Objective To analyze the correlation and clinical value of serum levels of soluble E selectin ( sES ) , matrix metalloproteinase-9 ( MMP-9 ) , tissue inhibitor of metalloproteinase-1 ( TIMP-1 ) and insulin to the degree of&nbsp;coronary artery ectasia ( CAE ) . Methods The 106 in-patients received with coronary angiography ( CAG ) were collected and divided into three groups according to the CAG outcome, which were control group (38 cases, normal coronary artery) , ectasia group (32 cases, coronary artery ectasia) and stenosis group (36 cases, coronary artery stenosis). The serum levels of sES, MMP-9, TIMP-1 and insulin were detected and compared among three groups during admission. The relative factors to the degree of CAE were confirmed by Pearson linear analysis. And the risk factors to the occurrence of CAE were confirmed by multivariate Logistic analysis. Results The serum levels of sES and MMP-9 of ectasia group were highest ( P <0. 05 ) , and the stenosis group was mediate and the control group was lowest ( P<0. 05 ) . The serum level of insulin of ectasia group were lowest ( P<0. 05 ) , and the normal group was mediate and the stenosis group was highest ( P<0. 05 ) . But the serum levels of TIMP-1 have no differ-ence among three groups. The positive relationship of the serum levels of sES, MMP-9 to the degree of CAE was confirmed by Pearson linear analysis ( r=0. 613 , P=0. 032; r=0. 671 , P=0. 027 ) . And the negative relation-ships of the serum levels of insulin to the degree of CAE were also confirmed ( r= -0. 754 , P=0. 023 ) . But there was no relationship of the serum levels of TIMP-1 to the degree of CAE ( r=0. 128 , P=0. 105 ) . Multivariant Lo-gistic analysis showed that the sES and MMP-9 were risk factors to the occurrence of CAE and the hyperinsulinemia was the protective factor to the occurrence of CAE. Conclusion Serum levels of sES, MMP-9 and insulin can as-sess the risk of CAE.

目的:分析冠状动脉扩张症(CAE)患者血浆胰岛素水平及其与基质金属蛋白酶-9(MMP-9)/基质金属蛋白酶组织抑制因子1(TIMP1)比例失衡的关系.方法:选择行冠脉造影患者80例,根据造影结果分为冠脉扩张组与冠脉正常组,各40例.再根据冠脉斑块情况分亚组:A1组18例,单纯冠脉扩张;A2组22例,冠脉扩张伴少量斑块;B1组25例,冠脉正常;B2组15例,冠脉无明显狭窄但有散在斑块.检测4组血浆胰岛素、MMP-9和TIMP1水平,计算MMP9/TIMP1比例.分析血浆胰岛素水平与MMP-9、TIMP1水平的相关性,应用多元Logistic回归分析评估CAE发生的危险因素.结果:与冠脉正常组相比,冠脉扩张组患者的血浆胰岛素、MMP-9水平及MMP-9/TIMP1比值较高,而TIMP1水平较低(均P＜0.05).亚组分析显示,血浆胰岛素、MMP-9水平及MMP-9/TIMP1比值顺序为A2组＞A1组＞B2组＞B1组(均P＜0.05),而TIMP1水平为B2组＞B1组＞A2组＞A1组(均P＜0.05).血浆胰岛素水平与MMP-9呈正相关(r=0.572,P＜0.01),与TIMP1呈负相关(r=-0.568,P＜0.01);MMP-9与TIMP1呈负相关(r=-0.468,P＜0.01).血浆胰岛素及MMP-9/TIMP1比值是CAE发生的危险因素(P＜0.05).结论:CAE患者血浆胰岛素水平较高,可能通过调节血浆MMP-9和TIMP1水平参与CAE损伤.

卵泡抑素样蛋白1(follistatin-like protein 1,Fstl1)是一种与卵泡抑素高度同源的分泌型糖蛋白,属于卵泡抑素家族成员,具有多种生理功能,参与调控细胞分裂增殖、凋亡和组织分化。在疾病发生、发展及转归过程中发挥重要的作用,与炎症反应、免疫性疾病、肿瘤发生和转移及心脑血管疾病等关系密切。Fstl1能够促进成年哺乳动物心肌梗死后残存的心肌细胞进入分裂期,通过增加心肌细胞数量来改善心脏功能。心肌和神经等组织,主要以永久性细胞构成,其损伤后修复再生的能力十分有限,致使组织器官功能恢复不良,严重降低了患者的生活质量。Fstl1在未来的研究中,关于损伤组织的修复再生机制将成为研究的热点和难点,尤其是如何促进永久性细胞构成的组织修复再生,这既是一个机遇又是一个挑战。

