肺炎衣原体抗体IgA和CRP与冠状动脉粥样硬化及再狭窄的相关性研究

目的探讨肺炎衣原体感染和炎症对冠状动脉粥样硬化和支架内再狭窄的影响.方法628例接受冠状动脉造影检查的患者根据造影结果分为冠状动脉粥样硬化组(n=433)和非冠状动脉粥样硬化组(n=195),记录两组基线临床资料、检测血清肺炎衣原体抗体IgA及C-反应蛋白(CRP).92例放置冠状动脉内支架的患者分感染组(n=49)和非感染组(n=53),随访0.5年,再次冠状动脉造影检查,测量支架内管腔丢失率.结果冠状动脉粥样硬化组肺炎衣原体抗体IgA的阳性率及滴度均高于非动脉粥样硬化组(48.32%,26.1%,P=0.000;1.31±1.19,0.92±1.12,P=0.000);血清CRP水平明显升高(34.67±3.24,23.22±3.27,P=0.008),且随着病变程度加重而增加.肺炎衣原体感染组和非感染组内膜增厚发生率分别为(64.7%,63.3%,P=0.909),差别无显著性.但有内膜增厚者血清CRP水平明显高于无内膜增厚者(36.13±4.04,16.51±3.92,P=0.042).结论肺炎衣原体感染与冠状动脉粥样硬化相关,但不能预示支架内再狭窄的发生;而炎症标志物与冠状动脉粥样硬化和再狭窄的发生均相关,提示炎症反应不仅在动脉粥样硬化而且在支架内再狭窄的发生中扮演重要角色.     

肺炎衣原体与动脉粥样硬化

近年来发现肺炎衣原体与心血管疾病有关，尤其是与动脉粥样硬化密切相关。人群中肺炎衣原体感染很普遍，其抗体检出率为40％～60％；在成年人中，男性肺炎衣原体抗体的阳性率高于女性，这与男性易患动脉粥样硬化的结论相一致。动脉粥样硬化患者肺炎衣原体抗体的阳性率明显高于对应的正常人群，在动脉粥样硬化病变中尤其是斑块中可以找到肺炎衣原体原体。经鼻接种肺炎衣原体的新西兰白兔喂正常饲料可以形成动脉粥样硬化病变。本文从诸多方面综合近五年的研究成果，讨论二者相关的证据并在此基础上推测肺炎衣原体致动脉粥样硬化可能的机制。     

肺炎衣原体与动脉粥样硬化

肺炎衣原体是新认识的人类呼吸系统重要病原菌，可引起急、慢性感染，尤其是近年来发现其慢性感染与动脉粥样硬化有密切的关系。本文从血清流行病学、分子形态学。分子生物学等方面综述这种关系，并简要阐明肺炎衣原体慢性感染诱发动脉粥样硬化的可能机制。     

肺炎衣原体感染与动脉粥样硬化

近年来大量的研究结果表明,肺炎衣原体很可能是动脉粥样硬化形成的始发因素.本文从血清流行病学、病理学、动物实验、体外细胞学实验及流行病学干预实验等几方面对肺炎衣原体与动脉粥样硬化的关系进行综述.     

肺炎衣原体与动脉粥样硬化研究进展

动脉粥样硬化 ( AS)及其相关疾病特别是冠心病在全世界发病率及死亡率均很高。传统的心血管危险因素如吸烟、高血压、脂质代谢异常等不能完全解释不同地区、不同时期冠心病患病率及严重程度的不同。这引发了人们浓厚的兴趣去寻找新的 AS危险因素。近10余年来关于一些感染性因素可能对 AS的发生和发展起作用的研究逐渐增多。其中肺炎衣原体( Chlamydia pneumoniae,Cpn)作为 AS发病因素的可能性最大。这基于大量的血清流行病学研究、形态学和分子生物学研究、细菌培养、接种动物模型和试验性的抗生素治疗的研究。本文旨在探讨 Cpn作为 A…     

肺炎衣原体感染致动脉粥样硬化机制的研究进展

本文阐述肺炎衣原体在体内的传播及其与血管内皮细胞、单核／巨噬细胞、平滑肌细胞的相互作用，以及肺炎衣原体感染对动脉粥样硬化斑块稳定性的影响，探讨肺炎衣原体感染致动脉粥样硬化的机制。     

