老年非瓣膜心脏病心房颤动患者血小板功能及血管性血友病因子的改变

结果:老年非瓣膜心脏病房颤患者(A组,22例)血小板膜上活化糖蛋白Ⅱb/Ⅲa复合物(GPⅡb/Ⅲa)荧光阳性率为9.23％,显著高于无房颤患者(B组,18例)的2.61％及健康老年组(C组,16例)1.71％(均为P<0.01)。而A组患者的糖蛋白Ⅰb(GPⅠb)     

心房颤动患者血小板膜糖蛋白水平及内皮功能改变

目的：研究心房颤动（房颤）患血小板活化和内皮损伤,探讨其临床意义。方法：采用全血法流式细胞术分别测定慢性房颤患（35例）、无房颤组（19例）和正常对照组（17例）血小板膜上活化糖蛋白Ⅱb/Ⅲa复合物（glycoprotein Ⅱb/Ⅲa complex,GPⅡb/Ⅲa)和糖蛋白Ib（glycoproteinIb,GPIb)水平。房颤患又根据是否服阿司匹林分为二组：房颤1组（17例）为未服阿司匹林,房颤2组（18例）为服阿司匹林。此外,用全自动血细胞分析仪测定平均血小板体积（mean platelet volume,MPV),用酶联免疫吸附法测定血浆血管血友病因子（von Willebrand factor,vWF)。结果：慢性房颤患血小板表面活化GPⅡb/Ⅲa水平显升高（P＜0．05）,GP Ib的水平显降低（P＜0．05）。此外房颤患MPV及vWF水平也显高于心脏病无房颤组及正常对照组（P＜0．05）。以上指标在房颤1组和房颤2组之间的差异无显性（P＞0．05）。vWF水平高于正常的房颤患活化GPⅡb/Ⅲa水平更高（P＜0．05）。结论：房颤患存在血小板活性增加和内皮细胞受损,这些异常可能与记颤患心房内血栓形成相关。阿司匹林对房颤患血小板膜糖蛋白以及vWF水平无影响。     

心房颤动住院患者1650例临床分析

目的分析心房颤动住院患者病因、临床特点和抗凝治疗现状.方法对广东省心血管病研究所1998～2001年共1650例心房颤动住院患者的临床资料进行回顾性分析.结果心房颤动患者中阵发性、持续性和持久性房颤各占13.94%、6.42%、79.64%,风湿性心脏病是最常见的病因(67.88%),其次是高血压及冠心病(13.88%、7.52%).持久性房颤患者中68.42%心功能Ⅲ～Ⅳ级,与阵发性房颤相比有较大的左房内径[(51.94±12.46)mm∶(34.96±7.64)mm, P<0.01]和较低的左室射血分数[(69.40±12.98)%∶(74.93±12.08)%, P<0.001].房颤患者血栓栓塞事件发生率为25.45%,其中风湿性房颤为非风湿性房颤的5.21倍;非风湿性房颤患者华法令应用率为24.53%,而32.83%的患者出院时未接受任何抗凝治疗.结论研究提供了有价值的房颤流行病学资料;血栓栓塞是房颤的重要并发症,应得到临床医生充分的认识和足够的重视.     

老年人特发性房颤和复律后对心脏功能的影响

目的观察老年特发性心房颤动(简称房颤)和复律后心脏功能的改变。方法采用彩色多普勒二维超声心动图仪测定老年人持续、阵发性房颤及房颤复律后左心功能的各项指标,并与健康老年人进行对照。结果(1)射血分数、每搏量、心输出量、心脏指数及左心房内径各指标持续、阵发性房颤组及房颤复律组与正常对照组比较,依次为差异非常显著(P<0.01);差异显著(P<0.05)及差异不显著(P>0.05);(2)房颤复律组E/A为0.71±0.14,与照对组比较差异非常显著(P<0.01);(3)持续、阵发房颤组的各项心功能指标与房颤复律组比较,分别为P<0.01,P<0.05。结论老年特发性持续房颤患者存在明显左心功能障碍;阵发性房颤者短时间内可出现左心功能改变;房颤复律后心脏收缩功能可恢复或接近正常,但仍存在不同程度舒张功能障碍。     

