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1.
替罗非班治疗急性冠脉综合征临床观察   总被引:20,自引:1,他引:19  
目的观察替罗非班治疗急性冠脉综合征的临床效果和安全性.方法符合急性冠脉综合征(不稳定心绞痛/非Q波心肌梗死)入选标准患者73例,按就诊顺序双盲随机分为受试组(n=37)和对照组(n=36).受试组微量泵持续泵入替罗非班,对照组微量泵持续泵入安慰剂,所有患者均静脉应用普通肝素和口服阿司匹林,疗程均为2.0~4.5 d.观察2组心电图改变、血小板聚集率、主要终点事件(顽固性缺血状态、新近心肌梗死和死亡)及不良反应发生情况.结果与对照组相比,受试组心电图缺血性改变有明显好转(P<0.05),血小板聚集率明显下降(P<0.01),主要终点事件有下降趋势,无严重不良反应.结论替罗非班治疗急性冠脉综合征是安全有效的.  相似文献
2.
The role of inflammatory stress in acute coronary syndrome   总被引:12,自引:2,他引:10       下载免费PDF全文
Objective To summarize current understanding of the roles of anti-inflammatory and proinflammatory mechanisms in the development of atherosclerosis and acute coronary syndrome and to postulate the novel concept of inflammation stress as the most important factor triggering acute coronary syndrome. Moreover, markers of inflammation stress and ways ,to block involved pathways are elucidated.Data sources A literature search(MEDLINE 1997 to 2002) was performed using the key words “inflammation and cardiovascular disease”. Relevant book chapters were also reviewed.Study selection Well-controlled, prospective landmark studies and review articles on inflammation and acute coronary syndrome were selected.Data extraction Data and conclusions from the selected articles providing solid evidence to elucidate the mechanisms of inflammation and acute coronary syndrome were extracted and interpreted in the light of our own clinical and basic research.Data synthesis Inflammation is closely linked to atherosclerosis and acute coronary syndrome.Chronic and long-lasting inflammation stress, present both systemically or in the vascular walls, can trigger acute coronary syndrome.Conclusions Inflammation stress plays an important role in the process of acute coronary syndrome.Drugs which can modulate the balance of pro- and anti-inflammatory processes and attenuate inflammation stress, such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin Ⅱ receptor blockers, statins, and cytokine antagonists may play active roles in the prevention and treatment of acute coronary syndrome when used in addition to conventional therapies (glycoprotein Ⅱ b/Ⅲ a receptor antagonists, mechanical intervention strategies, etc).  相似文献
3.
Background Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the combination of aspirin plus clopidogrel, a new antiplatelet agent, on inflammation. The purpose of this study was to determine whether aspirin plus clopidogrel can further suppress inflammation in patients with non-ST-segment elevation acute coronary syndrome (NSTEACS) . Methods One hundred and fifteen patients with NSTEACS were randomized into two groups: group A (aspirin alone, n =58) and group B (aspirin plus clopidogrel, n =57). Patients in group A received a loading dose of 300 mg aspirin, then 100 mg per day. The patients in group B received a loading dose of 300 mg aspirin and 300 mg clopidogrel, then 100 mg aspirin and 75 mg clopidogrel per day. Serum high sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor - α (TNF- α ) were measured in all patients at baseline prior to any drug treatment after admission, and at 7 and 30 days after beginning drug treatment. Thirty healthy volunteers on no medications were enrolled as controls (group C). Results Baseline levels of hs-CRP and TNF- α in group A and group B were significantly higher than those in group C. Seven days after administration, the levels of hs-CRP in both group A and group B decreased significantly [Group A: ( 6.15 ± 1.39) mg/L vs (9.18 ± 1.62) mg/L, P <0.01; Group B:(4.99 ± 1.62) mg/L vs (10.29 ± 1.47) mg/L, P <0.01] . Similarly, levels of TNF- α in both groups decreased at 7 days compared to baseline [Group A: ( 90.99 ± 28.91) pg/ml vs (117.20 ± 37.13) pg/ml, P <0.01; Group B: (74.32 ± 21.83) pg/ml vs (115.27 ± 32.11) pg/ml, P <0.01 ]. Thirty days after administration, the levels of hs-CRP in both group A and group B decreased further to ( 3.49 ± 1.53) mg/L, and (2.40 ± 1.17) mg/L respectively ( P <0.01 for both comparisons) . Levels of TNF- α in groups A and B also decreased significantly between 7 and 30 days, to 63.28 ± 29.01 pg/ml (group A) and (43.95 ± 17.10) pg/ml (group B; P <0.01 for both comparisons) . Significantly lower levels of hs-CRP and TNF- α were observed in group B compared to Group A at thirty days after initiating drug treatment (P <0.05). Conclusions A spirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF- α in patients with NSTEACS significantly more than aspirin alone. Because both aspirin and clopidogrel produce important anti-inflammatory effects, these results suggest the possibility that long-term treatment with aspirin plus clopidogrel may produce greater clinical benefits compared to treatment with aspirin alone.  相似文献
4.
