稳定性不稳定性心绞痛冠状动脉斑块形态和狭窄程度的对比研究

目的：探讨稳定性心绞痛、不稳定性心绞痛及急性心绞痛及急性心肌梗死发生的病理形态基础及其差异。方法：选取临床及心电图确认的稳定性心绞痛和死于急性心肌梗死的不稳定性心绞痛死亡病例的心脏作为研究材料,将冠状动脉剥离后固定、脱钙,然后连续取材,光镜观察两组冠状动脉斑块的形态、狭窄程度及血栓形成情况。结果：１５例稳定性心绞痛共取材８８９个块中,８４．０％为稳定斑块,斑块没有或仅有很小的脂质坏死中心,表面被覆的纤维帽较厚;而不稳定斑块（指斑块脂质坏殛中心超过４０％,表面被覆的纤维帽也较薄）仅占１６．０％。２０例伴有急性心肌梗死的不稳定性心绞痛共１２１０个取材块中,稳定斑块占６９．０％,与稳定性心绞痛组比较差异有显性（Ｐ〈０．０１）。冠状动脉各分支狭窄程度两组间差异无显性（Ｐ〉０．０５）。２０例伴有心肌梗死的不稳定性心绞     

不稳定性心绞痛患者的高胰岛素血症

检测冠心病不稳定性心绞痛２４例，稳定性心绞痛２９例，对照组３０例糖耐量前后血糖、胰岛素（ＩＳ）、Ｃ肽（ＣＰ）的变化。结果不稳定性心绞痛组和稳定性心绞痛组空腹和服糖后的ＩＳ、ＣＰ均明显升高，前组与后组相比，显示更高的ＩＳ、ＣＰ浓度（Ｐ〈０．０５￣０．００１）。提示冠心病的高胰岛素血症与其临床症状的严重程度相关，而高胰岛素血症对神经体液的影响可能会导致心绞痛的恶化。     

C-反应蛋白是急性冠状动脉综合征的一种危险因子

冠心病与炎症的关系日益受到人们的重视 ,尤其是反映急性炎症反应的血清Ｃ 反应蛋白 (Ｃ ｒｅａｃｔｉｖｅｐｒｏｔｅｉｎ ,ＣＲＰ)浓度在急性缺血和心肌梗死患者中明显升高。本研究以正常体检人群、稳定性心绞痛 (ｓｔａｂｌｅａｎｇｉｎａｐｅｃｔｏｒｉｓ ,ＳＡＰ)和陈旧性心肌梗死(ＯＭＩ)为对照研究急性冠状动脉综合征 [ａｃｕｔｅｃｏｒｏｎａｒｙｓｙｎｄｒｏｍｅ ,ＡＣＳ ,包括不稳定性心绞痛(ｕｎｓｔａｂｌｅａｎｇｉｎａｐｅｃｔｏｒｉｓ ,ＵＡＰ)、急性心肌梗死 (ａｃｕｔｅｍｙｏｃａｒｄｉａｌｉｎｆａｒｃｔｉｏｎ ,ＡＭＩ)…     

血小板活化功能检测在急性心肌梗死及不稳定性心绞痛时的临床初步应用

目的：观察急性心肌梗死和不稳定性心绞痛患者血小板的活化状态并探讨其临床意义。方法：分别采用抗人活化型血小板α－颗粒膜蛋白－１４０（ＧＭＰ－１４０）及血小板膜糖蛋白Ⅱｂ／Ⅲａ（ＧＰⅡｂ／Ⅲａ）的特异性单克隆抗体，以放射免疫法测定１７例急性心肌梗死和１５例不稳定性心绞痛患者血小板的活化状态，并将其与心肌酶、心肌梗死和缺血面积作相关分析。结果：急性心肌梗死组和不稳定性心绞痛组血小板ＧＭＰ－１４０数目明显高于正常对照组（Ｐ＜０．０１）。ＧＭＰ－１４０与血清肌酸激酶及其ＭＢ同工酶、血清乳酸脱氢酶（ＬＤＨ）、心肌梗死和缺血面积均呈正相关（Ｐ＜０．０５）。急性心肌梗死组和不稳定性心绞痛组血小板膜ＧＰⅡｂ／Ⅲａ分子数均明显高于正常对照组（Ｐ＜０．０５），但两组分子数与心肌梗死和缺血面积均不具有相关性。结论：血小板活化的检测在急性冠状动脉缺血时有一定应用价值     

