇综述中,我们总结和批判性地分析了关于(1)SVD 的触发因素和发病机制,(2)目前防止 BHVs 钙化的方法,(3)从基因修饰动物获得低免疫原性 BHV 组织,以及(4)在临床环境中预防 SVD 的潜在策略的相关研究。