Bian Weikang, Wang Zhicheng, Sun Chongxiu, Zhang Dai-Min
Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
Front Cardiovasc Med. 2021 Dec 23;8:765419. doi: 10.3389/fcvm.2021.765419. eCollection 2021.
Calcified aortic valve disease (CAVD) was previously regarded as a passive process associated with valve degeneration and calcium deposition. However, recent studies have shown that the occurrence of CAVD is an active process involving complex changes such as endothelial injury, chronic inflammation, matrix remodeling, and neovascularization. CAVD is the ectopic accumulation of calcium nodules on the surface of the aortic valve, which leads to aortic valve thickening, functional stenosis, and ultimately hemodynamic disorders. CAVD has become an important cause of death from cardiovascular disease. The discovery of therapeutic targets to delay or block the progression of CAVD and the clinical application of transcatheter aortic valve implantation (TAVI) provide new ideas for the prevention and treatment of CAVD. This article summarizes the pathogenesis of CAVD and provides insight into the future directions of CAVD diagnosis and treatment.
钙化性主动脉瓣疾病（CAVD）以前被认为是一种与瓣膜退变和钙沉积相关的被动过程。然而，最近的研究表明，CAVD的发生是一个活跃的过程，涉及内皮损伤、慢性炎症、基质重塑和新生血管形成等复杂变化。CAVD是主动脉瓣表面钙结节的异位积聚，导致主动脉瓣增厚、功能性狭窄，并最终引起血流动力学紊乱。CAVD已成为心血管疾病死亡的重要原因。延迟或阻断CAVD进展的治疗靶点的发现以及经导管主动脉瓣植入术（TAVI）的临床应用为CAVD的防治提供了新思路。本文总结了CAVD的发病机制，并对CAVD诊断和治疗的未来方向进行了探讨。
