冠心病患者血清甘油三酯水平与纤溶激活系统的关系

为研究冠心病患者血清甘油三酯水平与纤溶激活系统的关系,比较分析冠心病患者、高甘油三酯血症患者及正常对照者的血清甘油三酯水平、组织型纤溶酶原激活物及其抑制剂活性。纤溶酶原激活物抑制剂1、组织型纤溶酶原激活物活性测定采用发色低物法,血清甘油三酯浓度测定采用酶法。结果表明,高甘油三酯血症患者及冠心病患者纤溶酶原激活物抑制剂1活性较正常人升高,组织型纤溶酶原激活物活性较正常人下降。冠心病患者及高甘油三酯血症患者均有不同程度的纤溶活性下降,以急性心肌梗死、不稳定型心绞痛伴高甘油三酯组改变尤为明显。血清甘油三酯水平与血浆组织型纤溶酶原激活物活性呈负相关,与纤溶酶原激活物抑制剂1活性呈正相关。结果提示,甘油三酯通过影响纤溶功能参与冠心病的形成与发展。     

纤溶酶原激活抑制物活性与冠心病发病关系

目的 :探讨纤溶酶原激活抑制物 (PAI)与冠心病 (CHD)发病的关系。方法 :用免疫化学方法观察测定 145例CHD患者和 130例健康对照者的血浆PAI、纤溶酶原激活物 (PA)活性和胆固醇、甘油三酯 (TG)的血清水平。结果 :CHD组的PAI/PA比值 (1.83± 0 .5 2 )明显高于对照组 [(1.17± 0 .48) ,P <0 .0 5 ],PAI与TG具有显著相关性 (r =0 .45 ,P <0 .0 5 )。结论 :PAI与TG相关性在CHD发生、发展过程中具有重要作用。     

老年恶性肿瘤患者血浆组织因子途径抑制物、纤溶酶原激活物及抑制剂的变化

为探讨老年人恶性肿瘤凝血和纤溶异常的机制 ,我们于 2 0 0 0年 4～ 9月 ,测定了 6 0例老年恶性肿瘤患者血液中组织因子途径抑制物 (ＴＦＰＩ)、尿激酶型纤溶酶原激活物(ｕＰＡ)、ｕＰＡ受体 (ｕＰＡＲ)及组织纤溶酶原激活物抑制剂(ＰＡＩ 1)水平 ,现将结果报道如下。　　一、对象与方法　　 1.研究对象 :老年肿瘤组 6 0例 ,均为本院住院患者 ,并经有关病理或细胞学检查明确诊断的恶性肿瘤患者 ,男 38例 ,女 2 2例 ,年龄 6 0～ 86岁 ,平均 6 5 7岁。其中肺癌 18例 ,食管癌及大肠癌 12例 ,肝癌 6例 ,乳腺癌 10例 ,淋巴瘤8例及其他部位肿瘤 6…     

血浆纤溶酶原激活物抑制剂-1在年青冠心病患者中的表达

目的 研究血浆纤溶酶原激活物抑制剂-1(plasminogen activator inhibitor type-1,PAI-1)分子在年青冠心病患者中的表达以及与冠心病病情的关系.方法 入选患者按照年龄分为年青组和老年组,检测所有入选患者的PAI-1分子含量,年青组患者病情稳定后一月复查PAI-1含量.结果 年青组患者血清PAI-1为(44.27±2.8) mol/L,老年组PAI-1的血清含量为(39.14±3.60) mol/L,两组含量有统计学意义(P<0.05);一月后年青组复查PAI-1的血清含量为(33.85±2.4) mol/L,与发病急性期PAI-1分子含量相比,含量有统计学意义(P<0.05).结论 PAI-1是年青患者冠心病的独立预测因素之一,且PAI-1含量的高低与冠心病的时期有明显相关性.对于接受冠心病长期规范治疗的患者,PAI-1的血清含量与冠心病的病情相关性还需要进一步研究.     

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。     

冠心病组织型纤溶酶原激活物及其抑制物的活性变化

冠心病组织型纤溶酶原激活物及其抑制物的活性变化邱建钱学贤刘映峰刘兰平我们比较了不同类型冠心病血浆组织型纤溶酶原激活剂（ｔＰＡ）和纤溶酶原激活剂抑制物（ＰＡＩ）活性的变化，并探讨ｔＰＡ和ＰＡＩ活性变化与冠状动脉（冠脉）病变范围和冠脉狭窄程度的关系。对象...     

