心房颤动患者左心房血栓形成机制的初步研究
Preliminary study of the mechanisms of left atrium thrombosis of patients with atrial fibrillation
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摘要: 目的:探讨左心房重构、血管性血友病因子(von willebrand factor,vWF)、D-二聚体(D-dimer,D-D)、血小板膜活化糖蛋白Ⅱb/Ⅲa(platelet membrane glycoproteinⅡb/Ⅲa,GPⅡb/Ⅲa)同左心房血栓形成的关系,初步探讨左心房血栓形成的机制。方法:临床选取100例研究对象,分为心房颤动组(房颤组)60例、窦性心律组(窦律组)20例、正常对照组20例,其中房颤组中41例患者通过经胸及经食道超声心动图检查,又分为血栓阳性组(21例)和血栓阴性组(20例)。所有的研究对象均给予经胸超声心动图(trans-thoraial echocardiography,TTE)检查,记录以下指标:(1)左心房内径(left atrial diameter,LA-D);(2)左心房、左心耳血栓情况。测定全部研究对象的血浆凝血分子标志物水平:包括(1)酶联免疫双抗体夹心法测定vWF和D-D;(2)流式细胞仪检测全部研究对象的全血中GPⅡb/Ⅲa水平。结果:LA-D、vWF、D-D、GPⅡb/Ⅲa的测定值均为窦律组血栓阴性组血栓阳性组(P0.01);房颤组LA-D、vWF、D-D、GPⅡb/Ⅲa的测定值均高于窦律组和正常对照组(P0.01),而窦律组LA-D、vWF、D-D、GPⅡb/Ⅲa的检测值和对照组差异均无统计学意义(P0.05)。结论:心房重塑、内皮损伤、血小板激活和凝血酶增加等因素可能共同参与左心房血栓的形成。Abstract: Objective: To investigate the relationship between the left atrium remodeling, von Willebrand factor(vWF) ,D-dimer(DD) ,platelet membrane glycoprotein Ⅱb /Ⅲa(GP Ⅱb /Ⅲa) and left atrial thrombosis, and to explore the mechanisms of thrombosis.Methods: One hundred cases were divided into atrial fibrillation group(60 cases) , sinus rhythm group(20 cases) and normal control group(20 cases) .Fourty-one cases of atrial fibrillation group were subdivided into thrombosis positive group(21 cases) and thrombosis negative group (20 cases) according to the results of esophageal echocardiography.All cases were detected by transthoraial and transesophageal echocardiography(TTE) .The data of left atrial diameter(LA-D) and thrombosis of left atrium/left atrial appendage were observed.The levels of DD and vWF and GP Ⅱb /Ⅲa were measured using an enzyme linked immunosorbent assay(ELISA) and flow cytometry.Results: The levels of LA-D,vWF,D-D and GP Ⅱb /Ⅲa of sinus rhythm group, thrombosis negative group and thrombosis positive group were increased(P0.01) .The levels of LA-D、vWF、D-D and GP Ⅱb /Ⅲa of the atrial fibrillation group were significantly higher than that of sinus rhythm and normal control group(P0.01) ,while for the later two groups no significant difference(P0.05) .Conclusions: The atrium remodeling,endothelium damage,platelet activation and thrombin increasing may participate in the thrombosis of left atrium.