冠心病患者冠脉循环血浆内皮素-1水平变化33例分析

为了探讨冠心病患者冠脉循环血浆内皮素 (ET- 1)水平的变化及意义 ,我们对 33例冠心病患者进行了血浆 ET- 1测定 ,现报告如下。资料与方法 :本文冠心病组 33例 ,均经冠脉造影确诊 ,其中男 2 7例 ,女 6例 ;平均年龄 5 8.6± 7.0岁。急性心肌梗死(AMI) 13例 ,不稳定型心绞痛 (UAP) 12例 ,稳定性心绞痛(SAP) 8例。对照组 (冠脉造影排除冠心病 ) 18例 ,男 11例 ,女 7例 ;年龄 5 7.7± 9.1岁。检测方法 :冠脉造影前 ,先行股静脉穿刺置鞘管 ,进右冠脉造影管入冠状静脉窦 (CS)取血 2 ml,为CS血样。再行股动脉穿刺置鞘管 ,于动脉内注射肝素前…     

冠心病患者血浆神经肽Y水平的临床观察

选择符合WHO诊断标准的急性心肌梗塞(AMI)21例,心绞痛(AP)19例,应用放射免疫法动态观察血浆神经肽Y(NPY)含量变化,并以21例正常人作对照.结果显示:对照组NPY水平为 75.1±30.4Pg/ml,AMI组发病第1天NPY含量达峰值,为136.7±66.5pg/ml,显著高于正常组(P<0.05).发病第3天开始下降,第1周末趋于正常,为77.4±48.4pg/ml,与正常组比较无显著差异.AP组于心绞痛发作期NPY含量为159.3±98.5pg/ml,亦显著高于对照组(P<0.05);经治疗2周症状缓解后复查血浆NPY含量下降至118.9±54.3pg/ml,前后比较有显著差异(P<0.05).冠心病伴高血压者血浆NPY含量为186.9±103.1Pg/ml,显著高于不伴高血压者(111.7±45.5pg/ml,P<0.01);既往有吸烟史的冠心病患者,血浆NPY含量为181.8±193.1pg/ml,显著高于无吸烟史者(122.0±65.6pg/ml,P<0.05).提示:NPY水平在冠心病发病初期显著升高,其升高可能由于心肌缺血急性期交感神经兴奋性提高、释放活性增强所致,而高血压及吸烟可能也产生对NPY释放的影响.NPY参与了冠心病的发病机理及病理生理过程.     

血尿酸与冠心病关系的探计

目的检测血尿酸水平升高是否为冠心病的独立预测因子.方法采用回顾性分析选择经冠状动脉造影证实的连续性冠心病患者118例(稳定性心绞痛36人,不稳定性心绞痛28人,急性心肌梗死54人),年龄(65.79±10.03)岁,其中男94人,女24人;同期冠脉造影正常的连续性入院患者67例作为对照组,年龄(60.75±11.98)岁,其中男43人,女24人.入院第2天清晨取空腹12小时静脉血进行血尿酸、血脂等各种生化检查,详细询问包括吸烟、高血压等病史.入院期间行冠脉造影检查.结果冠心病组血尿酸水平高于对照组,(372.31±100.28)mmol/L vs(340.08±81.58)mmol/L(P=0.028),冠心病组之间血尿酸水平并无差异.但logistic回归分析显示血尿酸并非冠心病的独立危险因素.结论血尿酸水平升高可能只是动脉粥样硬化的一个标志,而非冠心病的独立危险因素.     