老年人单纯收缩期高血压血清瘦素、抵抗素及血浆同型半胱氨酸、神经肽的水平

目的探讨老年单纯收缩期高血压(ISH)患者血清瘦素(Lep)、抵抗素(Res)与血浆同型半胱氨酸(Hcy)、神经肽Y(NPY)的水平,及与其他类型老年高血压患者、健康老年人之间的差异. 方法对ISH组28例、全期型高血压(SDH)组26例、单纯舒张期高血压(IDH)组25例及老年健康对照组21例,采用酶免疫法检测血清Lep、Res,放射免疫法测定血浆Hcy、NPY,同时检测受试者体质指数(BMI)和体内脂肪(BF)百分比. 结果 ISH组、SDH组、IDH组血清Lep[(13.18±1.66)μg/L、(11.91±2.16)μg/L、(10.88±2.31)μg/L]、Res[(31.2±10.3)μg/L、(26.3±8.91)μg/L、(24.2±5.66)μg/L]水平均高于对照组[(7.71±1.28)μg/L和(19.8±7.21)μg/L,P<0.05或P<0.01],ISH组显著高于SDH、IDH组(P<0.05,P<0.01);3个不同类型高血压组患者的血浆Hcy、NPY较对照组增高(P<0.01,P <0.05),而老年ISH组又较SDH、IDH组增高(P<0.01);老年ISH组平均年龄较其他各组明显增高(P <0.01),老年SDH组较IDH组、对照组也增高(P<0.05, P<0.01);老年ISH组BMI也较其他各组明显增高(P<0.05,P<0.01),而且SDH组较老年健康组显著增高(P<0.05).ISH患者 BF百分比与IDH组、老年健康组差异均有显著性(P<0.05).收缩压与Lep、NPY呈正相关(γ=0.256,P <0.05;γ=0.374,P<0.01). 结论 Lep、Res、Hcy及NPY与老年人高血压发病,尤其是老年ISH的发病有关,控制患者血清Lep、Res、血浆Hcy及NPY浓度对预防老年高血压,尤其是ISH的发生或发展可能有积极作用.     

颈动脉粥样硬化致血小板活化及其与急性脑梗死的关系

为探讨颈动脉粥样硬化致血小板活化机制及其与急性脑梗死的关系,采用彩色多普勒血流显像仪和流式细胞仪分别测定115例急性脑梗死患者颈动脉及其周围血血小板表面CD62p、CD63的表达,并与30例非脑梗死头晕患者对照.结果发现,急性脑梗死患者颈动脉粥样硬化斑块较对照组明显增多,单侧脑梗死者同侧颈动脉斑块明显增加,达68.75%,双侧脑梗死者双侧颈动脉斑块达58.47%.斑块处狭窄,局部血流增快.颈动脉斑块患者血CD62p和CD63水平较正常动脉者明显增高,单侧颈内动脉粥样硬化斑块患者血CD62p和CD63的阳性率及荧光强度分别达4.72%±4.52%、5.38%±3.73%和1.50±0.26、1.38±0.14,双侧斑块者达7.72%±4.96%、6.78%±4.02%和1.59±0.37、1.41±0.18,后者较前者明显增高(P<0.05).脑梗死患者血小板活化率明显较对照组增高,并与颈动脉粥样硬化程度相关(P<0.05).结果提示,颈动脉粥样硬化构成"高剪切力+低剪切力"的特殊剪切力梯度活化血小板,可能是颈动脉粥样硬化导致急性脑梗死的一个重要发病因素.     

