论文部分内容阅读
目的:探讨无结构性心脏病房颤患者的左房或右房基质金属蛋白酶-9(MMP-9)、金属蛋白酶组织抑制因子-1(TIMP-1)、转化生长因子-β1(TGF-β1)和碱性成纤维细胞生长因子(bFGF)血清水平与心房结构重构的关系。方法:通过ELISA方法检测42例无结构性心脏病房颤患者及17例阵发性室上速或预激综合征患者左房和右房中血清的MMP-9、TIMP-1、TGF-β1和bFGF水平,并使用超声心动图测量左心房长径。分析血清中上述细胞因子的水平与房颤左房结构重构程度的关系。结果:房颤组左房内径(36±7)mm显著高于对照组(31±4)mm(P<0.01);房颤组左房血清MMP-9为(3037±804)ng/L,明显高于对照组(2439±663)ng/L(P<0.01)和右房(2635±9308)ng/L(P<0.05),但右房血清MMP-9与对照组相比未见显著性差异;与对照组相比,房颤组TIMP-1明显降低(P<0.05),TGF-β1明显升高(P<0.01),bFGF无显著性差异;MMP-9/TIMP-1与左房内径呈正相关。结论:MMP-9、TIMP-1和TGF-β1与房颤相关,并可提示房颤的结构重构程度。
Objective: To investigate the changes of left ventricular or right atrial matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1 (TIMP-1) and transforming growth factor-β1 (TGF-β1) in patients with structural heart disease without atrial fibrillation ) And basic fibroblast growth factor (bFGF) serum levels and atrial structural remodeling. Methods: The levels of MMP-9, TIMP-1, TGF-β1 in serum of left atrium and right atrium of 42 patients with structural heart disease without atrial fibrillation and 17 patients with paroxysmal supraventricular or anterior chamber syndrome were measured by ELISA And bFGF levels were measured and the left atrial diameter was measured using echocardiography. The relationship between serum cytokines levels and left atrial structural remodeling was analyzed. Results: The left atrium diameter (36 ± 7) mm in AF group was significantly higher than that in control group (31 ± 4) mm (P <0.01), while the atrial fibrillation group was (3037 ± 804) ng / L, (2439 ± 663) ng / L (P <0.01) and right atrium (2635 ± 9308) ng / L (P <0.05), but there was no significant difference between the right atrium serum MMP-9 and the control group Compared with the control group, TIMP-1 in atrial fibrillation group was significantly lower (P <0.05), TGF-β1 was significantly higher (P <0.01), bFGF had no significant difference, and MMP-9 / TIMP- Room diameter was positively correlated. Conclusion: MMP-9, TIMP-1 and TGF-β1 are associated with atrial fibrillation and may indicate the degree of structural remodeling of atrial fibrillation.