血浆纤溶酶原激活物抑制物-1基因4G/5G多态性及其抗原与冠心病的关系

目的探讨纤溶酶原激活物抑制物-1(PAI-1)与冠心病的关系及其对冠状动脉病变程度的预测价值.方法选择345例非糖尿病的住院患者(其中295例已行冠状动脉造影),分为对照组、心绞痛组及陈旧性心肌梗塞(OMI)组,通过等位基因特异引物聚合酶链反应法检测PAI-1基因4G/5G多态性,并测定血浆PAI-1抗原水平.为分析PAI-1基因型与冠心病、心肌梗塞的相关性,将心绞痛组与OMI组患者合称冠心病者,对照组与心绞痛组患者合称非心肌梗塞者.冠心病患者又分为稳定性心绞痛(SAP)者和不稳定性心绞痛(UAP)者.结果血浆PAI-1抗原水平在对照组、心绞痛组及OMI组间无统计学差异.UAP患者与SAP相比,PAI-1抗原水平显著升高,有显著性差异(25.0±7.2ng/ml比22.3±7.1 ng/ml,P<0.05),经Logistic回归分析,血浆PAI-1抗原水平与UAP仍有显著性相关,调整后的OR值为1.83(P=0.05).冠心病者4G和5G等位基因频率为56%和44%;对照组频率为62%和38%,冠心病者与对照组间无显著性差异.经一元直线相关分析发现,PAI-1基因型与PAI-1抗原水平间无相关性(P>0.05).PAI-1基因型分布及血浆水平均与冠状动脉病变支数无关.结论血浆PAI-1抗原水平升高可能与UAP有关,但PAI-1基因4G/5G多态性与血浆抗原水平及冠心病、心肌梗塞均无显著相关,且对冠状动脉病变范围无预测价值.     

肺心病伴发急性心肌梗死误诊漏诊13例分析

肺心病伴发急性心肌梗死 (AMI)临床上比较少见 ,我院1990 - 0 1～ 2 0 0 1- 0 6收治的肺心病伴发 AMI 19例 ,误诊漏诊13例 ,误诊漏率率高达 6 8%。现对误诊漏诊原因作一分析。1　临床资料　本组 13(男 11,女 2 )例 ,年龄 5 3～ 90 (6 9± 9)岁。肺心病病程 3～ 2 1年。基础疾患为慢性支气管炎 12例 ,支气管扩张 1例 ,同时并发高血压病史 2例 ,冠心病心绞痛病史 1例。肺心病按 1980年全国第 3次肺心病会议修订标准。 AMI按 WHO AMI诊断标准。临床表现 :全部病例均有慢性咳嗽、咳痰、胸闷、呼吸困难。同时有心前区压榨样疼痛 1例 ,恶心…     

糖代谢异常对急性心肌梗死患者血浆B型利钠肽和心功能的影响

【】目的：评价不同糖尿病状态对急性心肌梗死患者血浆B型利钠肽(BNP)和心功能的影响。方法：105例急性心肌梗死患者根据糖尿病史和OGTT检测结果将其分为糖耐量正常(NGT)、糖耐量异常(IGT)和糖尿病(DM)三组。应用美国博适Triage干式快速定量心肌梗死/心力衰竭诊断仪和 BNP检测板,测定三组患者入院时和发病第7天血浆BNP水平,同时对患者的心功能进行评价。结果：AMI＋DM 组患者入院时和发病第 7 天血浆 BNP水平分别为(347.78±122.02)pg/ml和(331.53±108.53)pg/ml,均明显高于AMI NGT组[(158.57±75.32)pg/ml和(102.85±60.52)pg/ml]和AMI IGT组[(167.86±72.56)pg/ml和(145.21±80.61)pg/ml],P＜0.05。AMI＋IGT组患者的BNP 水平亦高于AMI＋NGT 组,但差异无统计学意义,P＞0.05。三组患者发病第7 天血浆 BNP水平较入院时均有下降,但仅有AMI＋NGT组[(158.57±75.32)pg/ml比(102.85±60.52)pg/ml]BNP下降程度有统计学差异, P＜0.05。AMI DM组患者心功能Ⅲ-Ⅳ级比例(29.7%)明显高于其他两组(8.9%和8.7%),P＜0.05。结论：糖代谢异常影响急性心肌梗死患者血浆BNP的分泌,合并糖尿病的急性心肌梗死患者血浆BNP水平明显升高,心功能较差。     