急性冠状动脉综合征血清C-反应蛋白水平的变化及意义

为进一步了解急性冠状动脉综合征（ACS）患者血清C-反应蛋白（CRP）水平的变化及意义，我们测定了正常人群。非ACS冠心病组包括稳定性心绞痛（SAP）、急性心肌梗死恢复期（AMI恢复期）、陈旧性心肌梗死（OMI）和ACS组包括不稳定性心绞痛（UAP）、急性心肌梗死急性期（AMI）及心源性猝死（SCD）患者的血清CRP含量。并对其临床意义进行了探讨。     

急性冠状动脉综合征患者血清可溶性细胞间粘附分子1和妊娠相关血浆蛋白A的变化

目的 观察急性冠状动脉综合征患者血清可溶性细胞问粘附分子1、妊娠相关血浆蛋白A水平的变化，结合冠状动脉造影结果探讨其临床意义。方法 用酶联免疫吸附法检测46例急性冠状动脉综合征患者（其中急性心肌梗死20例，不稳定型心绞痛26例）、22例稳定型心绞痛患者和20例冠状动脉造影阴性对照者血清可溶性细胞问粘附分子1、妊娠相关血浆蛋白A水平，分析冠状动脉病变程度与可溶性细胞间粘附分子1、妊娠相关血浆蛋白A浓度的关系。结果急性冠状动脉综合征组血清可溶性细胞间粘附分子1和妊娠相关血浆蛋白A浓度较稳定型心绞痛组、对照组显著升高（P〈0．05或P〈0．01）。冠状动脉造影为单支、双支、三支病变者，其可溶性细胞问粘附分子1、妊娠相关血浆蛋白A浓度依次增高。相关分析发现，急性心肌梗死、不稳定型心绞痛患者血清可溶性细胞间粘附分子1浓度与妊娠相关血浆蛋白A浓度显著正相关（r=0．737和r=0．758，P〈0．001）。结论 急性冠状动脉综合征患者可溶性细胞阃粘附分子1、妊娠相关血浆蛋白A升高，二者可能是动脉粥样斑块不稳定的标志。     

老年不稳性心绞痛的冠脉造影特点

目的 了解老年患者不同类型不稳定性心绞主稳定性心绞痛的冠脉病变特点。方法 对６５例老年不稳定性心绞痛和３２例老年稳定性心绞痛患者进行冠脉造影。结果 血管病变最轻的类型为自发型心绞痛。初发劳力型心绞痛单支血管病变（占７１．４％）较其它类型多见（Ｐ〈０．０５）。稳定性心绞痛的复杂性病变、Ｃ型病变检出率较其它各型高（Ｐ〈０．０５）。恶化劳力型心绞痛与梗死后早期心绞痛病变特征介于上述两者之间。结论 稳定型     

