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Von Willebrand Factor: Multimeric Structure and Functional Activity inPatients With Atrial Fibrillation With and Without Oral Anticoagulation

机译:冯·威勒布兰德因子:中的多聚体结构和功能活性伴或不伴口服抗凝药的房颤患者

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摘要

von Willebrand factor (vWF) is a multimeric glycoprotein present in blood plasma. It is synthesized in megakaryocytes and endothelial cells, secreted into circulation in the form of high-molecular-weight multimers (HMWMs), and cleaved into shorter, less active multimers by ADAMTS13. It is essential for platelet adhesion and aggregation. Previous studies have investigated the relationship between vWF levels and thromboembolic events with little regard to vWF multimeric structure. Patients with atrial fibrillation (AF) exhibit higher plasma vWF and lower ADAMTS13 levels. One hundred seven patients with AF, 51 anticoagulated and 56 nonanticoagulated, were eligible for the study. Plasma samples were analyzed for vWF antigen, vWF activity, and ADAMTS13; vWF multimers were analyzed by Western blot in 1% to 1.3% sodium dodecyl sulfate agarose gel electrophoresis. Patients with AF without oral anticoagulation (OAC) had significantly higher vWF plasma levels (154.00 [75-201] UI/dL) and vWF activity (60.00% [20%-210%]) compared to patients with OAC (133.50 [90-192] UI/dL, P = <.001; 50.00% [20%-160%], P = .02). Both were specially decreased in patients treated with acenocumarin. Patients without OAC also showed lower ADAMTS13 levels and presence of vWF HMWMs. Patients with AF show higher plasma levels and vWF activity. Moreover, treatment with traditional OAC (acenocumarin) significantly reduced vWF levels. Patients without OACmight have an increased risk of thrombotic events showing lower ADAMTS13 and higher vWFlevels. Patients with stroke had higher plasma levels, vWF activity, and HMWMs. Our studysuggests that increased vWF levels and presence of HMWMs could be related tocerebrovascular disease and may represent useful biomarkers for stroke in AF.
机译:von Willebrand因子(vWF)是血浆中存在的一种多聚体糖蛋白。它在巨核细胞和内皮细胞中合成,以高分子量多聚体(HMWM)的形式分泌到循环中,并被ADAMTS13裂解为较短,活性较低的多聚体。它对于血小板粘附和聚集至关重要。先前的研究已经调查了vWF水平与血栓栓塞事件之间的关系,而很少考虑vWF多聚体结构。心房颤动(AF)患者的血浆vWF较高,而ADAMTS13水平较低。一百零七名房颤患者,其中51例抗凝和56例未抗凝,符合研究条件。分析血浆样品的vWF抗原,vWF活性和ADAMTS13;在1%至1.3%的十二烷基硫酸钠琼脂糖凝胶电泳中通过Western blot分析vWF多聚体。与没有OAC的患者(133.50 [90-90] 192] UI / dL,P = <.001; 50.00%[20%-160%],P = .02)。接受醋氨苄青霉素治疗的患者中两者均特别减少。没有OAC的患者还显示出较低的ADAMTS13水平和vWF HMWMs的存在。 AF患者表现出更高的血浆水平和vWF活性。此外,用传统的OAC(醋菌灵)治疗可显着降低vWF水平。没有OAC的患者血栓事件的风险可能增加,显示较低的ADAMTS13和较高的vWF水平。中风患者的血浆水平,vWF活性和HMWM较高。我们的研究提示vWF水平升高和HMWM的存在可能与脑血管疾病,可能代表房颤中风的有用生物标志物。

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