Tissue factor expression in atrial endothelia associated with nonvalvular atrial fibrillation: possible involvement in intracardiac thrombogenesis
Tissue factor expression in atrial endothelia associated with nonvalvular atrial fibrillation: possible involvement in intracardiac thrombogenesis
复制标题
DOI：
10.1016/s0049-3848(03)00405-5
复制
发表时间：
2003-01-01
影响因子：
7.5
通讯作者：
Ohe, T
中科院分区：
文献类型：
--
作者：
Nakamura, Y;Nakamura, K;Ohe, T
前言：组织因子在外源性凝血途径中起关键作用，由炎性细胞因子诱导。最近在一些孤立性心房颤动患者中发现了房性心肌炎。低血流量、高凝状态和内皮功能障碍的Virchow‘s三联症可促进血栓的形成。本研究旨在阐明内皮功能障碍在非瓣膜性心房颤动相关血栓形成中的作用。材料和方法：我们研究了7例非瓣膜性心房颤动和心源性血栓栓塞症患者左心耳内皮细胞中组织因子的表达。组织被分成7-13个切片，并与4名死于非心脏事件的患者的对照标本进行比较。免疫组织化学方法检测组织因子、von Willebrand因子和组织因子途径抑制物的表达。结果：组织病理学检查，7例患者心内膜均有炎性细胞浸润，均表现为持续性心肌炎。激活的T细胞[15.3+/-9.4个/高倍视野(HPF，Mean+/-S.D.)]心内膜内可见少量巨噬细胞[5.1+/-8.4cell/hpf vs对照2.4+/-3.5细胞/hpf(P=NS)]。与对照组相比，组织因子在内皮细胞中过度表达，尤其是在含炎性细胞和心内膜剥脱基质的组织中。Von Willebrand因子，但不是组织因子途径抑制物，在这些组织中也过表达。结论：局部炎症诱导的组织因子表达参与了非瓣膜性房颤患者血栓形成的发病机制。(C)2003爱思唯尔有限公司。保留所有权利。
Introduction: Tissue factor plays a key role in the extrinsic coagulation pathway and is induced by inflammatory cytokines. Atrial myocarditis has been detected recently in some patients with lone atrial fibrillation. Virchow's triad of low blood flow, hypercoagulability, and endothelial dysfunction, enhances thrombus formation. The present study was designed to elucidate the role of endothelial dysfunction in thrombogenesis associated with nonvalvular atrial fibrillation. Material and methods: We investigated tissue factor expression in the endothelia of left atrial appendages obtained from seven patients with nonvalvular atrial fibrillation and cardiogenic thromboembolism. Tissues were divided into 7-13 sections and compared with control specimens from four patients who died of noncardiac events. Expression of tissue factor, von Willebrand factor and tissue factor pathway inhibitor was evaluated by immunohistochemistry. Results: Histopathologically, inflammatory cells infiltrated the endocardium and all seven patients showed features of persistent myocarditis. Activated T cells [15.3 +/- 9.4 cells/high power field (HPF, mean +/- S.D.) vs. control 2.2 +/- 4.4/HPF (P = 0.0294)] and a few macrophages [5.1 +/- 8.4 cells/HPF vs. control 2.4 +/- 3.5 cells/HPF (P = NS)] infiltrated the endocardium. Tissue factor was overexpressed in the endothelia particularly in tissues containing inflammatory cells and denuded matrix of the endocardium, compared with the control group. Von Willebrand factor, but not tissue factor pathway inhibitor, was also overexpressed in these tissues. Conclusion: Tissue factor expression induced by local inflammation is involved in the pathogenesis of thrombosis in patients with nonvalvular atrial fibrillation. (C) 2003 Elsevier Ltd. All rights reserved.