冠心病患者血清视黄醇结合蛋白4与高敏C反应蛋白的相关性分析

目的 测定冠心病患者血清视黄醇结合蛋白4（RBP4）和高敏C反应蛋白（hs-CRP）水平,分析两者与冠心病的相关性.方法 将90例冠心病患者分为急性心肌梗死组30例,不稳定性心绞痛组30例,稳定性心绞痛组30例,另选择30例冠状动脉造影结果正常者为对照组.采用酶联免疫吸附法测定受试者血清RBP4水平,采用增强免疫透射比浊法测定血清hs-CRP水平.结果 急性心肌梗死和不稳定性心绞痛组患者血清RBP4、hs-CRP水平高于稳定性心绞痛组和对照组,差异具有统计学意义（P〈0.05）,稳定性心绞痛组血清hs-CRP水平与对照组比较,差异有统计学意义（P〈0.05）,而稳定性心绞痛组患者血清RBP4水平与对照组比较差异尤统计学意义.单支、双支、三支病变组患者血清RBP4、hs-cRP水平均高于对照组（P〈0.05）,但单支、双支与三支病变组之间比较差异均无统计学意义.经Pearson＇s相关分析,冠心病患者血清RBP4与hs-CRP的浓度呈显著正相关（r=0.469,P〈0.01）.结论 血清RBP4、hs-CRP与冠心病存在一定的相关性,可能与斑块稳定性有关,可作为预测斑块稳定性的血清标志物,但其并不能反映冠状动脉狭窄程度及范围.     

脂蛋白相关磷脂酶A2及血小板活化因子与急性冠脉综合征临床研究

目的探讨急性冠脉综合征患者血浆脂蛋白相关磷脂酶A2（1ipoprotein-associated phospholipaseA,Lp-PIA2）和血小板活化因子（platelet activating factor,PAF）浓度变化及其临床意义。方法选择经冠状动脉造影检查的260例心内科住院患者,按照临床表现及造影结果分组：急性冠脉综合征组115例,包括不稳定型心绞痛亚组70例、急性心肌梗死亚组45例;非急性冠脉综合征冠状动脉粥样硬化性心脏病（冠心病）组94例,包括稳定型心绞痛亚组56例、冠状动脉慢性完全闭塞亚组38例;正常冠状动脉对照组51例。采用夹心酶联免疫吸附法检血浆Lp-PLA2及PAF浓度。结果与对照组比较,急性冠脉综合征及非急性冠脉综合征患者血浆Lp-PLA2[（89．05±25．01）μg／Lvs．（11．85±4．17）μg／L,P〈0．001;（19．86±9．91）μg／Lvs．（11．85±4．17）μg／L,P〈O．01l及PAF[（139．44±56．49）μg／Lvs．（58．67±12．46）μg／L,P〈O．001;（64．36±13．89）μg／Lvs（58．67±12．46）μg／L,P〈0．05]浓度显著升高,差异均有统计学意义。与对照组比较,亚组中,除稳定型心绞痛亚组血浆Lp—PLA：及PAF浓度无明显升高外（P〉0．05）,其余亚组包括不稳定型心绞痛、急性心肌梗死、冠状动脉慢性完全闭塞亚组的Lp—PLA：及PAF浓度均显著升高,差异有统计学意义（均P〈O．01）。结论血浆Lp-PLA2及PAF浓度在急性冠脉综合征患者明显增高,可能提示粥样斑块不稳定性,有可能成为急性冠脉综合征的新的干预靶点。     

冠心病病人红细胞变形能力与血浆、红细胞膜硒浓度的关系

目的：从硒与红细胞膜收缩蛋白的关系探讨冠心病病人红细胞变形能力变化的机制。方法：检测１３５例冠心病病人（不稳定性心绞痛４８例，急性心肌梗死５０例，陈旧性心肌梗死３７例）和６６例健康人血浆硒，红细胞膜硒和脂质过氧化物浓度、收缩蛋白二聚体（下简称二聚体）、收缩蛋白四聚体（下简称四聚体）及红细胞变形能力的变化。结果：冠心病病人红细胞滤过指数明显增高，血浆、红细胞膜硒浓度明显降低，与对照组比较有极显著性差异（Ｐ＜０．００１）；冠心病病人红细胞膜脂质过氧化物、二聚体、二聚体与四聚体比值增高，四聚体明显减少，与对照组比较有极显著性差异（Ｐ＜０．００１）。急性心肌梗死病人上述变化均较不稳定性心绞痛和陈旧性心肌梗死病人更明显。冠心病病人红细胞滤过指数与血浆、红细胞膜硒浓度呈负相关（ｒ＝－０．５２４和－０．６６１，Ｐ＜０．００１），红细胞膜硒浓度与脂质过氧化物、二聚体、二聚体与四聚体比值呈负相关（ｒ＝－０．５２１、－０．５７９和－０．５８６，Ｐ＜０．００１），与四聚体呈正相关（ｒ＝０．５５０，Ｐ＜０．００１）。结论：冠心病病人硒缺乏引起的膜骨架结构蛋白异常是红细胞变形能力降低的原因之一。     

