冠状动脉造影和PTCA术对冠心病纤溶活性的影响

目的 :观察选择性冠状动脉造影 （SCA）和 PTCA对冠心病纤溶活性的影响。方法 :对接受 SCA的 45例患者和 PTCA术后 19例患者的血浆组织型纤溶酶原激活物抗原 （t- PA:Ag）、纤溶酶原激活物抑制物 （PAI1 ）和纤维蛋白二聚体 （DD）含量进行动态观测。结果 :1SCA后 SCA正常组、稳定型和不稳定型心绞痛组 t- PA:Ag含量均显著升高 （P<0 .0 1） ,前者 2 4h,后者 72 h内恢复 ;活性无显著变化 ;t- PA:Ag升高程度以 SCA正常组最明显 ,显著高于稳定和不稳定型心绞痛组。 2 PTCA术后 t- PA:Ag,DD含量和 PAI1 活性均显著升高 ,PAI1 活性 3d内、t- PA :Ag 7d内恢复 ,DD含量 7d内仍高于术前。结论 :冠心病患者有 t- PA:Ag储存和释放障碍 ,SCA和 PTCA术后纤溶活性有增加趋势 ,可能与术前、术后抗血小板药物及术中、术后肝素应用有关。     

缬沙坦治疗原发性高血压对内源性纤溶活性的影响

目的 :观察缬沙坦治疗原发性高血压 (EH)的同时对内源性纤溶活性的影响。方法 :用发色底物分解显色法测定 6 4例EH患者 (EH组 )和 35例正常对照者 (对照组 )的组织型纤溶酶原激活因子 (t PA)、纤溶酶原激活抑制物 (PAI 1)的活性 ,然后EH组口服缬沙坦 80mg ,每日 1次 ,共 8周 ,比较治疗前后的t PA和PAI 1活性变化。结果 :EH组治疗前t PA活性较对照组明显降低 ,PAI 1活性明显升高 (P <0 .0 5 )。经缬沙坦治疗 8周后 ,t PA活性较治疗前显著上升 ,PAI 1活性降低 (P <0 .0 5 )。结论 :缬沙坦在降低血压的同时 ,有改善内源性纤溶活性的作用。     

急性心肌梗死患者内皮纤溶储备功能的研究

目的 :探讨急性心肌梗死 (AMI)患者全身纤溶状态及内皮纤溶储备功能的变化规律。方法 :2 1例 AMI患者于入院第 1天和入院后第 10天采集静脉血测定纤溶指标 ,并与 15例正常人作对比 ,同时做静脉闭塞试验以确定最大内皮组织纤溶酶原激活剂 (t PA)释放。结果 :AMI患者 t PA含量、纤溶酶原激活剂抑制物 - 1(PAI- 1)活性均较正常人明显为高。最大内皮 t PA释放于入院第 1天降低为 (2 .3± 0 .9) μg/ L(P<0 .0 1) ,第 10天恢复至(4.5± 1.2 ) μg/ L(P >0 .0 5 )。结论 :内皮纤溶功能紊乱与血管内血栓形成的联系要比全身纤溶指标的变化更为密切 ,在 AMI早期纠正内皮纤溶功能异常更为重要     

缺血性脑血管病患者血脂、凝血及纤溶指标的变化

目的　观察缺血性脑血管病 (ICVD)患者血脂、凝血及纤溶指标的变化。方法　对缺血性脑血管病 113例 [包括脑梗死 (CI)急性期 2 5例 ,恢复期 30例 ;短暂性脑缺血发作 (TIA) 5 8例 ]和正常对照组 77名进行血脂、血浆组织型纤溶酶原激活物 (t PA)、纤溶酶原激活物抑制物 (PAI)和D 二聚体浓度进行测定。结果　CI组甘油三酯 (TG)、总胆固醇 (TC)、载脂蛋白B10 0 (ApoB10 0 )、氧化型低密度脂蛋白 (ox LDL)水平显著高于对照组 ;CI急性期、恢复期和TIA组PAI高于对照组 ,而t PA活性均低于对照组 ;TIA伴有梗死灶者血浆D 二聚体和PAI含量明显高于无梗死灶者 ,t PA含量低于无梗死灶者。结论　ICVD患者不仅存在血脂代谢紊乱 ,且体内凝血活性增强 ,纤溶功能下降。     