目的 分析冠状动脉扩张(CAE)患者胰岛素敏感性与CAE病变程度的相关性.方法 选取96例CAE患者作为研究对象,检测稳态模型胰岛素抵抗指数(HOMA-IR)指数并作为分组依据,分为冠脉扩张合并胰岛素抵抗(IR-CAE)组(57例)与冠脉扩张合并胰岛素敏感(IS-CAE)组(39例).比较两组的一般指标及生化指标差异性,以及CAE病变程度的差异性.应用Pearson相关分析HOMA-IR指数与CAE病变程度的相关性,应用多元Logistic回归分析各种指标与CAE发生的危险因素.结果 与IR-CAE组相比,IS-CAE组患者的BMI、腹围、收缩压、舒张压、空腹胰岛素(FINS)、总胆固醇、三酰甘油均显著较低(P＜0.05),而高密度脂蛋白胆固醇显著较高(P＜0.05).两组CAE病变严重程度差异有统计学意义(P＜0.05).Pearson相关分析显示HOMA-IR指数与CAE病变程度呈正相关(r=0.703,P=0.025).多元Logistic回归分析显示,FINS及HOMA-IR指数为CAE发生的危险因素(P＜0.05).结论 CAE患者胰岛素敏感性越差,其CAE病变程度越严重.

冠状动脉扩张(coronary artery ectasia，CAE)是指心外膜下冠状动脉的局限性或弥漫性扩张，目前定义为超过临近正常血管节段的1.5倍，若大于2倍则为冠状动脉瘤，是一种非梗塞性、缺血性冠状动脉疾病。随着冠状动脉造影、血管内超声及无创性检查手段如多排螺旋CT、心脏磁共振、超声心动图的广泛开展，越来越多的CAE患者得以检出，冠状动脉扩张越来越受到临床关注，因CAE缺乏临床表现的特异性，需一些特殊辅助检查才能诊断，本文就其相关辅助检查作一综述。

Background-Tissue factor (TF) and coagulation proteases are involved in promoting atherosclerosis, but the molecular and cellular bases for their involvement are unknown.Methods and Results-We generated a new strain (ApX4) of apolipoprotein E-deficient mice expressing a membrane-tethered human tissue factor pathway inhibitor fusion protein on smooth muscle actin-positive cells, including vascular smooth muscle cells (SMCs). ApX4 mice developed little atherosclerosis on either a normal chow or high-fat diet. Lipid levels were similar to those in parental ApoE(-/-) mice, and there was no detectable difference in systemic (circulating) tissue factor pathway inhibitor levels or activity. The small lipid-rich lesions that developed had markedly reduced leukocyte infiltrates, and in contrast to ApoE(-/-) mice, SMCs did not express macrophage migratory inhibitory factor (MIF), including at sites distant from atheromatous lesions. Low levels of circulating MIF in ApX4 mice normalized to levels seen in ApoE(-/-) mice after injection of an inhibitory anti-human tissue factor pathway inhibitor antibody, which also led to MIF expression by tissue factor-positive medial SMCs. MIF production by SMCs in ApoE(-/-) mice in vitro and in vivo was shown to be dependent on tissue factor and protease-activated receptor signaling, which were inhibited in ApX4 mice.Conclusions-Our data indicate that tissue factor plays a hitherto unreported role in the generation of MIF by SMCs in atherosclerosis-prone ApoE(-/-) mice, inhibition of which significantly prevents the development of atherosclerosis, through inhibition of leukocyte recruitment. These data significantly enhance our understanding of the pathophysiology of this important pathology and suggest new potential translational strategies to prevent atheroma formation.

DNA甲基化是一种重要的表观遗传调控方式,可在转录前水平调节基因的表达.近年来的研究表明,动脉粥样硬化的发生发展与DNA甲基化密切相关.对DNA甲基化模式改变在动脉粥样硬化发病的相关机制做深入研究,可能为动脉粥样硬化的诊治提供一种新的途径.本文将从基因组低甲基化、相关基因异常甲基化以及动脉粥样硬化危险因素的DNA甲基化等方面重点阐述DNA甲基化与动脉粥样硬化的关系.