老年非瓣膜心脏病心房颤动患者脂蛋白(a)与纤维蛋白原及血小板聚集率改变的临床探讨

心房颤动(房颤)是常见的快速性心律失常,可导致心房内血栓形成,脱落引起栓塞,使患者致死或致残,其中血小板及纤溶系统的激活在血栓形成中起重要作用,通过测定血小板聚集功能及纤维蛋白原(FIB)、脂蛋白(a)[Lp(a)],旨在了解老年非瓣膜心脏病房颤患者的血小板聚集功能、FIB及Lp(a)改变的临床意义.     

老年胰腺癌患者外周血CD44表达及其临床意义

目的探讨黏附分子CD44在老年胰腺癌外周血淋巴细胞中的表达及其意义.方法用流式细胞检测法(FCM)测定60例老年胰腺癌患者外周血中CD44水平并与正常人及胰腺炎患者进行相互比较,对照分析手术前后或热疗前后CD44的变化.结果胰腺癌组外周血CD44含量为564.51±16.64,明显高于正常对照组(382.46±15.28,P<0.01)及慢性胰腺炎组(396.37±16.32,P<0.01),且手术前或热疗前胰腺癌患者外周血CD44的表达也明显高于手术后或热疗后(P<0.01).亦发现CD44的表达水平与患者的临床分期和组织学分级有关(P<0.01).结论外周血淋巴细胞中CD44含量可作为老年胰腺癌诊断的参考指标,其表达水平的高低可判定临床疗效及预后.     

心房颤动患者心房肌细胞离子重塑及缬沙坦的干预研究

目的研究心房颤动(房颤)患者心房肌电生理重塑机制并探讨缬沙坦在房颤患者治疗中的作用及可能机制. 方法经典两步酶解法分离单个心房肌细胞,膜片钳全细胞法记录离子电流,并分别观察缬沙坦(10 μmol/L)对房颤组和窦性心律(窦律)组心房肌细胞各离子电流的影响. 结果 (1)与窦律组比较房颤组心房肌细胞L型钙电流(ICa-L)密度降低(P<0.001),瞬间外向钾电流(Ito1)密度降低(P<0.001),内向整流性钾电流(IK1)在超极化状态密度增加(P<0.05).两组超速激活延迟整流性钾电流(IKur)和快速内向钠电流(INa)差异无显著性.(2) 缬沙坦灌流前后两组心房肌细胞各离子电流自身前后对比以10 μmol/L缬沙坦灌流后,房颤组心房肌细胞INa密度峰值减少65.68%(P<0.001),膜电位+50 mV时IKur密度减少30.70%(P<0.05),膜电位-120 mV时IK1密度减少23.32% (P<0.05);窦律组心房肌细胞仅INa密度峰值减少59.49%(P<0.001),IKur和IK1无显著改变.缬沙坦对房颤和窦律组心房肌细胞Ito1及ICa-L无显著影响. 结论心房肌细胞ICa-L、Ito1密度降低而超极化状态时IK1密度增加,是房颤患者心房肌电生理重塑的重要离子基础;缬沙坦对房颤患者心房肌细胞离子电流表现出异于窦律患者的作用,可能有利于改善房颤导致的心房电重塑.     

二尖瓣狭窄并发心房颤动的危险因素探讨

目的探讨二尖瓣狭窄并发心房颤动(房颤)的危险因素。方法采用非条件Logistic回归模型对连续行二尖瓣球囊扩张术(PBMV)的260例二尖瓣狭窄患者进行并发房颤的危险因素分析。PBMV后对房颤患者进行复律治疗并随访。结果二尖瓣狭窄并发房颤的预测因子是左心房内径(P<0.0001)、年龄(P<0.0001)及病程(P=0.0007)。PBMV后左心房内径缩小,113例患者经药物或直流电转复窦性心律;随访(12±6.8)个月,31例(28.2％)患者房颤复发,左心房内径(P<0.0001)是转复窦性心律患者房颤复发的独立预测因子。结论左心房内径、年龄和病程是决定二尖瓣狭窄患者发生房颤的最重要的因素。左心房内径也是决定PBMV后转复窦性心律患者能否维持窦性心律的主要因素。     

Interaction of porcine von Willebrand factor with the platelet glycoproteins Ib and IIb/IIIa complex