高血压并发不同程度糖代谢异常血浆PAI-1水平变化

目的探讨高血压患者并发不同程度糖代谢异常血浆纤溶酶原激活物抑制剂-1(PAI-1)的相关性及其影响。方法160例高血压病患者,根据空腹血糖(FPG)和OGTT检查2h血糖(2HPG)试验结果分为三组:糖耐量正常(NGT)组、糖耐量异常(IGT)组和糖尿病(DM)组。用酶联免疫双抗体吸附法(ELISA法)测定三组患者血浆PAI-1抗原。结果①单因素方差分析(ANOVA)显示,NGT、IGT和DM三组PAI-1水平差异有统计学意义[(30.25±6.17)ng/ml、(43.12±5.52)ng/ml和(55.04±8.03)ng/ml;P<0.01]。②以PAI-1与年龄、收缩压(SBP)、舒张压(DBP)、FPG、2HPG作直线回归分析,能进入该方程的变量为年龄、SBP、DBP、2HPG。结论高血压患者伴发糖代谢异常及其严重程度与PAI-1升高正相关;年龄、SBP、DBP、2HPG为PAI-1独立影响因素。     

ST段抬高急性冠脉综合征并高血压患者心电图特征对近期预后影响

目的:急性冠状动脉综合征(ACS)的概念是目前冠心病研究的重要进展,本文作者探讨高血压患者首发ST段抬高ACS心电图特点及其临床意义。方法:25年连续收治ST段抬高急性心肌梗死(AMI)患者1529例,并发高血压者367(男219,女148)例,对照组随机选血压正常AMI患者60(男33,女27)例;观察该组心电图某些指标及近期临床特征。结果:观察组PTFV1(≤0.03mm.s)负值增长0.04±0.01mm.s,ΣST段抬高振幅26.1±4.2mm,Q波导联数6.7±1.3,QTc间期460.0±50.2ms,对照组PTFV1、ΣST、Q波导联数、QTc分别为0.02±0.01mm.s;12.1±1.9mm;4.0±0.8;420.0±4…     

左室运动协调性与心功能、心率变异性及心肌复极离散度的关系

作者观察左心室运动协调性与心肌缺血程度及心脏收缩和舒张功能、心率变异性、心肌复极离散度的关系 ,以了解其变化规律。1　对象和方法1.1　对象　病例组 :选择 1997年以来门诊和住院治疗的冠心病和高血压心脏病 (高心病 ) 4 8(男 4 1,女 7)例 ,年龄 6 0± 8岁。冠心病中心绞痛 14例 ,陈旧性心肌梗死 (OMI) 12例 ,急性心肌梗死 (AMI) 3例。高心病 19例。对照组 32 (男 2 4 ,女8)例 ,年龄 6 0± 7岁。经询问病史、体格检查、心电图、动态心电图、心脏 B超、胸片及实验室检查排除心血管病、糖尿病、高血压病等其他系统严重疾病者。两组成…     

血浆D-二聚体水平与冠状动脉疾病的关系及相关因素分析

目的 :探讨血浆D 二聚体水平与冠心病 (CHD)及其危险因素的关系。方法 :检测经冠状动脉造影证实的 6 7例CHD患者和 4 3例健康对照者的D 二聚体水平 ,以性别 ,年龄 ,体重指数 (BMI) ,是否并发高血压、糖尿病、CHD家族史 ,白细胞计数、总胆固醇 (TC)、三酰甘油 (TG)、高密度脂蛋白胆固醇 (HDL L)、低密度脂蛋白胆固醇 (LDL C)、血清同型半胱氨酸 (Hcy)、尿酸、纤维蛋白原 (Fib)浓度、血清高敏感C反应蛋白 (hs CRP)水平为危险因素 ,进行统计分析。结果 :CHD组的D 二聚体水平为 ( 338.5 2± 15 6 .92 ) μg/L ,对照组为 ( 2 2 1.72± 4 2 .0 2 ) μg/L ,两者之间差异有统计学意义 (P <0 .0 5 )。采用多样本的秩和检验发现稳定型心绞痛 (SAP)、不稳定型心绞痛(UAP)、陈旧性心肌梗死 (OMI)、急性心肌梗死 (AMI)患者的D 二聚体水平之间差异均有统计学意义 (均 P <0 .0 1) ,AMI患者最高 ,依次为AMI >UAP >SAP和OMI≥对照者。与血浆D 二聚体水平具有等级相关关系的因素有年龄、BMI、吸烟量、Fib、Hcy、hs CRP、并发高血压和糖尿病。逐步多元回归分析发现只有年龄、Hcy和hs CRP与D 二聚体独立相关 ,Fib与其有独立相关的趋势。结论 :CHD患者血浆D 二聚体水平明显增高 ,不同类型的CHD患者的血浆D 二聚体水平也不同 ;     