肺炎衣原体感染对老年患者冠状动脉粥样硬化及再狭窄的影响

目的　探讨肺炎衣原体感染和炎症对老年患者冠状动脉粥样硬化和支架内再狭窄的影响。方法　 5 5 5例接受冠状动脉造影检查的患者根据造影结果分为冠状动脉粥样硬化组和无冠状动脉粥样硬化组 ,检测血清肺炎衣原体抗体IgA及C反应蛋白 (CRP)。 89例放置冠状动脉内支架的患者分感染组和非感染组 ,随访半年 ,再次行冠状动脉造影检查 ,测量支架内管腔丢失率。结果　冠状动脉粥样硬化组肺炎衣原体抗体IgA的阳性率及滴度显著高于非冠状动脉粥样硬化组 ;血清CRP水平明显升高 ,且随着病变程度加重而增加。肺炎衣原体感染组和非感染组内膜增厚发生率差异无显著性意义。但内膜增厚者血清CRP水平明显高于无内膜增厚者。结论　肺炎衣原体感染与冠状动脉粥样硬化相关 ,但不能预示支架内再狭窄的发生 ;而炎症标志物与冠状动脉粥样硬化和再狭窄的发生均相关。     

肺炎衣原体感染致动脉粥样硬化的作用机制

近年来研究发现肺炎衣原体( Cpn)感染与动脉粥样硬化( AS)及冠心病密切相关。这一研究结论已得到了血清流行病学、病理学、动物实验及小规模的流行病学干预实验研究结果的支持〔1〕。Cpn可能作为一损伤因素触发炎症反应,促进AS发生发展。1　Cpn对人体心血管组织有亲嗜性Cpn易导致机体的慢性持续感染,其核酸序列被从单核细胞中检出,提示Cpn可通过呼吸道由肺巨噬细胞播散至全身其他系统。Cpn对人心血管组织有亲嗜性〔2〕,对不同患者多种组织研究发现,Cpn在心血管组织中检出率最高。在病变动脉采用特异性单克隆抗体进行检查,仅检测到Cpn,…     

肺炎衣原体与动脉粥样硬化关系的研究进展

动脉粥样硬化是由单核细胞、淋巴细胞黏附并激活内皮细胞所导致的一种慢性炎性疾病。动脉粥样斑块的形成过程,是以低密度脂蛋白为主的各种脂质成分在血管内皮下聚集,继而白细胞渗出、泡沫细胞形成、血管平滑肌增生以及大量结缔组织形成的病理过程。     

肺炎衣原体和巨细胞病毒感染与动脉粥样硬化的关系

肺炎衣原体和巨细胞病毒感染与动脉粥样硬化的关系尹瑞兴（广西医科大学心血管病研究所，南宁５３００２１）关键词肺炎衣原体；巨细胞病毒；动脉粥样硬化；病因学动脉粥样硬化是心血管系统的常见病，严重危害全世界中老年人的身体健康。虽然临床和流行病学研究表明，吸烟...     

Chlamydia pneumoniae seropositivity predicts the risk of restenosis after percutaneous transluminal coronary angioplasty