Porcine von Willebrand factor (PvWF) induces platelet aggregation which is thought to be responsible for the thrombocytopenia that occurs in haemophilic patients treated with commercial preparations of porcine factor VIII. This study demonstrates that such aggregation can be completely inhibited by a monoclonal antibody against human platelet glycoprotein GPIb and partially inhibited by an antibody directed against platelet GPIIb/IIIa. The interaction of PvWF with GPIb is also demonstrated by the inhibitory effect of purified glycocalycin on aggregation. The binding site of PvWF to GPIb is very close to that of human vWF, since a recombinant peptide blocks the binding of both molecules to GPIb. When platelets are incubated with PvWF, the GPIIb/IIIa receptor is activated and binds fibrinogen. PvWF also binds to GPIIb/IIIa when platelets are stimulated with thrombin, suggesting that the molecule has the same RGD sequence as other adhesive proteins (human vWF, fibrinogen, fibronectin and vitronectin). These findings identify the dual mechanisms responsible for in vivo platelet aggregation induced by PvWF, i.e. binding to GPIb and activation of the GPIIb/IIIa receptor.     

血小板激活及内皮损伤血液标志物对心房颤动血栓栓塞危险性的评价

目的:研究心房颤动(Af)患者是否存在血小板激活和内皮损伤,探讨其对评价Af血栓栓塞危险性的价值。方法:Af患者共89例,按是否接受了经食管超声心动图(TEE)检查分为两个亚组:①TEE检查亚组:35例,发现左心房和(或)左心耳有血栓者10例,有明确外周动脉血栓栓塞并发症者8例,无血栓者17例;②未检查亚组:54例。另选33例非Af者为对照组。用ELISA法测定两组的血浆可溶性P选择素(sP选择素)、血管性血友病因子(vWF)、D二聚体(DD)水平,用全自动生化分析仪测定平均血小板体积(MPV),对其结果进行对照分析。结果:Af患者血浆sP选择素、vWF、MPV、DD水平显著升高(P<0.05),其中血浆sP选择素、DD、MPV水平在血栓和无血栓者中差异有统计学意义(P<0.05)。且sP选择素与DD水平呈正相关(r=0.311,P<0.05)。结论:Af患者存在有血小板激活及内皮损伤,与其血栓形成及栓塞并发症有一定关系。     

On the role of von Willebrand factor in promoting platelet adhesion to fibrin in flowing blood

Platelet adhesion to fibrin at high shear rates depends on both the glycoprotein (GP) IIb:IIIa complex and a secondary interaction between GPIb and von Willebrand factor (vWF). This alternative link between platelets and vWF in promoting platelet adhesion to fibrin has been examined in flowing whole blood with a rectangular perfusion chamber. Optimal adhesion required both platelets and vWF, as shown by the following observations. No binding of vWF could be detected when plasma was perfused over a fibrin surface or when coated fibrinogen was incubated with control plasma in an enzyme-linked immunosorbent assay. However, when platelets were present during perfusion, interactions between vWF and fibrin could be visualized with immunoelectron microscopy. Exposure of fibrin surfaces to normal plasma before perfusion with severe von Willebrand's disease blood did not compensate for the presence of plasma vWF necessary for adhesion. vWF mutants in which the GPIIb:IIIa binding site was mutated or the GPIb binding site was deleted showed that vWF only interacts with GPIb on platelets in supporting adhesion to fibrin and not with GPIIb:IIIa. Complementary results were obtained with specific monoclonal antibodies against vWF. Thus, vWF must first bind to platelets before it can interact with fibrin and promote platelet adhesion. Furthermore, only GPIb, but not GPIIb:IIIa is directly involved in this interaction of vWF with platelets.     