冠状动脉扩张（coronary artery ectasia,CAE）为心外膜冠状动脉的局限性或弥漫性扩张,管径扩大超过临近正常段或大于正常值上限的1.5~2.0倍。大约20%~30%的CAE患者被认为是先天性的[1]。目前关于CAE的发病机制仍不明确,有关其病因、临床意义和预后也知之甚少。随着近年来无创影像学检查技术的不断发展,以及经皮冠状动脉介入治疗和抗凝剂、硝酸酯和钙通道阻滞剂等药物的应用,将有

<正>冠心病(coronary heart disease,CHD)是一种临床常见的慢性进展性疾病,由多因素综合所致,病理基础是动脉粥样硬化(atherosclerotic,AS)。而冠状动脉粥样斑块的稳定性能很好地反映急性冠状动脉事件的可能性。研究不稳定斑块特点、寻找反映易损斑块的早期指标成为近年心血管疾病的讨论热点。基质金属蛋白酶(matrixmetalloproteinases,MMPs)是一种可以降解细胞外基质(ECM)的蛋白水解酶,多在斑块肩部降解ECM,引起斑块破裂出血,引发急性冠状动脉综合征(acute coronary syndrome,ACS),并在冠状动脉重建过程中发挥重要作用。其中基质金属蛋白酶-9(MMP-9)通过过度降解血管基底膜的主要结构成分——Ⅳ型胶原,介导了冠状动脉斑块的发生、发展和破裂,而最终导致临床严重后果。现就MMP-9在CHD中的作用作一综述。

<正>单纯收缩期高血压(ISH)作为临床常见的一种高血压类型,无论从其发病机制、临床表现、预后和治疗均与经典的收缩压(SBP)和舒张压(DBP)同时升高有所不同,是临床心血管事件的独立危险因素之一。其病理生理机制主要表现为大动脉血管壁中层弹性减退,胶原含量增加,弹性纤维减少、断裂、钙

Objective To explore the relationship smoking index and coronary artery disease degree and cardiovascular disease prognosis.Methods Retrospective analysis of collection patients with coronary heart disease(CHD) and it' suspected in the Digital Subtraction Angiography(DSA) of the first affiliated hospital of the university of south china in January 2010 to August 2011,1203 cases of coronary angiography were entered in.according to the international standards of CHD and smoking index Coronary artery pathological damage through the Gensini quantitative evaluation scoring system,divided into 5 groups.Results With smoking index increased coronary artery disease severity and disease extent increase significantly,the relationship has the remarkable concentration-response smoking is independent risk factors of coronary heart disease;It also found that age and men is also the risk factors of coronary heart disease.Conclusion Smoking index and coronary artery pathological changes has a significant relationship between the degree,a serious threat to human health and life safety,quit smoking and tobacco control is urgently needed.

脂蛋白(a)[Lp(a)]是由载脂蛋白(a)(apo(a))与载脂蛋白B100 (apoB100)通过共价键连接的脂蛋白.高血浆水平Lp(a)是心血管疾病的独立风险因子,Lp(a)的血浆水平主要受遗传因素调控,主要有LPA [lipoprotein,Lp(a)]基因的三环结构域kringle Ⅳ/2拷贝数和单核苷酸多态性(SNP).欧洲动脉粥样硬化协会(EAS)和美国心脏病协会(AHA)建议对于高Lp(a)的人群应当考虑降高Lp(a)的治疗.目前已有多种降高Lp(a)的药物和方法,如血浆分离置换法、雌激素治疗、反义核苷酸治疗、类法尼醇X核内受体(farnesoid X receptor,FXR)激动治疗等,但应用于临床的降高Lp(a)的药物和方法依然缺乏.本文拟就降Lp(a)的药物和方法进展情况进行综述.

冠心病是当今威胁人类健康的主要疾病之一,动脉粥样硬化是一种脂质代谢紊乱、血凝因素异常、细胞因子、平滑肌细胞增殖和血流动力学改变等多种因素相互作用的结果。近年来,越来越多的研究提示炎症与免疫在动脉粥样硬化的发生、发展中起重要作用。炎症的激活可能是导致斑块不稳定的主要因素。在与冠心病相关的众多炎症介质中,血浆可溶性CD40配体(sCD40L)已成为研究热点。sCD40L通过促进血小板聚集、刺激趋化蛋白表达和释放、增强免疫活性细胞的粘附、诱导金属蛋白酶表达等多种机制促进动脉粥样硬化的演变。

Objective To study the benefits about cTnT and BNP in early diagnosis and prognosis for non-ST elevated myocardiac infarction(NSTEMI).Methods To collect patients with acute NSTEMI and healthy volunteers as study objects,dynamically monitor serum cTnT and BNP and compare their relationship.Results The level of serum cTnT and BNP in study group was significantly higher than the control group(P0.01),and the peak of BNP lasted significantly longer than cTnT(P0.01),and there was significant relationship between high BNP and the incidence of heart failure(P0.01).Conclusions There are no differences between cTnT and BNP in early diagnosis about NSTEMI,but BNP is important to the prognosis of myocardial infarction.