急性心肌梗死与不稳定型心绞痛患者血栓前体蛋白和肌酸激酶的检测

为了解检测血栓前体蛋白对急性冠状动脉综合征转归的早期诊断价值 ,5 1例临床确诊冠心病患者分为不稳定型心绞痛和急性心肌梗死两组 ,采用酶联免疫吸附法检测各组血浆中血栓前体蛋白含量 ,采用干化学法同步检测患者血清磷酸肌酸激酶及其同工酶。结果发现 ,急性心肌梗死组 2 5例患者血栓前体蛋白均值为 9.9± 3.9mg L ,不稳定型心绞痛组 2 6例患者血栓前体蛋白均值为 2 .6± 1.7mg L ,前者明显升高 ,差别有显著性意义 (P <0 .0 1) ;急性心肌梗死组磷酸肌酸激酶均值为 5 95± 4 32u L ,磷酸肌酸激酶同工酶均值为 10 1± 74u L ,不稳定型心绞痛亚组磷酸肌酸激酶均值为 137± 4 0u L ,磷酸肌酸激酶同工酶均值为 10± 7u L ,前者亦明显升高 ,差别均有显著意义(分别为P <0 .0 5和P <0 .0 1)。结果提示 ,血栓前体蛋白对急性冠状动脉综合征具有早期诊断和鉴别价值     

不同炎性标志物对冠状动脉病变的预测价值

目的 探讨可溶性CD40L、单核细胞趋化蛋白1、白细胞介素8和白细胞介素6等炎性标志物对冠状动脉病变严重程度和稳定性的预测价值.方法 应用流式细胞术检测129例冠心病患者血浆可溶性CD40L、单核细胞趋化蛋白1、白细胞介素8和白细胞介素6水平,计算各类型冠心病患者冠状动脉病变的Gensini积分,分析上述炎性标志物与Gensini积分的相关关系以及对急性冠状动脉综合征的预测价值.结果 四种炎性标志物血浆浓度在冠心病组均显著高于对照组(P均<0.01),其中可溶性CD40L、单核细胞趋化蛋白1和白细胞介素6的浓度在急性心肌梗死组高于稳定型心绞痛组(P=0.001、P=0.009和P=0.011).血浆单核细胞趋化蛋白1和白细胞介素6水平与冠状动脉Gensini积分呈正相关关系(r=0.322, P<0.00001;r=0.203,P=0.026);多因素Logistic回归分析显示白细胞介素6对急性冠状动脉综合征有预测价值(OR=1.275,P=0.037).结论 血浆可溶性CD40L、单核细胞趋化蛋白1、白细胞介素8和白细胞介素6等炎性标志物与冠状动脉粥样硬化病变有关;血浆单核细胞趋化蛋白1和白细胞介素6能反映冠状动脉病变的严重程度;白细胞介素6对预测冠状动脉病变不稳定的冠心病急性冠状动脉综合征有一定价值.     