A study of cardiovascular risk factors in Delhi, India

Acute myocardial infarction (AMI) is a leading cause of mortality and disability of adults in urban and rural India, and occurs at younger age than in western populations. In this paper an attempt has been made to determine the risk factors for non- fatal AMI among Indian men and women and to study the difference in proportion of risk factors by taking non- AMI group along with healthy group as controls. Mantel Haenzel test showed that while comparing AMI with non-AMI group, diabetes mellitus (p < 0.05), family history of MI (p < 0.0001) and smoking (p < 0.0001) are significantly associated with AMI after adjusting the effects of hypertension. The same test was carried out in comparing AMI with healthy group which showed that diabetes mellitus (p < 0.05), family history of MI (p < 0.0001) and smoking (p < 0.0001) are significantly associated with AMI after adjusting the effects of hypertension. Similarly, while comparing CVD group with healthy group, family history of MI (p < 0.0001) and smoking (p < 0.0001) are significantly associated with CVD after adjusting the effects of hypertension. Stepwise logistic regression showed that while comparing AMI cases with non- AMI controls, arrhythmias (odds ratio (OR) = 5.196, p < 0.0001), angina (OR = 3.599, p < 0.0001), CHF (OR = 3.121, p < 0.0001), hypertension (OR = 2.717, p < 0.0001), smoking (OR = 1.993, p < 0.0001) and family history of MI (OR = 1.819, p < 0.01) were important risk factors for a first myocardial infarction. Moreover, while comparing AMI cases with healthy controls, family history of AMI (OR = 15.925, p < 0.0001), smoking (OR = 2.806, p < 0.001), hypertension (OR = 2.718, p < 0.0001), gender (OR = 2.410, p < 0.01) and age (OR = 2.410, p < 0.05) were important predictors of AMI; and while comparing CVD cases (AMI and non-AMI) with healthy group, family history of MI (OR = 10.377, p < 0.01), hypertension (OR = 8.237, p < 0.01) and smoking (OR = 4.454, p < 0.01), were important predictors of cardiovascular disease.     

冠心病患者细胞间粘附分子-1变化的研究

目的:观察心绞痛、急性心肌梗死时血清细胞问粘附分子-1(ICAM-1)水平的变化,以探讨其与冠心病的关系及意义。方法:选择健康体检者(正常对照组)30例、稳定性心绞痛(SAP)患者(SAP组)20例、不稳定性心绞痛(UAP)患者(UAP组)25例和急性心肌梗死(AMI)患者(AMI组)30例,采用酶联免疫吸附分析法(ELISA法)检测血清中ICAM-1浓度的变化。结果:(1)SAP组、UAP组、AMI组与正常对照组比较;血清中ICAM-1水平显著升高(P<0.01);(2)与SAP组比较,UAP组、AMI组血清ICAM-1水平显著升高(P均<0.01);(3)与UAP组比较,AMI组血清ICAM-1水平显著升高(P<0.05)。结论:血清中ICAM-1水平的高低与冠心病的严重程度有关,具有判断病情和预后的价值。     

Prognostic role of plasminogen-activator-inhibitor-1 levels in treatment with streptokinase of patients with acute myocardial infarction

BACKGROUND: The antifibrinolytic effect of plasminogen-activator-inhibitor type 1 (PAI-1) may be responsible for delays in reperfusion and/or reinfarctions after streptokinase (STK) therapy in patients with acute myocardial infarction (AMI). HYPOTHESIS: This study aimed to demonstrate the prognostic role of pretreatment PAI-1 levels for the outcome of STK therapy in patients with AMI, depending on reperfusion and/ or reinfarction. METHODS: The mean pretreatment PAI-1 level of 104 patients with AMI, treated with STK, determined by chromogenic method, was 5.8 +/- 8.6 U/ml, range 0.3-66.2 U/ml. Streptokinase therapy was successful when reperfusion was achieved, as assessed noninvasively, without subsequent reinfarction; it failed when reperfusion was delayed and/or reinfarction developed. RESULTS: Fibrinolysis with STK failed significantly in patients with elevated pretreatment PAI-1 levels (p < 0.05), especially with levels >4.0 U/ml (p< 0.01). The mean pretreatment PAI-1 level was significantly higher in unsuccessfully treated patients. Multivariate statistical testing demonstrated that among pretreatment variables, elevated PAI-1 activity was the most significant independent risk factor of failed fibrinolysis with STK. CONCLUSIONS: Among pretreatment variables, elevated pretreatment PAI-1 activity in patients with AMI was the most significant independent risk factor of failed fibrinolysis with STK, especially at levels > 4.0 U/ml.     