C-反应蛋白浓度反映急性冠脉事件严重程度的临床意义   总被引:11,自引:2,他引:9  
目的 探讨C -反应蛋白在冠心病不同程度的表现及临床意义。方法 测定 39例急性冠脉综合征患者 ,2 3例稳定性心绞痛患者及 2 5例对照组患者的血清CRP浓度 ,比较 3组之间的血清CRP浓度的差异。结果 稳定性心绞痛组与对照组相比 ,两者的血清CRP浓度差别无显著性意义 (P >0 0 5 )。急性冠脉综合征患者的血清CRP浓度与对照组及稳定性心绞痛组比较差别均有显著性意义 (P均 <0 0 5 )。结论 急性冠脉综合征的发生与炎症反应有关 ,CRP可作为评价冠状动脉斑块不稳定性的一个客观指标。  相似文献
5.
目的 探讨急性冠脉综合症 (ACS)病人外周血单核细胞表达CD4 0L及血清可溶性CD4 0L(sCD4 0L)变化的临床意义。方法 应用流式细胞术和ELISA分别对正常对照组 16例、稳定心绞痛 2 4例、不稳定心绞痛 2 0例、急性心肌梗死12例患者血单核细胞表达CD4 0L及血清可溶性sCD4 0L水平进行检测。结果 UA组及AMI组血单核细胞表达CD4 0L及血清sCD4 0L水平明显较SA和对照组高 (P <0 0 1)。AMI患者血清sCD4 0L水平与UA组无差异 (P >0 0 5 ) ,但AMI发病后 2 4小时sCD4 0L有一峰值。PTCA后血清sCD4 0L明显高于PTCA前 (P <0 0 1) ,但血单核细胞表达CD4 0L无差异 (P >0 0 5 )。结论 血清可溶性CD4 0L升高是判断ACS的可靠血清学指标 ,且可能是冠脉病变的活动性标志物  相似文献
6.
冠心病患者血清sCD40L和MMP-9的变化及相关性   总被引:10,自引:0,他引:10  
目的:观察不同类型冠心病患者中可溶性CD40配体(sCD40L)水平的变化及其与金属蛋白酶-9(MMP-9)之间的关系, 进一步探讨急性冠脉综合征临床识别和预测的炎症指标。方法:采用酶联免疫吸附法测定79例冠心病患者血清sCD40L,MMP-9的浓度。结果:急性冠脉综合征患者sCD40L水平[在不稳定心绞痛(UAP)和急性心肌梗死组(AMI)分别为(1.96± 0.84) ng/ml,(2.23 ±0.99 )ng/ml]显著高于稳定性冠心病组(1.20±0.76)ng/ml (P<0.05),而在UAP和AMI组间比较差异无显著性(P>0.05),sCD40L水平与MMP-9呈显著正相关(r=0.401, P<0.01)。sCD40L水平与甘油三酯呈正相关(r=0.254, P=0.039),与高密度脂蛋白胆固醇呈负相关(r=-0.234, P=0.031)。结论:急性冠脉综合征患者外周血清sCD40L和MMP-9水平升高,可能与急性冠脉综合征的发生有关,可能是动脉粥样硬化不稳定的标志,CD40L可能通过促使MMP-9的表达而促发急性冠脉综合征。  相似文献
7.