经皮冠状动脉介入治疗对冠心病患者内皮功能、纤溶活性及炎症指标的影响

本研究测定经皮冠状动脉腔内成形术(PTCA)及支架置入术(CS)前后C 反应蛋白(CRP)、血管性血友病因子(VWF)、D 二聚体(DD)、纤溶酶原激活物抑制物 1(PAI 1)、肌钙蛋白I(cTnI)的变化,以了解PTCA CS术对冠心病患者血管内皮功能、纤溶活性及炎症指标的影响。一、资料与方法1.研究对象:PTCA CS组4 0例,冠状动脉造影(CAG)阳性组2 0例,CAG阴性组15例,三组临床基线资料无统计学差异。排除入选对象的标准为:(1) 3周以内的急性心肌梗死;(2 )肝、肾功能异常;(3)并存影响CRP水平的其他疾患及因素;(4)存在血液病。PTCA CS组术前3…     

尿激酶治疗下肢深静脉血栓的纤溶研究

35例下肢深静脉栓塞(lower legs deep venous thrombosis,LDVT)患者,应用尿激酶治疗,探讨治疗前后纤溶酶原活性(PLG:A),纤溶酶活性(pL:A),组织纤溶酶原激活物(t-PA),组织纤溶酶激活物抑制物(PAI)和纤维蛋白原抗原性(Fg:Ag)的变化,结果显示PAI和Fg:Ag明显降低(P值分别<0.05和<0.001),pl:A呈显著增高(P值<0.001)。同时,下肢深静脉栓塞部分与完全再通24例(24/35例),疗效达68.5%,无1例出血与过敏。由此证实尿激酶具有明显溶栓效应,且安全可靠。     

高血压患者胰岛素抵抗与纤溶系统的关系

目的　研究高血压病 (EH)患者胰岛素抵抗 (IR)与纤溶系统的关系。方法　EH病人 71例 ,采用 75g葡萄糖口服负荷法 (OGTT) ,将EH患者分为糖耐量正常组 (NGT) 44例和糖耐量异常组 (IGT) 2 7例 ,正常对照组 3 1例。测定血浆组织型纤溶酶原激活物活性 (t PA)、纤溶酶原激活物抑制物 -1活性 (PAI 1)、纤溶酶原活性 (PLG) ,在OGTT测定的同时作血胰岛素 (INS)测定 ,并根据Cederholm公式计算出胰岛素敏感指数 (ISIc)。结果　NGT组和IGI组相比t PA无明显差别 (P >0 0 5) ,但两组均较正常对照组降低 (P <0 0 5)。NGT组和IGT组PAI -1与正常对照组比较均无明显差别 (P >0 0 5)。IGT与NGT相比PLG增高 (P <0 0 5) ,与正常对照比较PLG明显增高 (P <0 0 1)。ISIc在NGT组和IGT组较正常对照组明显降低 (P <0 0 5,P <0 0 1) ,且IGT组较NGT组更低 (P <0 0 1)。ISIc与t PA ,PAI 1不相关。结论　高血压病人存在胰岛素抵抗 ,当高血压病合并IGT时 ,胰岛素抵抗更明显。EH病人存在纤溶活性的下降 ,当合并IGT时 ,纤溶活性的降低更为明显。t PA和PAI 1与ISIc无明显相关性     

纤溶酶原对星形胶质细胞纤溶酶原激活因子及其抑制的调节作用

目的 探讨纤溶酶原（PGn)对大鼠脑星菜胶质细胞纤溶酶原激活因子（PAI）及其抑制剂(PA)的调节作用。方法 利用大鼠血纤溶酶原对体外培养的星形胶质细胞进行诱导刺激,采用酶谱分析法、反射酶谱分析法、免疫印迹法对所产生的PAs和PAIs进行分析测定。结果 实验所用PGn调uPA和PAI－1,下调tPA活性,并且诱导产生一个28kDa的低分子量的uPA活性分子。结论 在体外,纤溶酶原有调节星形胶质细胞的功能。     

缺血性脑血管病纤溶活性和血清同型半胱氨酸含量测定的临床意义

目的　探讨缺血性脑血管病 (ICVD)患者血浆纤溶活性和血清同型半胱氨酸 (Hcy)含量的变化及其临床意义。方法　入选ICVD患者 86例 (ICVD组 ) ,根据病情又分为短暂脑缺血发作 (TIA)组 14例 ,脑梗死组 72例 ,并入选非脑血管病患者 4 3例作为对照组 ,分别采用产色法测定血浆纤溶酶原 (Plg)、组织型纤溶酶原激活物 (t PA)、纤溶酶原激活抑制物 1(PAI 1)活性 ,荧光偏振光法测定血清Hcy,电化学发光法测定叶酸 ,同时常规测定血脂水平。结果　ICVD组 ,TIA患者和脑梗死患者血浆Plg、t PA活性均较对照组显著降低 (P <0 .0 5 )。ICVD组血清Hcy水平较对照组明显升高 (P <0 .0 1) ,t PA活性降低和高Hcy对ICVD的发生均有显著作用。结论　t PA活性降低和高Hcy分别是ICVD的独立危险因素     