Spontaneous platelet aggregation during pregnancy in a patient with von Willebrand disease type IIB can be blocked by monoclonal antibodies to both platelet glycoproteins Ib and IIb/IIIa

Spontaneous platelet aggregation appeared in a patient with von Willebrand disease type IIB during the 37th week of pregnancy. This phenomenon was not associated with symptoms of thrombosis and the patient delivered by caesarean section with no complications. Her platelet-poor plasma (PPP) aggregated normal platelet-rich plasma (PRP) and washed platelets. Aggregation was inhibited by monoclonal antibodies with known specificity for the platelet receptors of von Willebrand factor (vWF), i.e. the glycoprotein Ib (GPIb) and the GPIIb/IIIa complex. A monoclonal antibody, which selectively inhibits the binding of vWF to the GPIIb/IIIa complex, did not block aggregation, suggesting that spontaneous aggregation is not dependent on the binding to GPIIb/IIIa of vWF from patient plasma. Aggregation induced by patient plasma could also be blocked either by two monoclonal antibodies raised against vWF or by a fragment derived from trypsin digestion of normal vWF which blocks the ristocetin-induced binding of normal vWF to platelets. These findings indicate that the spontaneous platelet aggregation in this patient results from the binding of her vWF to GPIb but is independent from the binding of her vWF to GPIIb/IIIa.     

Platelet membrane abnormalities in myeloproliferative disorders: decrease in glycoproteins Ib and IIb/IIIa complex is associated with deficient receptor function

The number and functional activity of membrane glycoproteins (GP) Ib and IIb/IIIa were investigated in platelets from 11 patients with myeloproliferative disorders (MPD). Three patients had essential thrombocythaemia, two had chronic myeloid leukaemia and six had polycythaemia vera. The numbers of GPIb and GPIIb/IIIa molecules were detected on the platelet surface using different 125I-labelled monoclonal antibodies. The functional properties of GPIb and GPIIb/IIIa were evaluated using purified 125I-labelled asialo von Willebrand factor (vWF) and purified 125I-labelled fibrinogen, respectively, in a binding assay. Binding of the anti-GPIIb/IIIa antibody was decreased by 40% in almost all patients studied and, when measured, it was accompanied by decreased fibrinogen binding to activated platelets. Binding of anti-GPIb antibodies to platelets was also slightly decreased or virtually the same in eight out of 11 patients. The decrease correlated with decreased binding of asialo vWF. The increased plasma glycocalicin levels, measured in four patients, depended on the high platelet count. Scatchard analysis revealed normal receptor binding affinity for all ligands tested in all but one patient. In this report we demonstrate that abnormalities in the concentrations of GPIIb/IIIa membrane proteins are commonly present in patients with MPD, while a decrease in GPIb concentration is also seen, although in fewer patients. These abnormalities are accompanied by a concurrent decrease in the respective receptor functions. These findings may explain part of the haemorrhagic tendency often encountered in MPD.     

In vivo effects of eltrombopag on platelet function in immune thrombocytopenia: no evidence of platelet activation

The effects of eltrombopag, a thrombopoietin-receptor agonist, on platelet function in immune thrombocytopenia (ITP) are not fully characterized. This study used whole blood flow cytometry to examine platelet function in 20 patients receiving eltrombopag treatment at days 0, 7, and 28. Platelet surface expression of activated GPIIb/IIIa, P-selectin, and GPIb was measured with and without low and high adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP) concentrations. Before eltrombopag treatment with no ex vivo agonist, platelet activation was higher in ITP patients than controls. Platelet GPIb and activated GPIIb/IIIa expression without added agonist was unchanged following eltrombopag treatment, whereas a slight increase in P-selectin was observed. Expression of P-selectin and activated GPIIb/IIIa in response to high-dose ADP was lower during eltrombopag treatment than at baseline. Eltrombopag led to a slight increase in platelet reactivity to TRAP only in responders to eltrombopag but not to levels above those in controls; whole blood experiments demonstrated that this increase was probably because of higher platelet counts rather than higher platelet reactivity. In conclusion, although thrombocytopenic ITP patients have higher baseline platelet activation than controls, eltrombopag did not cause platelet activation or hyper-reactivity, irrespective of whether the platelet count increased.     