冠心病患者血浆脑钠肽N末端前体浓度的变化及临床意义   总被引:9,自引:0,他引:9  
目的 分析稳定型心绞痛(SAP)、不稳定型心绞痛(UAP)和非ST段抬高型心肌梗死(NSTEMI)患者以及冠脉介入治疗前后血浆中的脑钠肽(BNP)N末端前体(NT-proBNP)水平的变化,评价血浆NT-proBNP水平与不同冠心病类型的关系,以及心肌缺血改善后血浆NT-proBNP水平的变化.方法 选择住院冠心病患者345例,其中NSTEM组29例,UAP组151例,SAP组165例:同时设正常对照组140例.采用电化学发光双抗体夹心免疫法检测血浆NT-proBNP水平,同时对180例急性冠状动脉综合征(ACS)患者经皮冠状动脉介入治疗(PCI)后的上述指标进行分析.结果 NSTEMI组NT-proBNP水平明显高于其他三组(P<0.05),UAP组高于SAP组(P<0.05),SAP组高于正常对照组(P<0.05),其中180例ACS患者在经皮冠脉介入术后12~24 h内,血浆NT-proBNP水平UAP组从术前的(1720.53±610.77)ng/L降为(1020.52±510.70)ng/L(P<0.05),NSTEMI组从术前的(5660.23±1290.53)ng/L降为(2640.20±890.50) ng/L(P<0.05);术后1周NT-proBNP水平,UAP组降为(359.05±230.33) ng/L;NSTEMI组降为(360.30±210.26)ng/L;与对照组比较均无显著性差异(P>0.05).血浆NT-proBNP值与心肌TIMI血流评分相关(r=-0.402,P<0.001).结论 冠心病患者血浆NT-proBNP浓度增高;NT-proBNP水平增高可以预测冠心病的严重程度;ACS患者冠脉介入治疗后血浆NT-proBNP含量明显降低,可作为观察疗效的指标,对临床病情的评估具有重要价值.  相似文献
8.
目的:检测急性冠脉综合征(ACS)患者外周血单核细胞中环氧化酶2(COX-2)mRNA的表达水平并探讨其意义。方法:选择典型急性冠脉综合征患者42例,分离和培养单核细胞,并采用不同浓度的选择性COX-2抑制药(塞来昔布)体外干预。采用RT-PCR法半定量COX-2 mRNA的表达,夹心酶联免疫吸附法(ELISA)测定培养上清液中IL-6和基质金属蛋白酶9(MMP-9)浓度。结果:ACS患者外周血单核细胞中COX-2 mRNA表达(0.61±0.17)较健康对照组(0.11±0.09)明显增强(P<0.05);ACS患者外周血单核细胞培养上清液中IL-6浓度[(97.24±11.21)ng/L]较健康对照组 [(22.15±6.30)ng/L]显著升高(P<0.05),MMP-9浓度[(41.20±8.41)μg/L]较健康对照组 [(11.76±4.23)μg/L]显著升高(P<0.05);ACS患者外周血单核细胞经塞来昔布干预后, 塞来昔布以浓度依赖性方式降低培养上清液中IL-6和MMP-9浓度分别达48%和50%(均P<0.05)。结论:COX-2可能在急性冠脉综合征的炎症反应中起重要作用。  相似文献
9.
目的:测定急性冠脉综合征(ACS)患者血清基质金属蛋白酶(MMP-9)水平,与高敏C-反应蛋白进行相关性分析,探讨MMP-9对ACS患者斑块易损性的判断价值。方法:选择ACS患者50例,稳定性心绞痛(SA)26例及30例健康人作为对照,用ELISA法检测血清MMP-9水平,同时检测血清高敏C-反应蛋白(hs-CRP),比较各组患者血清MMP-9、hs-CRP水平变化,并进行相关性分析。结果:ACS组患者外周血清MMP-9、hs-CRP水平明显高于SA组及健康对照组,差异有统计学意义,ACS组内血清MMP-9、hs-CRP水平呈直线正相关。结论:血清MMP-9水平升高与冠状动脉斑块易损性相关,临床检测MMP-9浓度水平的高低可以预测动脉粥样斑块易损性的大小。  相似文献
10.
目的研究急性冠脉综合征(ACS)患者血清妊娠相关血浆蛋白-A(PAPP—A)水平和外周血单核细胞PAPP—AmRNA表达的变化及其与血清高敏C反应蛋白(hsCRP)水平的相关性。方法从18例不稳定性心绞痛(UAP)、37例急性心肌梗死(AMI)和15例稳定性心绞痛(SAP)及15例正常对照者中分离外周血单核细胞,应用RT—PCR检测PAPP—A的mRNA表达,同时检测血清PAPP—A和hsCRP水平。结果SAP组血清PAPP—A水平与正常对照组差异无显著性;UAP组和AMI组血清PAPP—A水平均显著高于正常对照组(P〈0.01)和SAP组(P〈0.01),但UAP组与AMI组差异无显著性。SAP组血清hsCRP水平明显高于正常对照组;UAP组明显高于正常对照组和SAP组,但低于AMI组。正常对照者和SAP患者外周血单核细胞存在PAPP—AmRNA低水平表达,ACS患者的表达显著增加。ACS的血清PAPP—A水平和单核细胞PAPP—AmRNA表达与血清hsCRP水平呈正相关(r=0.616,0.706,P〈0.01)。结论急性冠脉综合征时活化的单核细胞表达和合成释放PAPP—A增加,与hsCRP水平正相关,提示PAPP—A可能通过炎症机制参与ACS的发生发展。  相似文献
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