血管紧张素Ⅱ和血管紧张素1-7对内皮细胞释放组织纤溶酶原激活物及其抑制剂-1的影响

目的 :研究血管紧张素Ⅱ (AngⅡ )和血管紧张素 1 7[Ang ( 1 7) ]对内皮细胞分泌组织纤溶酶原激活物 (t PA)和纤溶酶原激活物抑制剂 1(PAI 1)的影响。方法 :培养内皮细胞株 (ECV30 4 ) ,分为AngⅡ和Ang ( 1 7)刺激组 ,培养基中AngⅡ和Ang ( 1 7)加至终浓度为 5、10、2 5、5 0、10 0nmol/L ,2 4h后测定上清液中的t PA和PAI 1的含量。结果 :内皮细胞在AngⅡ终浓度为 5 0、10 0nmol/L组刺激 2 4h后 ,其分泌的PAI 1含量较对照组有明显升高 ,差异有统计学意义 (P <0 .0 5 )。而Ang ( 1 7)在同样浓度组却显著降低PAI 1(P <0 .0 5 ) ,AngⅡ和Ang ( 1 7)两组t PA含量差异无统计学意义 ( P >0 .0 5 )。结论 :AngⅡ对内皮细胞株分泌的PAI 1有显著的升高作用 ,而Ang ( 1 7)对PAI 1作用相反。两者对t PA均无显著影响。提示AngⅡ和Ang ( 1 7)对纤溶系统的调节有一定作用     

冠心病患者血清脂蛋白(a)与纤溶功能的变化及其相关性

目的:观察冠心病(CHD)患者血清脂蛋白a[Lp(a)]、血浆组织型纤溶酶原激活剂(tPA)与纤溶酶原激活剂抑制物-1(PAI-1)活性的变化特点,并探讨它们之间的关系。方法:对124例CHD患者和26例正常人采用双抗体ELISA法测定Lp(a)浓度,发色底物法测定tPA、PAI-1活性。结果:CHD患者中,急性心肌梗死(AMI)和不稳定性心绞痛(UAP)组患者Lp(a),浓度和PAI-1活性均非常显著高于对照组(P<0.01):tPA活性显著低于对照组(P<0.01);陈旧性心肌梗死(OMI)和稳定性心绞痛(SAP)组患者Lp(a)浓度和PAI-1活性均亦高于对照组(P<0.05);tPA活性亦低于对照组(P<0.05)。124例CHD患者相关分析显示:Lp(a)与PAI-1活性呈显著正相关,与tPA活性呈显著负相关(P均<0.001)。结论:冠心病患者Lp(a)显著升高,且与tPA、PAI-1活性有密切相关关系。     

苯那普利对急性冠状动脉综合征患者凝血及纤溶系统的影响

目的 :探讨血管紧张素转换酶抑制剂对凝血及纤溶系统的影响。方法 :急性冠状动脉综合征患者 48例 ,随机分为对照组 (1 6例 )和苯那普利组 (32例 ) ,对照组按临床常规处理 ,苯那普利组在此基础上加用苯那普利 1 0 mg/ d,分别于入院后即刻和第 3天采血测激活的凝血时间(ACT)和血浆组织型纤溶酶原激活剂 (t- PA)及其抑制物 (PAI- I)。结果 :治疗前后及组间比较ACT均无显著变化 ;两组的 t- PA活性治疗后均比治疗前明显升高 ,而 PAI- I活性明显降低 (均 P<0 .0 5及 <0 .0 1 ) ,组间比较苯那普利组升高及降低的幅度显著高于对照组 (P <0 .0 1 )。结论 :苯那普利对急性冠状动脉综合征患者的凝血系统无明显影响 ,但可使 t- PA活性增高而 PAI- I活性降低     