This study was done to evaluate whether anti-Chlamydia pneumoniae seropositivity can be a predictor of restenosis after coronary intervention. Recent studies indicate that latent infection with C. pneumoniae is associated with and could possibly cause atherosclerosis. However, it is unknown whether chronic infection with this microorganism is involved in the mechanism of restenosis after percutaneous transluminal coronary angioplasty. We prospectively studied 78 consecutive patients (90 target lesions) with symptomatic coronary artery disease who underwent successful coronary intervention to a de novo lesion (conventional balloon angioplasty to 31 lesions and stent implantation to 59 lesions). At angioplasty, blood samples were collected to measure the serum level of anti-C. pneumoniae IgG to examine whether seropositive patients were prone to restenosis and whether the seropositivity could predict the risk of restenosis determined by follow-up coronary angiography performed within 6 months after the angioplasty. Restenosis, defined as more than 50% stenosis with an increase of 15% or more in the degree of stenosis from that measured on cineangiograms after angioplasty, developed in 36 of 62 seropositive patients and in 4 of 16 seronegative patients (58% vs 25%, P = 0.025). Lesions in the seropositive patients had a greater mean loss index (mean ± SD 0.75 ± 0.45 vs 0.35 ± 0.41, P < 0.001), which was defined as late loss (luminal diameter reduction at follow-up angiography) divided by acute gain (luminal diameter gain by angioplasty), in late loss (1.07 ± 0.64 mm vs 0.65 ± 0.79 mm, P = 0.019), in percentage of diameter stenosis (57% ± 20% vs 41% ± 21%, P = 0.003) and a lesser mean in minimal luminal diameter (1.18 ± 0.58 mm vs 1.67 ± 0.63 mm, P = 0.002) at follow-up angiography. In a multivariate logistic regression model, anti-C. pneumoniae IgG seropositivity was a strong independent predictor of restenosis compared to the other risk factors (odds ratio = 6.2, P = 0.01). C. pneumoniae could play an important role in the mechanism of restenosis and evaluation of the IgG seropositivity, and may help to identify patients at high risk for restenosis. Received: June 13, 2001 / Accepted: December 7, 2001     

N-WASP在肺炎衣原体感染促进血管新生中的作用

目的探讨N-WASP在肺炎衣原体感染诱导血管新生中的作用及其可能机制。方法肺炎衣原体增殖培养后感染人血管内皮细胞(VEC),免疫荧光染色确认感染成功。Western blot检测肺炎衣原体感染的VEC内N-WASP磷酸化水平;CCK-8检测N-WASP特异性抑制剂Wiskostain对VEC活力的影响;免疫荧光实验检测工作浓度的Wiskostain对肺炎衣原体感染率的影响;肺炎衣原体感染以5μmol/L Wiskostain预处理的VEC后,管腔形成实验观察各组VEC形成新生血管能力的变化。结果在荧光显微镜下,感染的VEC胞浆内可见典型的肺炎衣原体包涵体。肺炎衣原体感染VEC 10、24 h后N-WASP磷酸化水平均明显上调且高于正常对照组(P0.05)。管腔形成实验结果显示,肺炎衣原体感染VEC 16 h后,其所形成的微管腔节点数明显多于正常对照组(P0.05);经Wiskostain预处理后,肺炎衣原体感染促进微管腔节点形成的作用被显著削弱,几乎不能形成微管腔结构(P0.05)。结论肺炎衣原体感染可能通过N-WASP促进人VEC形成新生血管。     

肺炎衣原体与动脉粥样硬化关系的病理学探讨

目的近年来感染作为动脉粥样硬化(AS)发病的新的危险因素受到格外关注,特别是肺炎衣原体(C.pn)感染和AS两者是否具有因果关系一直是争议的焦点。本研究试从病理学的角度探讨C.pn在动脉组织检出的意义及其在AS发生发展过程中的作用。方法利用高灵敏度的nestedPCR法对90例尸检材料采取的右冠状动脉(RCA)组织切片进行C.pn检测,同时根据美国心脏学会的AS组织学分类标准将所有标本进行分类。结果使用Nested PCR法除正常RCA之外在不同程度的AS病变组织中均有C.pn特异性DNA片段检出。90例中C.pn阳性检出率为48%(43/90),其中心脑血管病死因组为50%(15/30),其他死因组为41%(28/60),C.pn阳性检出组和阴性对照组的尸检患者临床特征如性别比例、死亡时的平均年龄及是否为心血管病死因等进行对照分析,结果显示均无显著性差异。在对90个标本4个病变内膜组中C.pn阳性检出率进行对照分析的结果显示,C.pn阳性检出率在病变初期组高于进展组,但随病变程度的增强却有意义的呈现低值。结论本研究结果提示C.pn普遍存在于AS的各类病变中,C.pn感染可能是AS形成初期阶段的启始因子,但对AS病变的发展没有直接的促进作用。     