恶性肿瘤患者血液中尿激酶型纤溶酶原激活系统测定的临床意义

目的 研究恶性肿瘤患者血液中尿激酶型纤溶酶原激活物（ＵＰＡ）及其特异性受体（ＵＰＡＲ）和纤溶酶原激活物掏抑制物－１（ＰＡＩ－１）含量对肿瘤转移和预后的影响。方法用ＥＬＩＳＡ法测定５０例恶性肿瘤患者和２０例正常人血液中ＵＰＡ、ＵＰＡＲ和ＰＡＩ－１含量。结果 淋巴瘤ＵＰＡ,肺癌ＵＰＡ、ＰＡＩ－１,食管癌、肠癌和乳腺癌ＵＰＡ、ＵＰＡＲ和ＰＡＩ－１均显著升高（Ｐ〈０．０５～０．０１）;肿瘤组中,中、晚期组     

老年高血压病患者早期肾损害中组织型纤溶酶原激活物和纤溶酶原激活物抑制剂的作用

为研究老年高血压病患者纤溶活性异常与肾脏损害的关系 ,选择 5 2例血清肌酐正常的老年原发性高血压患者和 2 2例血压正常的老年人 ,用发色底物法测定血浆组织型纤溶酶原激活物和纤溶酶原激活物抑制剂活性 ,用酶联免疫吸附法测定尿微量转铁蛋白和视黄醇结合蛋白含量 ,并进行相关分析。结果发现 ,老年高血压病患者与正常血压者比较 ,血浆组织型纤溶酶原激活物活性显著下降 ,血浆纤溶酶原激活物抑制剂活性和尿微量转铁蛋白、视黄醇结合蛋白含量显著升高 ;血浆组织型纤溶酶原激活物活性与尿转铁蛋白 (r =- 0 .792 8)、视黄醇结合蛋白 (r=- 0 .85 2 2 )含量呈显著负相关 (P <0 .0 0 0 1) ,而血浆纤溶酶原激活物抑制剂活性与尿转铁蛋白 (r =0 .7497)、视黄醇结合蛋白 (r=0 .82 69)含量呈显著正相关 (P <0 .0 0 0 1) ,提示老年高血压病患者存在的纤溶活性异常可能在其肾脏损害进程中起重要作用     

纤溶酶原激活物抑制剂-1与动脉粥样硬化

纤溶酶原激活物抑制剂-1可能是动脉粥样硬化的危险因素,它通过影响动脉附壁血栓形成、内皮再生、新内膜形成和基质沉积等环节参与动脉粥样硬化.     

纤溶酶原激活剂的抑制剂与动脉粥样硬化关系的研究进展

纤溶酶原激活剂的抑制剂－1是血浆中主要纤溶酶原激活剂的抑制物。它主要是由血管内皮细胞产生。纤溶酶原激活剂的抑制剂－1所致的纤溶系统损伤,导致纤维蛋白沉积清除减少,在动脉血栓的发生和发展中起着主要作用。纤溶酶原激活剂的抑制剂－1已被很多学者认为是冠心病的独立危险因素。本文就纤溶酶原激活剂的抑制－1与动脉粥样硬化的关系作一综述。     

纤溶酶原激活物抑制剂-1在冠状动脉疾病时表达的变化

目的：研究纤溶酶原激活物抑制剂（PAI）-1分子在吸烟患者中的表达以及与冠状动脉粥样硬化病变的关系。方法：入选冠心病患者98例,根据吸烟时间和吸烟支数分为：强吸烟组（45例）和弱吸烟组（53例）;又根据冠脉造影分为：单支病变组（56例）和多支病变组（42例）,比较各组血清PAI-1分子含量。结果：强吸烟组患者血清PAI-1含量明显高于弱吸烟组[（41．17±8．5）mol／L比（34．26±7．8）,mol／L,P〈0．055;多支病变组PAI-1含量明显高于单支病变组[（43．21±8．3）mol／L比（31.16±6．4）mol／L,P〈0．05]。结论：冠状动脉病变严重程度与纤溶酶原激活物抑制剂-1含量有关,吸烟可破坏机体的内环境平衡,对纤溶起到明显的抑制作用。     

复方丹参滴丸对冠心病患者纤溶系统t-PA、PAI-1含量与活性的调控

目的观察复方丹参滴丸对冠心病患者内源性纤溶活性及血管内皮功能的影响，探讨其作用机制。方法冠心病患者78例，随机分为对照组和复方丹参滴丸组。对照组采用常规治疗；复方丹参滴丸组在常规治疗基础上加用复方丹参滴丸每次10粒，每日3次。两组用药时间均为4周。比较治疗前后血浆组织型纤溶酶原激活剂（t-PA）、纤溶酶原激活剂抑制因子-1（PAI-1）活性及浓度。结果复方丹参滴丸治疗4周后，患者血浆PAI-1活性及浓度下降（P〈0．05），t—PA活性及浓度含量升高（P〈0．05），与治疗前比较差异有统计学意义；常规治疗组治疗前后t-PA和PAI-1活性差异无统计学意义。结论复方丹参滴丸可有效地调控改善冠心病患者内源性纤溶活性及血管内皮功能。     

