论文部分内容阅读
目的 研究瓣膜性心房颤动 (房颤 )和非瓣膜性房颤患者左心房自发声学显影 (SEC)的形成机制。方法 患者 6 1例分为 3组 ,其中健康对照组 17例 ,非瓣膜性房颤组 2 3例和瓣膜性房颤组 2 1例。测定血浆纤维蛋白原 (Fg)、血管性血友病因子 (vWF)、D 二聚体 (DD)、血小板颗粒膜糖蛋白 14 0 (GMP 14 0 )、凝血酶抗凝血酶Ⅲ复合物 (TAT)和纤溶酶原激活物抑制物 1(PAI 1) ;应用经食管超声心动图技术测量房颤患者左心耳和肺静脉血流速度 ;应用背向散射积分 (IBS)技术定量测定左心耳SEC。结果 与对照组比较 ,房颤患者血浆Fg、vWF、DD、TAT和PAI 1显著升高 (P <0 0 5 ) ,GMP 14 0差异无显著性 (P >0 0 5 ) ;房颤两组间差异无显著性。相关分析结果 ,瓣膜性房颤组左心房SEC与TAT正相关 (r =0 6 4 ,P =0 0 0 2 6 ) ,与肺静脉血流D波平均流速负相关 (r =-0 4 9,P =0 0 4 4 ) ,其余无相关性 ;非瓣膜性房颤组左心房SEC与左心耳排空血流流速积分负相关 (r= - 0 4 3,P =0 0 4 5 ) ,与肺静脉血流D波平均流速负相关 (r =- 0 4 3,P =0 0 4 8) ,其余无相关性。结论 血液高凝状态和局部血流淤滞可能是瓣膜性房颤左心房SEC形成的主要机制 ;局部血流动力学紊乱可能是非瓣膜性房颤左心房SEC形成的主要机制 ,血浆凝血?
Objective To investigate the mechanism of spontaneous acoustic contrast (SEC) formation in left atrium of patients with valvular atrial fibrillation (AF) and nonvalvular atrial fibrillation. Methods Sixty-one patients were divided into three groups, including 17 healthy controls, 23 non-valvular atrial fibrillation patients and 21 atrial valve atrial fibrillation patients. Plasma fibrinogen (Fg), von Willebrand factor (vWF), D dimer (DD), platelet granulocyte membrane glycoprotein 140 (GMP 140), thrombin antithrombin III complex TAT) and plasminogen activator inhibitor 1 (PAI 1). The left atrial appendage and pulmonary venous flow velocity were measured by transesophageal echocardiography. The left atrial appendage SEC was measured by backscatter integration (IBS) . Results Compared with the control group, the plasma levels of Fg, vWF, DD, TAT and PAI 1 were significantly increased in patients with atrial fibrillation (P <0.05), while there was no significant difference in GMP 14 0 (P> 0.05) There was no significant difference between the two groups. Correlation analysis showed that there was a positive correlation between SEC and TAT (r = 0.64, P = 0.0026) in left atrial valvular atrial fibrillation group, and negatively correlated with the average velocity of D wave in pulmonary venous blood flow (r = -0.49, P = 0 0 4 4). There was no correlation between the left atrial septum and left atrial appendage flow velocity (r = - 0 43, P = 0 0 455) in non-valvular atrial fibrillation group The average velocity of D wave in pulmonary vein was negatively correlated (r = - 0 4 3, P = 0 0 48), and the rest had no correlation. Conclusions Hypercoagulable state and local blood stasis may be the main mechanism of left atrial septum formation in valvular atrial fibrillation. Local hemodynamic disorder may be the main mechanism of SEC atrial fibrillation in non-valvular atrial fibrillation.