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目的:探讨非瓣膜病心房颤动(房颤)对内皮功能的影响。方法:选择中老年非瓣膜病房颤患者92 例(房颤组)和窦性心律者60例(对照组),采用放射免疫分析法(RIA法)测定血浆内皮素-1(ET-1)和6-酮-前列腺素F1α(6-k-PGF1α)水平,采用酶联免疫吸附双抗体夹心法(ELISA法)测定血浆血管性血友病因子(vWF)水平,观察2组间各指标的差异,并对可能影响ET-1、vWF、6-k-PGF1α水平的性别、年龄和血清肌酐、尿酸、血糖、三酰甘油、胆固醇等因素采用协方差方法分析。结果:①单因素分析,房颤组ET-1(115．11±81．84)ng／L显著高于对照组(83．81±20．60)ng／L,P<0．05,房颤组vWF(163．04±36．58)％也显著高于对照组(71．14±43．40)％, P<0．01,房颤组6-k-PGF1α(205．81±100．96)ng／L显著低于对照组(300．79±118．02)ng／L,P<0．01。②多因素分析,调整其他可能影响因素后,房颤组ET-1和vWF水平仍高于对照组(P>0．05和P<0．01),6-k- PGF1α水平仍低于对照组(P<0．05)。结论:非瓣膜病房颤患者存在内皮细胞受损和功能异常。因此应重视非瓣膜病房颤患者改善内皮功能的治疗。
Objective: To investigate the effect of non-valvular atrial fibrillation (AF) on endothelial function. Methods: Ninety-two elderly patients with atrial fibrillation (AF) and 60 patients with sinus rhythm (control group) were included in this study. Plasma ET-1 was measured by radioimmunoassay (RIA) And 6-keto-prostaglandin F1α (6-k-PGF1α) were detected by enzyme-linked immunosorbent assay (ELISA). Plasma von Willebrand factor (vWF) The differences of sex, age, serum creatinine, blood glucose, triglyceride, cholesterol and other factors that may affect the levels of ET-1, vWF and 6-k-PGF1αwere analyzed by the covariance method. Results: ① In univariate analysis, ET-1 (115.11 ± 81.84) ng / L in AF group was significantly higher than that in control group (83.81 ± 20.60) ng / L, P <0.05 The vWF (163.04 ± 36.58)% in AF group was also significantly higher than that in control group (71.14 ± 43.40%), P <0.01. The 6-k-PGF1α (205.81 ± 100 .96) ng / L was significantly lower than that of the control group (300.79 ± 118.02) ng / L, P <0.01. (2) Multivariate analysis showed that the levels of ET-1 and vWF in atrial fibrillation group were still higher than those in control group (P> 0.05 and P <0.01) after adjusting for other possible influencing factors, and the level of 6-k-PGF1α was still lower than that in control group Group (P <0.05). Conclusion: There is endothelial cell damage and dysfunction in patients with nonvalvular atrial fibrillation. Therefore, attention should be paid to the treatment of non-valvular atrial fibrillation to improve endothelial function.