心房颤动患者心房组织中明胶酶的基因表达及活性变化

目的　检测明胶酶及其内源性抑制剂金属蛋白酶组织抑制因子(TIMPs)和基质金属蛋白酶(MMPs)在心房颤动(房颤)患者心房组织中的表达和明胶酶活性的变化,探讨房颤患者心房结构重构的分子机制。方法　75例风湿性心脏瓣膜病(风心病)接受换瓣手术者分为三组,其中窦性心律组 34例,阵发性房颤组 11例,持续性房颤组 30例;于术中获取右心耳组织,分别采用半定量逆转录 聚合酶链反应技术和免疫印迹法测定MMP 2、MMP 9、TIMP 1、TIMP 2的mRNA含量和蛋白含量,酶谱法测定MMP 2、MMP 9的活性。结果　(1)与窦性心律组比较,MMP 2的mRNA水平在阵发性房颤组、持续性房颤组心房组织中均明显增加(P<0 01,P<0 001);各组患者MMP 9的mRNA水平相似。持续性房颤组MMP 2、MMP 9的蛋白表达水平较窦性心律组、阵发性房颤组均明显增加 (P<0 01)。阵发性房颤组MMP 2、MMP 9的蛋白表达水平较窦性心律组亦明显增加 (均为P<0 05 )。(2)与窦性心律组比较,持续性房颤组TIMP 1、TIMP 2的mRNA及蛋白表达水平均明显下调 (P<0 05~0 01)。(3)与窦性心律组比较,持续性房颤组、阵发性房颤组MMP 2、MMP 9的活性均明显增加(P<0 05~0 01),持续性房颤组的MMP 9活性较阵发性房颤组亦明显增加 (P<0 01 )。( 4 )MMP 2、MMP 9的mRNA及蛋白表达水平与左心房内     

心房颤动患者碱性成纤维细胞生长因子基因表达的研究

目的：检测碱性成纤维细胞生长因子（bFGF）在心房颤动（房颤）患者心房组织中的基因表达,探讨其与心房纤维化的关系。方法：75例风湿性心脏瓣膜病（风心病）接受换瓣手术者被分为三组：窦性心律组（34例）,阵发性房颤组（11例）,慢性房颤组（30例）;于术中切取右心耳组织,分别采用半定量逆转录聚合酶链反应和免疫组化技术测定bFGFmRNA含量和蛋白含量。结果：与窦性心律组比较,bFGF的mRNA和蛋白在阵发性房颤组和慢性房颤组的表达均显著上调（P均〈0．001）,而且慢性房颤组的较阵发性房颤组的明显上调（P〈0．05）。同时,bFGF的mRNA和蛋白水平均与房颤持续时间（分别为r=0．330．P=0．005和r=0．299,P=0．010）及左心房内径呈正相关（分别为r=0．342,P=0．003和r=0．285,P=0．015）。结论：心房组织中bFGF的基因表达上调可能参与房颤的发生和维持．与房颤的心房纤维化密切相关。     

Coagulation, fibrinolytic system activation and endothelial dysfunction in patients with mitral stenosis and sinus rhythm

Anticoagulation treatment can prevent systemic embolism in patients with mitral stenosis (MS) and atrial fibrillation (AF), but this treatment is under debate if patients are in sinus rhythm. The authors aimed to determine the hemostatic changes in patients with MS and sinus rhythm. Forty-six patients (28 in sinus rhythm and 18 in AF) with mitral stenosis were enrolled in this study. They studied systemic venous fibrinogen, D-dimer, antithrombin-III, tissue plasminogen activator (tPA), plasminogen activator inhibitor-I (PAI-I), von Willebrand factor (vWF), and platelet factor 4 (PF 4) in these patients. The patients were first classified according to their rhythm as sinusal and AF, and then according to the presence of left atrial spontaneous echo contrast (LASEC). Fibrinogen, D-dimer, antithrombin-III, vWF, and PF 4 levels were significantly greater in patients with MS and sinus rhythm or atrial fibrillation compared to the control group (p < 0.05). Whether the rhythm was sinus or AF, fibrinogen, D-dimer, antithrombin-III, vWF, and PF 4 levels were significantly higher in patients with LASEC than in the control group (p < 0.05). Only PF 4 was higher in the AF group than in those with sinus rhythm (p < 0.05). As to plasminogen activator and PAI-I levels, only tissue plasminogen activator levels were found to be higher in the AF group than in those with sinus rhythm and the control group (p < 0.05). In patients with mitral stenosis and sinus rhythm, if LASEC is present, coagulation activation, platelet activation, and endothelial dysfunction are similar in patients with AF, and anticoagulation should be considered in these patients.     