Reactive protein,plasminogen activator inhibitor type-1 （PAI-1） levels,PAI-1 promoter 4G/5G polymorphism and acute myocardial infarction

Objective To investigate the relationship between CRP, plasminogen activator inhibitor type 1 （PAI-1） levels, PAI-1 gene promoter 4G/5G polymorphism and the type of acute myocardial infarction （ST elevation myocardial infarction, STEMI vs the non-ST elevation Myocardial infarction, NSTEMI）. Methods One hundred seventy-six consecutive patients with AMI were included for the study, of whom 60 had STEMI and 56 had NSTEMI, and 60 adults without cardiovascular and cerebrovascular disease were selected as controls. Blood samples were obtained from patients within 6 h of AMI and the plasma PAI-1, CRP, and the gene polymorphism were measured. Results Plasma levels of PAI- 1 and CRP were higher in AMI groups, compared those in the control group, and plasma levels of PAI-1 were significantly higher in patients with STEMI compared to those with NSTEMI （80.12ng/ml VS.73.01ng/ml, P 〈0.01）, while CRP levels were not significantly different between patient with STEMI and NSTEMI （3.87 ± 0.79 mg/ml VS.4.01 ±0.69mg/ml, P〉0.05）. PAI-1 levels presented a significant correlation with CRP levels in the NSTEMI subjects. However, PAI-1 and CRP levels could explain the lack of a significant relationship between them in control and STEMI subjects.The frequencies of 4G/4G genotype in the AMI group were higher than those in the control group and higher in patient with STEMI than in patient with NSTEMI. Plasma levels of PAI-1 in subjects with 4G/4G genotype were significantly increased as compared to those in subjects with 4G/5G and 5G/5G genotype. Conclusions Plasma PAI-1 levels were associated with different myocardial infarction type, and PAI-1 promoter 4G/5G polymorphisms and CRP may be related to plasma PAI-1 levels     

青年男性急性心肌梗死的危险因素及介入治疗后1年随访分析

目的分析青年男性急性心肌梗死患者的临床危险因素,及接受冠状动脉介入治疗患者的1年期预后。方法纳入2008年1月至2012年1月在我院诊断为急性心肌梗死的男性患者727例,其中年龄≤40岁的急性心肌梗死患者322例,年龄≥60岁的急性心肌梗死患者405例,对比两组临床资料;对两组中行冠状动脉介入治疗的537例患者进行1年随访研究。结果青年组患者的吸烟、饮酒、肥胖、早发冠心病家族史比例及血三酰甘油、血浆纤维蛋白原水平高于老年组,apoA1水平低于老年组,差异有统计学意义(均为P<0.05),两组间糖尿病史比例、总胆固醇、HDL-C、LDL-C、apoB及尿酸水平差异无统计学意义(均为P>0.05)。Logistic回归分析显示,吸烟(P=0.008)、肥胖(P=0.013)、早发冠心病家族史(P=0.022)、高三酰甘油(P=0.021)是青年男性患AMI的独立危险因素。青年组PCI术后1年全因死亡率、复合MACE发生率、靶血管重建率、心力衰竭再住院发生率较老年组低(均为P<0.05)。结论 40岁以下青年男性急性心肌梗死的危险因素是吸烟、早发冠心病家族史、肥胖、高三酰甘油;青年男性急性心肌梗死患者行介入治疗1年随访预后良好。     

Lack of association between the angiotensin-converting enzyme insertion/deletion polymorphism and plasminogen activator inhibitor-1 antigen levels in the National Heart, Lung, and Blood Institute Family Heart Study.