Intracoronary temperature in patients with coronary artery disease

OBJECTIVES: Measurements of changes in plaque temperature may predict plaque rupture. The present study investigated variations in temperature within the atherosclerotic coronary artery using a pressure guide wire with thermal sensor (dual sensor guide wire). METHODS AND RESULTS: Seventy-seven patients (78 lesions), who had no significant lesion at the orifice of the culprit coronary artery, were studied. The patients had acute myocardial infarction (22 patients), unstable angina pectoris (20 patients), and stable angina pectoris (35 patients). The thermal sensor was calibrated at the orifice of the coronary artery, and then inserted into the culprit coronary artery. deltaT was defined as the difference between the intracoronary temperature at the position of the pressure gradient and at the orifice. deltaT was higher in patients with acute myocardial infarction and unstable angina pectoris than in patients with stable angina pectoris (0.09 +/- 0.07 and 0.07 +/- 0.07 vs 0.03 +/- 0.04 degrees C, p < 0.001, p = 0.02, respectively). There was no significant difference in deltaT between patients with acute myocardial infarction and unstable angina pectoris (p = 0.48). Patients with acute myocardial infarction and unstable angina pectoris showed a significant relationship between deltaT and C-reactive protein (r = 0.59, p = 0.0004). CONCLUSIONS: The variations in intracoronary temperature of the culprit coronary arteries in patients with acute coronary syndrome were higher than those in patients with stable angina pectoris. These variations may be related to inflammation of vulnerable plaque.     

Procalcitonin in patients with acute coronary syndromes and cardiogenic shock submitted to percutaneous coronary intervention

Procalcitonin (PCT) is known to be a biological diagnostic marker for severe sepsis, or septic shock in critically ill patients. There are still contrasting data about a role of procalcitonin in patients with acute myocardial infarction or cardiogenic shock, and in those with acute coronary syndromes, that is, non-ST-elevation myocardial infarction or unstable angina. We evaluated plasma levels of procalcitonin and C-reactive protein (CRP) in 52 patients admitted to our intensive cardiac care unit (ICCU): 14 patients with cardiogenic shock (CS) following ST-elevation myocardial infarction (STEMI), 15 patients with uncomplicated ST-elevation myocardial infarction (STEMI), and 24 with non-ST-elevation myocardial infarction or unstable angina (NSTEMI/UA). In all patients, infective processes were excluded. Procalcitonin values were significantly higher in CS patients with respect to the other two subgroups (P < 0.001, P < 0.001) while CRP levels were higher than NSTEMI/UA patients (P < 0.001) but not with respect to STEMI patients (P = 0.063). No correlations were found in cardiogenic shock patients between CRP and PCT values (R = 0.02; P = 0.762, ns). Procalcitonin levels measured on ICCU admission are significantly higher in patients with cardiogenic shock following the acute myocardial infarction, and they are not correlated with those of CRP. The degree of myocardial ischemia (clinically indicated by the whole spectrum of ACS, from unstable angina to cardiogenic shock ST-elevation following myocardial infarction) and the related inflammatory-induced response are better reflected by CRP (which was positive in most acute cardiac care patients of all our subgroups), than by PCT which seems more reflective of a higher degree of inflammatory activation, being positive only in all CS patients.     

The role of aspirin resistance on outcome in patients with acute coronary syndrome and the effect of clopidogrel therapy in the prevention of major cardiovascular events

Background: Aspirin resistance may increase up to more then threefold the risk of major cardiovascular events (MACE) in patients with stable coronary artery disease. Aim:The aim of our study was to determine; the prevalence of aspirin resistance in patients with acute coronary syndromes, the role of aspirin resistance on outcome in the follow-up and the effect of clopidogrel therapy in the prevention of MACE in aspirin resistant subjects. Material and methods: We detected the prevelance of aspirin resistance in 105 patients with acute coronary syndrome. Platelet functions were analyzed in Platelet Function Analyzer (PFA)-100 (Dade Behring, Germany) with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP (Col/ADP) cartridges. Primary end points of the study were myocardial infarction, unstable angina, cardiac death. Results: 19% (n = 20) of patients were aspirin resistant by PFA-100. In the follow-up, MACE occured in 9 patients (45%) with aspirin resistance and in 10 patients (11.7%) with aspirin sensitive platelet aggregation (p = 0.001). Multivariate analysis showed that aspirin resistance was an independant predictor of MACE. The prevalence of MACE in patients who were on clopidogrel treatment for 12 months were lower compared to those who were on a clopidogrel treatment for the first six months (p = 0.040). Conclusions: We determined that the MACE risk in patients with acute coronary syndromes having detected aspirin resistance, was higher at statistically significant levels compared to patients having aspirin sensitive platelet aggregation. Our results showed that aspirin resistance, was an independant predictor of MACE in patients with acute coronary syndrome.     