目的观察复方丹参滴丸对急性冠脉综合征患者血小板聚集与活化的影响。方法将56例急性冠脉综合征患者随机分成2组:对照组采用常规治疗;治疗组在常规治疗基础上加服复方丹参滴丸10粒/次,每天3次。检测2组用药前、用药后24 h、用药后48 h的血小板最大聚集率、血栓素A2水平。结果治疗48 h后,治疗组血小板最大聚集率、血栓素A2水平较对照组显著降低(P均<0.01)。结论复方丹参滴丸可显著抑制血小板聚集与活化。

Aim To investigate the effect of Shensongyangxin capsule on QT dispersion and connexin43 expression in heart failure rats. Methods Heart failure rats models were built by constricting abdominal aorta,and were lavaged with Shensongyangxin capsule for 8 weeks.Ventricular electrophysiology were measured by inserting home-made electrode into subcutaneous,left ventricular morphostructure,myocardial fibrosis,and connexin43 distribution were respectively observed by HE staining,Masson staining,immunohistochemical staining. Results Heart failure rats QT dispresion were significantly longer(37.20±9.94 ms,P<0.05),cardiomyocytes were misaligned,myocardial fibrosis area were significantly increased(101217.30±33970.02 μm2,P<0.05),and connexin43 distribution were significantly decreased(55.93±11.61,P<0.05).Shensongyangxin capsule can shorten QT dispresion(25.50±8.21 ms) of heart failure rats,increase connexin43 distribution(69.09±16.59) and decrease myocardial fibrosis area(13580.64±8213.73 μm2) in myocardium of heart failure rats. Conclusion Shensongyangxin capsule can shorten QT dispresion of heart failure rats,increase connexin43 distribution and decrease myocardial fibrosis area in myocardium of heart failure rats.

Objective To analysis the application value of DES and tirofiban to AMI patients.Methods 78 AMI patients were divided into observation group that were treated with DES and tirofiban and control group that were treated with DES.TIMI,MBG,drop of ST-segment,cardiac index and MACE were compared and analysised.Results Observation group's MBG,one week's drop of ST-segment after operation,cardiac index were better than control group's Obviously,observation group's rate of MACE was lower than control group's(7.5% Vs 23.7%).There were significant difference between the two groups(P <0.05).Conclusion Application of DES and tirofiban to AMI patients can make myocardial ischemia reperfusion,reduce no-reflow phenomena,reduce the incidence of heart attacks,can significantly improve patients' cardiac and prognosis.

BACKGROUND: Adiponectin plays a regulatory role in insulin resistance and metabolic syndrome, and the synthesis of which is regulated by peroxisome proliferator-activated receptor γ (PPAR γ). Studies demonstrated that angiotensin receptor blocker can affect the metabolism of adiponectin via activating PPAR γ, but the precise mechanism remains unclear. OBJECTIVE: To investigate the effect of telmisartan on the adiponectin expression in 3T3-L1 adipocytes in vitro, and to compare the results with candesartan. METHODS: 3T3-L1 adipocytes were cultured and differentiated in vitro. The differentiated 3T3-L1 adipocytes were cultured with vehicle or candesartan (10 μmol/L) or telmisartan (10 μmol/L). The expression level and secretary level of adiponectin were detected by RT-PCR, Western blot and ELISA. RESULTS AND CONCLUSION: Compared with the control and candisartan groups, telmisartan significantly increased the expression of adiponectin mRNA and protein in adipocytes (P < 0.05, P < 0.01), but there was no significant difference in secretion levels of adiponectin between groups (P > 0.05). The results demonstrated that telmisartan can increase the adiponectin expression in 3T3-L1 adipocytes, but can not increase the secretion by 3T3-L1 adipocytes. The promotive effect of telmisartan is superior to candesartan.

Brain natriuretic peptide (BNP) is a polypeptide with multiple physiological actions. It can be used for the judgement of the left ventricular function and prediction of the prognosis patients with acute coronary syndrome (ACS)or underwent Percutaneous coronary intervention (PCI). Recombined BNP is effective in cases of decompensated heart failure and acute myocard infarction(AMI).