Experimental and clinical research supports a direct link between activation of the renin-angiotensin system and production of plasminogen activator inhibitor-1 (PAI-1), the primary physiologic inhibitor of tissue plasminogen activator. Several studies have reported higher PAI-1 levels in individuals carrying the deletion (D) allele of the angiotensin-converting enzyme (ACE) gene. We investigated the association between ACE genotypes and plasma PAI-1 levels in a family study of 577 women and 428 men from four US communities. Participants were between 25 and 84 years of age without evidence of coronary heart disease (CHD). Mean geometric plasma PAI-1 levels adjusted for ethnicity were 17.4, 17.9, and 18.1 ng/ml in participants with the DD, insertion-deletion (ID), and II genotypes, respectively (P = 0.89 for difference). We found no associations between ACE I/D genotypes and plasma PAI-1 antigen concentrations in a subset of participants without major CHD risk factors (hypertension, hypercholesterolemia, overweight, smoking, diabetes) or in a small sample of African-Americans. Our findings suggest that the ACE insertion/deletion polymorphism has relatively little, if any, influence on circulating PAI-1 levels in the population at large.     

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。     

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。     

Plasminogen activator inhibitor-1 in patients with atrial arrhythmias during acute myocardial infarction, treated with streptokinase.

Atrial arrhythmias (AA), especially atrial fibrillation (AF), during acute myocardial infarction (AMI) are often associated with increased mortality and heart failure. Impaired fibrinolysis with elevated plasminogen activator inhibitor-1 (PAI-1) activity is associated with resistance to fibrinolytic therapy in AMI patients, but it is also found in patients with AF. Our aim was a prospective study of the role of pre-treatment PAI-1 levels for the presence of AA in AMI patients and the influence of AA on in-hospital mortality. In 116 AMI patients, treated with streptokinase, pre-treatment PAI-1 levels were estimated by the chromogenic method (normal levels, 0.3-3.5 U/ml) and in-hospital AA were assessed as atrial fibrillation, flutter and/or tachycardias. Between patients with and without AA, a significant difference was observed in mean pre-treatment PAI-1 levels, in several in-hospital complications and mortality (24 versus 4.4%; P < 0.01; odds ratio, 6.45; 95% confidence interval, 1.66-25.0). The PAI-1 level > 7 U/ml was the most significant independent pre-treatment risk factor for AA (P < 0.05; odds ratio, 3.5; 95% confidence interval, 1.15-10.6). We conclude that AA were a significant risk for in-hospital mortality of AMI patients, treated with streptokinase. A pre-treatment PAI-1 level > 7 U/ml was the most significant pre-treatment risk for AA in these patients.     

Relation of depressive mood to plasminogen activator inhibitor, tissue plasminogen activator, and fibrinogen levels in patients with versus without coronary heart disease

The increased risk of coronary heart disease (CHD) associated with depression is well documented. We hypothesized that impaired fibrinolysis is involved in this link. To explore the association of depressive mood and/or vital exhaustion with various measurements of fibrinolysis activity, 231 men (40 to 65 years old; 123 without CHD and taking no medication and 108 with documented CHD), completed the Center of Epidemiologic Studies Depression Scale and the Maastricht Questionnaire for vital exhaustion. Using classic cut-off points (Center of Epidemiologic Studies Depression Scale score >or=17, Maastricht Questionnaire score >or=8), 6.5% and 9.8% of subjects without CHD and 38% and 48.1% of those with CHD were classified as depressed and exhausted, respectively. Patients with CHD were older, had a higher body mass index, and higher levels of total cholesterol, glucose, plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (t-PA) antigen, and fibrinogen; 47% were treated for hypertension. Depressed subjects had higher levels of PAI-1 activity (p = 0.006) and exhausted patients had higher levels of PAI-1 activity (p = 0.011) and fibrinogen (p = 0.009). After adjusting for clinical condition (with or without CHD), smoking, hypertension, triglyceride concentration, and body mass index, PAI-1 activity remained higher in depressed subjects (p = 0.03). This association persisted after further adjustment for vital exhaustion or for t-PA antigen and fibrinogen levels. t-PA antigen and fibrinogen levels were not associated with depressive mood in multivariate analyses. No fibrinolytic variable was associated with vital exhaustion in multivariate analyses. In conclusion, depressive mood, but not vital exhaustion, is associated with higher levels of PAI-1 activity, suggesting a possible impairment of fibrinolysis and indicating a potential additional mechanism by which depressive mood may act as a cardiovascular risk factor.