老年冠心病患者冠状动脉内支架置入术的临床评估

目的　评估老年冠心病患者的冠状动脉内支架置入术(支架术)的安全性和有效性。　方法　将我院123例年龄≥60岁(老年组)和265例年龄＜60岁(非老年组)已行支架术的冠心病患者的临床病灶特点、手术成功率、手术并发症及近、远期临床随访结果进行了回顾性对照分析。　结果　老年组在经皮冠状动脉腔内成形术（PTCA）的基础上行支架术总成功率与非老年组比较差异无显著性(96.7%与99.6%,Ｐ＞0.05);老年组手术死亡率为1.6%（2/123）,但与非老年组相比差异无显著性（Ｐ＞0.05）,两组间冠状动脉血管、外周血管并发症无明显差异;老年组因冠状动脉扩张后发生急性血管闭塞或严重内膜撕裂而置入支架比例明显高于非老年组（23.7%与14.3%,Ｐ＜0.001）;老年组左主干病变比例明显高于非老年组（3.2%比0.3%,Ｐ＜0.001）。随访6～54个月,两组患者恶性心脏事件发生率无明显差异,但老年组患者血运重建率明显高于非老年组（16.3%与7.8%,Ｐ＜0.05）。　结论　随着PTCA及支架置入技术的日臻完善,老年患者行支架术的成功率与非老年患者无明显差异,均达国内先进水平,老年患者的围手术期死亡率、急性期并发症及长期临床疗效与非老年患者比较无明显差异,均与全国注册水平相似,因此支架术是治疗老年冠心病患者安全、有效的方法。     

血浆纤溶酶原激活物抑制因子基因启动子多态性与2型糖尿病伴发冠心病的关系

目的从分子遗传水平进行基因多态性研究，以探讨２型糖尿病易伴发冠心病的内在原因。方法对８１例２型糖尿病患者、９３例非糖尿病（非ＤＭ）患者进行口服糖耐量试验、血脂分析、血浆纤溶酶原激活物抑制因子（ＰＡＩ１）基因多态性分析。结果２型糖尿病和非ＤＭ相比ＰＡＩ１基因启动子４Ｇ频率明显增加（４２％和３１％，Ｐ＜０００１）；２型糖尿病伴冠心病与不伴冠心病相比，ＰＡＩ１基因启动子４Ｇ频率及４Ｇ／４Ｇ基因型频率存在明显差异（５２％和３０％，３２％和１４％；Ｐ分别＜０００１、００５）；非２型糖尿病伴冠心病与不伴冠心病相比，ＰＡＩ１基因启动子４Ｇ频率及４Ｇ／４Ｇ基因型频率则无明显差异（３１％和３１％，８％和１６％，均为Ｐ＞００５）。结论ＰＡＩ１基因４Ｇ等位基因可能是糖尿病合并冠心病的内在危险因素     

老年人冠状动脉疾病的外科治疗

目的探讨老年人冠状动脉疾病外科治疗的疗效。方法３５例老年患者接受了冠状动脉旁路移植术。按ＮＹＨＡ心功能分级,Ⅲ级１７例,Ⅳ级１８例。其中３支血管病变２４例,左主干病变６例;左室射血分数小于５０％者２５例。结果人均移植血管３．１根,无手术死亡。术后所有患者心绞痛均消失,心功能恢复至Ⅰ级者３３例,Ⅱ级２例。随访３～６４个月,平均３７个月,无死亡。结论对于老年冠状动脉疾病患者,冠状动脉旁路移植术是一种安全、有效的治疗方法。     

老年冠心病患者与抑郁障碍的相关性研究

目的 探讨抑郁障碍是否为老年冠心病的危险因素并观察冠心病伴抑郁障碍患者炎性标记物水平变化.方法 对188例入选者进行临床情况调查、汉密顿抑郁量表评分和血清炎性标记物水平测定,分析冠心病伴抑郁障碍患病率及影响冠心病发病的危险因素.结果 冠心病患者87例,其抑郁障碍患病率为29.9%(26例),非冠心病入选者101例,患病率为11.9%(12例),抑郁障碍在两组间差异有统计学意义(P＜0.01).年龄、高血压、糖尿病、脂代谢异常和抑郁障碍是冠心病的危险因素之一.冠心病伴抑郁障碍组和冠心病不伴抑郁障碍组入选者在突发生活事件、心功能分级差异有统计学意义(均P＜0.05).两组入选者在冠状动脉病变、冠状动脉病变治疗差异无统计学意义(P＞0.05).冠心病伴抑郁障碍组和冠心病不伴抑郁组外周血炎性标记物水平比较显示,伴抑郁障碍组血清单核细胞趋化因子-1水平增高,高敏C反应蛋白和肿瘤坏死因子α差异无统计学意义.结论 老年冠心病患者伴抑郁障碍患病率高于老年非冠心患者群.抑郁障碍是影响冠心病发病的危险因素之一.老年冠心病患者抑郁障碍与炎性标记物之间可能存在一定关系.