Prognosis by C-reactive protein and matrix metalloproteinase-9 levels in stable coronary heart disease during 15 years of follow-up

Background and AimElevated CRP and matrix metalloproteinase-9 associate with increased risk of cardiovascular events, possibly because these plasma proteins mark vulnerable atherosclerotic plaques.We tested the hypothesis that levels of C-reactive protein (CRP) and matrix metalloproteinase-9 associate with prognosis in patients with stable coronary heart disease.Methods and ResultsWe measured baseline plasma CRP and matrix metalloproteinase-9 in 1090 patients with stable coronary heart disease and as the primary composite endpoint detected incident unstable angina, myocardial infarction and any death during 15 years of follow-up.CRP above versus below the median of 3.0 mg/L was associated with an increased cumulative incidence of unstable angina, myocardial infarction and any death combined (log-rank p < 0.0001). CRP above versus below the median had a corresponding hazard ratio of 1.5(95% CI, 1.3–1.8) after age adjustment, of 1.4(1.2–1.6) after multifactorial adjustment, and of 1.4(1.2–1.6) after multifactorial adjustment including degree of coronary disease. In contrast, matrix metalloproteinase-9 above versus below the median was not associated with risk of unstable angina, myocardial infarction and death.ConclusionsElevated CRP, but not elevated matrix metalloproteinase-9, associates with increased risk of unstable angina, myocardial infarction and death in patients with stable coronary heart disease.     

血浆白介素-37水平与冠状动脉病变程度的相关性研究

目的 探讨急性冠状动脉综合征(acute cornary syndrome,ACS)患者血浆白介素-37(interleukin-37,IL-37)水平与冠状动脉病变程度的关系.方法 选取2016年1-12月因胸闷、胸痛等症状就诊于河北医科大学第二医院并行冠状动脉造影的患者作为研究对象,依据患者的症状、心电图、心肌酶、...     

C-reactive protein and coronary artery disease

Evidence suggests that inflammation plays a key role in the pathogenesis of atherosclerosis. The chronic inflammatory process can develop to an acute clinical event by the induction of plaque rupture and therefore cause acute coronary syndromes. The aim of this study was to determine the serum levels of the circulating acute-phase reactant C-reactive protein (CRP), which is a sensitive indicator of inflammation, in patients with chronic stable coronary artery disease (CAD) and acute coronary syndromes (ACS). We studied 56 subjects: 1) 25 consecutive patients (18 men, 7 women; mean age, 68.5 +/- 14.3 years, range, 40-86) with unstable angina (UA) or acute myocardial infarction (AMI); 2) 31 consecutive patients (25 men, 6 women; mean age 64 +/- 12.7; range, 47-83, years) with signs and symptoms of clinically stable CAD. High-sensitivity-C-reactive protein (hs-CRP) levels were determined with a commercially available enzyme-linked immunoassay method. In patients with unstable angina and AMI before reperfusion therapy, CRP levels were not significantly different to those in patients with stable CAD (5.96 +/- 2.26 versus 4.35 +/- 2.6 mg/L; P = 0.12), but tended to be higher in patients with unstable angina and AMI. Baseline CRP levels in the subgroup of patients with AMI (6.49 +/- 2.28 mg/L) were significantly higher than levels in patients with stable CAD (4.35 +/- 2.6 mg/L; P = 0.02). CRP levels in patients with unstable angina and AMI were measured four times during a 72-hour period (0, 12, 24, and 72 hours). The lowest value was observed at baseline and differed significantly from values measured at any other time of the observation period (P < 0.001; 5.96 +/- 2.26; 9.5 +/- 9.04, 18.25 +/- 11.02; 20.25 +/- 10.61). CRP levels after 12, 24, and 72 hours were also significantly different to the initial values for patients with stable CAD (P < 0.01). There was no correlation between CRP and creatine kinase (CK), CK-MB isoenzyme, or troponin I positivity as markers for the extent of the myocardial injury during the observation period. Baseline levels of serum CRP tended to be higher in patients with unstable angina or AMI but were not significantly different from levels in patients with chronic stable CAD. In the subgroup of patients with AMI, baseline CRP levels were significantly higher than the levels in patients with stable CAD. CRP as a marker of inflammation is significantly increased in patients with AMI and unstable angina shortly after the onset of symptoms (after a period of 12 hours), supporting the hypothesis of an activation of inflammatory mechanisms in patients with an acute coronary syndrome or AMI.     

