Natorska J, Undas A
Anetta Undas, Institute of Cardiology, Jagiellonian University School of Medicine, 80 Pradnicka St., 31-202 Cracow, Poland, Tel.: +48 12 6143004, Fax: +48 12 6143143, E-mail:
Thromb Haemost. 2015 Aug;114(2):217-27. doi: 10.1160/TH14-10-0861. Epub 2015 Mar 26.
Aortic valve stenosis (AS) increasingly afflicts our aging population. However, the pathobiology of the disease is still poorly understood and there is no effective pharmacotherapy for treating those at risk for clinical progression. The progression of AS involves complex inflammatory and fibroproliferative processes that resemble to some extent atherosclerosis. Accumulating evidence indicates that several coagulation proteins and its inhibitors, including tissue factor, tissue factor pathway inhibitor, prothrombin, factor XIII, von Willebrand factor, display increased expression within aortic stenotic valves, predominantly on macrophages and myofibroblasts around calcified areas. Systemic impaired fibrinolysis, along with increased plasma and valvular expression of plasminogen activator inhibitor-1, has also been observed in patients with AS in association with the severity of the disease. There is an extensive cross-talk between inflammation and coagulation in stenotic valve tissue which contributes to the calcification and mineralisation of the aortic valve leaflets. This review summarises the available data on blood coagulation and fibrinolysis in AS with the emphasis on their interactions with inflammation and calcification.
主动脉瓣狭窄（AS）日益困扰着我们的老年人群。然而，该疾病的病理生物学仍知之甚少，且对于有临床进展风险的患者尚无有效的药物治疗方法。AS的进展涉及复杂的炎症和纤维增生过程，在一定程度上类似于动脉粥样硬化。越来越多的证据表明，几种凝血蛋白及其抑制剂，包括组织因子、组织因子途径抑制剂、凝血酶原、因子XIII、血管性血友病因子，在主动脉狭窄瓣膜内的表达增加，主要在钙化区域周围的巨噬细胞和成肌纤维细胞上。在AS患者中还观察到全身纤维蛋白溶解功能受损，以及血浆和瓣膜中纤溶酶原激活物抑制剂-1的表达增加，且与疾病严重程度相关。狭窄瓣膜组织中炎症和凝血之间存在广泛的相互作用，这促进了主动脉瓣叶的钙化和矿化。本综述总结了关于AS中血液凝固和纤维蛋白溶解的现有数据，重点是它们与炎症和钙化的相互作用。