非瓣膜性心房颤动患者内皮和血小板功能及β受体阻滞剂干预的临床意义

目的 探讨非瓣膜性心房颤动(房颤)与内皮细胞功能及血小板功能的关系,观察β受体阻滞剂治疗对房颤患者内皮功能及血小板功能的影响.方法 非瓣膜性持续性房颤患者(房颤组)25例,窦性心律组(窦律组)35例,通过竞争性酶联免疫(ELASA)分析定量测定两组血清血管性血友病因子(von Willebrand Factor,vWF)和可溶性P选择素水平,及房颤组β受体阻滞剂治疗后上述指标的变化.结果 房颤组血清vWF水平(1945.2±111.3)g/L高于窦律组(1862.3±101.6)g/L,差异有统计学意义(P＜0.05).房颤组患者服用β受体阻滞剂(阿替洛尔)后,血清vWF水平下降至(1758.3±152.4)g/L,与服药前比较差异有统计学意义(P＜0.01).血清可溶性P选择素水平房颤组与窦律组[分别为(24.32±9.21)g/L与(24.68±11.70)g/L]比较,差异无统计学意义(P＞0.05),服用β受体阻滞剂后血清可溶性P选择素水平下降至(21.05±8.94)g/L,但与服药前相比差异无统计学意义(P＞0.05).vWF与可溶性P选择素无相关性(Pearson相关系数为-0.008,P＞0.05).结论 房颤患者血清vWF水平较窦性心律者升高,提示存在心血管内皮损伤.服用阿替洛尔后,房颤患者血清vWF水平下降,提示阿替洛尔用于房颤患者除能有效控制心室率外,还可能具有内皮保护功能.

Abstract：

Objective To examine the serum von Willebrand factor (vWF) and soluble Pselectin levels in patients with non-valvular atrial fibrillation (NVAF), and to observe the influence of beta-blocker treatment on endothelial function and platelet activation in NVAF patients. Methods The 25 subjects, 17 males and 8 females, with persistent NVAF and left ventricular ejection fraction (LVEF)≥50%, were enrolled in NVAF group. Those with myocardial infarction, cardiomyopathy or hyperthyroidism were excluded. Another 35 subjects with sinus rhythm were as control (age,gender and LVEF matched with NVAF group, and with similar cardiovascular diseases). Serum vWF and soluble P-selectin levels were tested by enzyme-linked immunosorbent assay. Results The serum vWF level was significantly higher in NVAF group than in control group [(1945.2±111.3) g/L vs. (1862.3±101.6) g/L, P＜0.05]. However, there was no significant difference in serum soluble P-selectin level between NVAF group and control group [(24.32±9.21) g/L vs. (24.68±11.70) g/L, P＞0. 05]. After administration of beta-blocker, a down-regulation was found in serum vWF level [(1758. 3±152. 4) g/L, P＜0. 01], but not in soluble P-selectin level [(21.05±8. 94) g/L, P＞0. 05]. There was no relationship between serum level of vWF and soluble P-selectin (r=-0.008,P＞0. 05). Conclusions High serum level of vWF is found in patients with persistent NVAF as compared with control, indicating endothelial damage/dysfunction in those patients. After administration of beta-blocker, serum level of vWF drops dramatically in NVAF patients, indicating possible endothelial function protection of beta-blocker.