The effect of aspirin on C-reactive protein as a marker of risk in unstable angina

OBJECTIVES: This study was designed to assess the interaction between aspirin and C-reactive protein (CRP) release in unstable angina. BACKGROUND: C-reactive protein release in acute coronary syndromes may be a response to myocardial necrosis or may reflect the inflammatory process that drives atherogenesis. Aspirin has the potential to influence CRP release, either by its anti-inflammatory activity or by reducing myocardial necrosis. The clinical significance of this potential interaction has not previously been tested. METHODS: We conducted a prospective cohort study of 304 consecutive patients admitted with non-ST-elevation acute coronary syndromes. Serial blood samples were obtained for CRP and troponin I assay. End points were cardiac death and nonfatal myocardial infarction during follow-up for 12 months. RESULTS: A total of 174 patients (57%) were taking aspirin before admission. Patients taking aspirin had lower troponin I concentrations throughout the sampling period, only 45 (26.0%) having concentrations >0.1 mg/l compared with 48 (37.8%) patients not taking aspirin (p = 0.03). Maximum CRP concentrations were also lower in patients taking aspirin (8.16 mg/l [3.24 to 24.5]) than in patients not taking aspirin (11.3 mg/l [4.15 to 26.1]), although the difference was not significant. However, there was significant interaction (p = 0.04) between prior aspirin therapy and the predictive value of CRP concentrations for death and myocardial infarction at 12 months. Thus, odds ratios (95% confidence intervals) for events associated with an increase of 1 standard deviation in maximum CRP concentration were 2.64 (1.22-5.72) in patients not pretreated with aspirin compared with 0.98 (0.60-1.62) in patients pretreated with aspirin. CONCLUSIONS: The association between CRP and cardiac events in patients with unstable angina is influenced by pretreatment with aspirin. Modification of the acute-phase inflammatory responses to myocardial injury is the major mechanism of this interaction.     

血清瘦素、脂联素与冠心病病变程度的相关性研究

目的探讨血清瘦素、脂联素(APN)水平与冠心病(CHD)病变程度的相关性。方法应用ELISA法对稳定型心绞痛(SA)组(21例)、不稳定型心绞痛(UA)组(23例)、急性心肌梗死(AMI)组(24例)和正常对照(CO)组(20例)进行血清瘦素、脂联素水平检测,并进行统计学分析。结果血清瘦素水平冠心病各组明显高于正常对照组(P<0.05),UA组及AMI组高于SA组(P<0.05),AMI组高于UA组(P<0.05),血清瘦素水平与冠心病病变程度呈正相关(r=0.60,P<0.05);血清APN水平UA组及AMI组明显低于SAP组和对照组(P<0.05),冠心病各组与正常对照组比较有统计学意义(P<0.05),AMI组与UA组比较有统计学意义(P<0.05),脂联素与冠心病病变程度呈负相关(r=-0.59,P<0.05)。结论血清瘦素、脂联素与冠心病发病密切相关,冠心病患者血清瘦素水平升高,血清瘦素水平与冠心病病变程度呈正相关。冠心病患者血清APN水平下降,血清脂联素与冠心病病变程度呈负相关。