辛伐他汀对冠心病患者纤溶参数的影响

目的了解冠心病患者纤溶参数的变化,并观察辛伐他汀对冠心病患者纤溶参数的影响。方法测定87例正常对照者和108例冠心病患者血浆组织型纤溶酶原激活物(t-PA)活性和纤溶酶原激活物抑制物-(1PAI-1)活性,随后108例冠心病患者被随机分成常规治疗组和常规治疗+辛伐他汀40mg每日一次(辛伐他汀组)。治疗14d后复测t-PA活性和PAI-1活性。结果与正常对照组相比较,冠心病患者纤溶参数异常,t-PA活性下降,PAI-1活性上升(P<0.01)。常规治疗组治疗后纤溶参数无显著变化(P>0.05)。辛伐他汀组纤溶参数明显改善,表现为t-PA活性上升,PAI-1活性下降(P<0.01)。结论冠心病患者纤溶参数明显异常,辛伐他汀能改善冠心病患者纤溶参数。     

Plasminogen activator inhibitor activity and other fibrinolytic variables in patients with coronary artery disease.

Several fibrinolytic variables, including plasminogen activator inhibitor activity, were studied before and after exercise in 67 normolipidaemic patients with coronary artery disease and in 25 hyperlipidaemic patients with coronary artery disease. Before exercise plasminogen activator inhibitor activity was higher in the patient groups than in a group of 10 healthy volunteers. For those who were normolipidaemic plasminogen activator inhibitor activity was greater in patients with angina pectoris who had had a myocardial infarction. The concentration of antigenic tissue-type plasminogen activator was similar in all the patients with coronary artery disease and higher than in the control group. After the exercise test fibrinolytic capacity was lower in the patients with angina pectoris and a previous history of myocardial infarction. After exercise both the released immunological tissue-type plasminogen activator and fibrinolytic capacity were lower in the hyperlipidaemic patients than in the normolipidaemic patients. The concentration of plasminogen activator inhibitor was also higher in the hyperlipidaemic patients. Patients with hyperlipidaemia IV had the highest plasminogen activator inhibitor activity. The increase in plasminogen activator inhibitor activity found in the patients was partially inhibited by antiserum against plasminogen activator inhibitor-1 in vitro. The formation of a complex of about 115,000 daltons between plasminogen activator inhibitor and purified tissue-type plasminogen activator was detected by a zymographic fibrin technique. These findings show that in patients with coronary artery disease fibrinolytic activity is impaired by an increase in plasminogen activator inhibitor. Impaired fibrinolysis may be related to the clinical evolution of coronary artery disease in these patients.     

Fibrinolytic Variables in Postmenopausal Women with Unstable Coronary Artery Disease

Objectives: Many women with typical anginal chest pain have normal coronary angiograms. The pathogenetic mechanisms behind the chest pain in these patients is unknown but may be due to altered fibrinolytic function enhancing thrombosis formation. We evaluated the two key components of the fibrinolytic system, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in women with clinical signs of unstable coronary artery disease (CAD). Methods and results: 158 patients with unstable CAD and 101 controls were examined. Of the patients 16% had normal vessels and 84% coronary atherosclerosis at coronary angiography. Mean plasma concentration of t-PA-ag, but not of PAI-1-act was higher in patients than in controls (t-PA-ag: 2.12 (2.05;2.19) vs. 1.98 (1.89;2.07), p<0.05; PAI-1-act: 1.55 (1.35;1.74) vs. 1.49 (1.24;1.73), p=n.s.). Patients with coronary atherosclerosis had significantly higher mean plasma levels of both t-PA-ag and PAI-1-act than patients with normal coronary vessels (t-PA-ag: 2.16 (2.08;2.33) vs. 1.94 (1.78;2.10), p<0.05; PAI-1-act: 1.68 (1.47;1.90) vs. 0.82 (0.43;1.21), p<0.01), and these differences were seen whether markers of myocardial damage were elevated or not. Mean plasma levels of PAI-1-act in patients with normal coronary vessels were even lower than in the control group (p<0.05). Almost all significant differences in mean plasma t-PA-ag and PAI-1-act disappeared after adjustments for known covariates. Conclusion: Our results indicate, regardless of myocardial marker elevation or not, an activated fibrinolytic system in postmenopausal women with unstable CAD and coronary atherosclerosis, but not in the same group of patients with normal coronary vessels. This argues against reduced fibrinolytic capacity in the latter patients and therefore against thrombosis formation as the cause of chest pain in these women. However, we cannot exclude that the differences can be an effect of inequality among some common risk factors between the groups.     