Abstract：

Objective To explore whether depressive disorder is one of risk factors for coronary artery disease (CAD) in enrolled patients and observe the level of inflammation markers in coronary artery disease patients with depression. Methods In all patients, we recoded clinical information and data from Hamilton Depression Rating Scale for Depression( HRSD)and measured concentration of monocyte chemoattractant protein-1 (MCP-1), tumour necrosis factor α (TNFα) and hypersensitive C-reaction protein (hsCRP). Results Among 87 patients with coronary artery disease, depressive disorder was diagnosed in 26 patients, the prevalence of depressive disorder was 29. 9%. Among 101 patients without coronary artery disease, 12 patients were suffering from depressive disorder, the prevalence of depressive disorder was 11.90%. The prevalence of depressive disorder in coronary artery disease group was statistically higher than that in non-coronary heart disease group (29.8% vs.11.9%, P<0. 01). The incidence of coronary artery disease was associated with age, hypertension,diabetes mellitus, hypercholesterolemia and depression. Life events and stage of heart function occurred differently between CAD patients with and without depression (P<0. 05). There were no differences in the degree of coronary artery stenosis and the type of treatment (P>0. 05) between the two groups. There were higher concentration of MCP-1 in coronary artery disease patients with depression, but no remarkable difference in hsCRP and TNFa. Conclusions There is high prevalence of depressive disorder, which is one of risk factor for coronary artery disease. The depressive disorder may be associated with inflammation biomarker in patients with coronary artery disease.     

急性冠状动脉综合征患者内皮组织纤溶酶原激活剂储备功能的研究

目的 探讨急性冠状动脉综合征９ＡＣＳ）患者内皮组织纤溶酶原激活剂（ｔＰＡ）储备功能的变化规律。方法 ３５例ＡＣＳ患者,其中急性心肌梗死１５例和不稳定心绞痛２０例,于入院当日和入院后第１０天采集静脉血样以测定纤溶、凝血指标,以评价内皮ｔＰＡ储备功能;同时做静脉闭塞试验以确定最大内皮ｔＰＡ释放,并与稳定性心绞痛９ＳＡＰ）和正常人作对比。结果 ＡＣＳ患者ｔＰＡ含量、纤溶酶原激活剂抑制物－１（ＰＡＩ－１）     

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.     

Plasminogen activator inhibitor-1 4G4G genotype is associated with myocardial infarction but not with stable coronary artery disease

Background  A case control study was conducted to test the hypothesis that plasminogen activator inhibitor type-1 (PAI-1) 4G/5G gene polymorphism confers an increased risk for myocardial infarction (MI) in patients with known coronary atherosclerosis. Methods  One hundred fifty-six consecutive patients who presented with acute MI and 111 stable coronary artery disease (SCAD) patients with documented critical coronary artery stenoses were prospectively enrolled. PAI-1 4G/5G gene polymorphism and conventional atherosclerotic risk factors were studied in all patients. PAI-1 4G/5G gene polymorphism was studied in another 281 healthy blood bank donors. Results  The frequency 4G4G genotype was significantly higher in the MI group as compared to SCAD group (32.7% vs. 15.3%, P = 0.001) while it was not statistically significant between MI and healthy control groups (32.7% vs. 26.0%, P = 0.136). Comparing with healthy controls SCAD group had significantly lower frequency of 4G4G genotype (P = 0.024). In comparison with SCAD group PAI-1 4G/4G genotype, male sex and smoking habits favored to MI in univariate analysis with a P value of less than 0.2. These variables were included in multivariate regression model to estimate the associated risk for MI. PAI-1 4G/4G genotype was the only independent variable (OR 2.67, 95%CI 1.43–4.96, P = 0.002) associated with MI in this regression model. Comparing with healthy control group 4G4G genotype was not associated with MI (OR 1.38, 95%CI 0.90–2.12). However, presence of 4G4G genotype had a protective effect against development of SCAD (OR 0.52, 96%CI 0.29–0.92). Conclusion  Compared to patients with critical coronary stenoses, PAI-1 4G/4G genotype was found to be an independent predictor for development of MI in this population. PAİ-1 4G4G genotype have a protective effect against development of high grade stable coronary stenoses.