Evidence for reduced fibrinolytic activity in unstable angina at rest. Clinical, biochemical, and angiographic correlates

BACKGROUND. The goal of this study was to evaluate the role of the fibrinolytic system in patients with unstable angina at rest associated with transient electrocardiographic changes. METHODS AND RESULTS. Tissue plasminogen activator activity in plasma was comparable among patients with unstable angina (n = 17), patients with stable exertional angina (n = 10), and control patients with normal coronary arteriograms (n = 8). In contrast, plasminogen activator inhibitor-1 (PAI-1) activity in plasma was elevated in the unstable angina group (21.67 +/- 9.52 AU/ml) as compared with either the stable angina group (12.01 +/- 7.06 AU/ml, p less than 0.02) or the controls (12.49 +/- 8.54 AU/ml, p less than 0.02). Coronary angiography performed within 24 hours after the last anginal episode showed a similar extent of coronary artery disease in the unstable and stable angina groups. However, intracoronary thrombi were observed in eight patients in the unstable angina group while no thrombus was noted in the stable angina group (chi 2 = 7.22, p less than 0.01). CONCLUSIONS. We conclude that patients with unstable angina at rest have a reduced fibrinolytic activity and an increased incidence of intracoronary thrombi. It is postulated that elevated PAI-1 activity in the presence of coronary arterial wall injury may be an important factor leading to the development of acute coronary syndromes.     

Fibrinolytic activities and their relations to esophageal variceal bleeding in patients with liver cirrhosis]

BACKGROUND/AIMS: Esophageal variceal bleeding in liver cirrhosis is a major complication and has high mortality rate. We tried to find fibrinolytic parameters, which correlated with variceal bleeding in cirrhotic patients. METHODS: We divided the cirrhotic patients into two groups: bleeding group (group A, n=15) and non-bleeding group (Group B, n=17). Fibrinolytic parameters (fibrinogen, D-dimer, plasminogen, tissue plasminogen activator [t-PA], fibrin degradation product [FDP], and plasminogen activator inhibitor type-1 [PAI-1]) were compared between two groups. In the group A, serial samplings were taken at the initial period, 3 days, 8 days, 15 days and 6 weeks after the bleeding onset. RESULTS: Plasma levels of FDP and D-dimer in the group A were significantly higher than the group B (1.7 +/- 1.16 vs. 0.95 +/- 1.27 mg/L and 10.96 +/- 6.58 vs. 4.99 +/- 3.50 micro gram/mL, respectively, p value<0.05). The clinical, biochemical, and coagulation parameters didn't show significant differences in both groups. The fibrinolytic parameters were improved along with the hemodynamic stabilization in group A. CONCLUSIONS: Cirrhotic patients with increased fibrinolytic activity were at higher risk of bleeding. Thus, the measurement of these parameters would be useful to identify patients at higher risk of esophageal variceal bleeding.     

冠心病介入治疗前后患者血浆P-选择素、血栓调节蛋白、纤溶酶原激活剂抑制剂-1的变化

目的旨在了解冠心病患者行经皮冠状动脉成形术(PTCA)前后血小板、内皮功能及纤溶活性的变化.方法以26例冠状动脉造影(CAG)阴性者为阴性对照,以16例CAG阳性但不宜行PTCA者为阳性对照,观察24例行PTCA术冠心病患者术前后P-选择素(Ps)、血栓调节蛋白(TM)及血浆纤溶酶原激活剂抑制物-1(PAI-1)的动态变化.结果PTCA组Ps、TM在术后5分钟较术前显著增加(P均<0.05),且较同时间点的阴性组有非常显著增高(P均<0.001);术后5minCAG阳性组Ps较CAG阴性组显著增加(P<0.02);在术前PTCA组和CAG阳性组PAI-1均高于CAG阴性组(P均<0.05).结论PTCA术后Ps、TM的增高,提示血小板的激活及内皮细胞的损伤,急性冠脉闭塞与PTCA后再狭窄可能与此相关.     

冠心病伴高血脂症患者的纤溶功能改变及血脂康的影响

目的:研究冠心病并高血脂症患者纤溶、纤溶储备功能的改变及血脂康的影响。方法:40例冠心病人[其中12例总胆固醇(TC)升高;10例甘油三酯(TG)升高;18例TG、TC均升高],于入院第1天采集静脉血测定纤溶指标后服用血脂康(0.6mg,每日2次);于4周后再次行纤溶指标检查,同时做静脉闭塞实验以确定最大内皮组织纤溶酶原激活物(t-PA)水平并与10例正常者对比。结果:经4周血脂康治疗后,t-PA活性、t-PA/PA I比值明显升高(P<0.01)纤溶储备功能明显改善(P<0.05)。结论:血脂康能明显改善冠心病高脂血症患者的纤溶储备功能。