Chlamydia pneumoniae IgG and the severity of coronary atherosclerosis

BACKGROUND: The aim of this study was to compare Chlamydia pneumoniae IgG and the extent of coronary atherosclerosis. METHODS: We investigated 92 patients with stable angina pectoris who underwent coronary angiography to assess chest pain. Before angiography, C. pneumoniae IgG was analyzed. The number of major coronary arteries (1-3) having at least one diameter narrowing (>/=50%) stenosis was determined. The patients were divided into two groups of equal size, according to C. pneumoniae IgG levels. One group included individuals with C. pneumoniae IgG levels exceeding 46 enzyme-immuno-units (EIU)/L and the other consisted of subjects with IgG concentrations below 46 EIU/L. RESULTS: Subjects with higher antibody concentrations had a more severe disease. The number of diseased arteries was 2.1+/-0.8 (S.D.) and 1.4+/-0.6 (S.D.) for the two groups, respectively. The difference is highly significant (p<0.0001). CONCLUSIONS: This study suggests a causative relationship between C. pneumoniae IgG and the degree of coronary atherosclerosis. It does not, however, prove causality.     

高敏C反应蛋白和肺炎衣原体感染与颈动脉粥样硬化及缺血性脑卒中的相关性研究

目的探讨高敏C反应蛋白水平、肺炎衣原体抗体与颈动脉粥样硬化及缺血性脑卒中TOAST亚型的关系。方法缺血性脑卒中组135例,对照组135例,测定2组的高敏C反应蛋白水平、肺炎衣原体IgG抗体、颈动脉内膜中层厚度及颈动脉粥样硬化程度。结果(1)高敏C反应蛋白水平升高与颈动脉内膜中层厚度及颈动脉粥样硬化程度相关,OR值分别为3.44和6.82;高敏C反应蛋白水平升高与大动脉粥样硬化性脑卒中危险性升高相关,OR值为10.11。(2)肺炎衣原体抗体的阳性率与颈动脉内膜中层厚度及颈动脉粥样硬化程度相关,OR值分别为1.76和4.89。结论高敏C反应蛋白水平和慢性肺炎衣原体感染与颈动脉粥样硬化密切相关,同时高敏C反应蛋白水平升高,可增加发生大动脉粥样硬化性脑卒中的风险。     

Chlamydia pneumoniae in atherosclerosis

Chlamydia pneumoniae is currently the infectious agent most often associated with the inflammation found in atherosclerosis. The seroepidemiological association and the actual presence of pathogen in lesions has been confirmed in numerous studies, in which technical difficulties seem to be the only limitation. Besides animal experiments and intervention trials, we need information of possible pathogenic mechanisms. Recently, several studies have suggested mechanisms by which C. pneumoniae infection could participate in the development of atherosclerosis.     

Evidence for persistent Chlamydia pneumoniae infection of human coronary atheromas

To date, structures representing developmental stages of Chlamydia pneumoniae, especially persistent forms of this intracellular bacteria, have not been described in human atherosclerotic tissues using specific antibody labeling and transmission electron microscopy.Staining of atherosclerotic tissue from five patients seeking heart transplantation with gold-labeled antibodies specific for up-regulated chlamydial heat shock proteins, GroEL and GroES, and visualisation via transmission electron microscopy revealed intracellular, atypical, round to oval structures of variable diameter. These structures resembled reticulate bodies of Chlamydia, were surrounded by membranes and were located within smooth muscle cells, macrophages or fibroblasts. By using double immunogold electron microscopy technique (GroEL and GroES in combination with chlamydial LPS/MOMP antibodies), we demonstrated these structures were of chlamydial origin.In the current study, we demonstrated the presence of aberrant bodies of C. pneumoniae in vivo in archival coronary atheromatous heart tissues by the immunogold electron microscopy technique.     

Seropositivity against Chlamydia pneumoniae in patients with coronary atherosclerosis

BACKGROUND: Results of therapy in patients with unstable coronary syndromes with antibiotics directed against Chlamydia pneumoniae have been variable, perhaps due to the heterogeneity of patients in these trials. HYPOTHESIS: The aim of the present study was to correlate the severity of coronary artery disease (CAD) with seropositivity against C. pneumoniae prospectively. METHODS: We measured the frequency of seropositivity (IgG levels > or = 1/64 and IgA levels > or = 1/16 against Chlamydia pneumoniae) in 110 patients with CAD and in 49 controls. RESULTS: As expected, traditional CAD risk factors were seen more often in patients with CAD than in controls. Mean values of total cholesterol (184 +/- 52 and 166 +/- 44 mg/dl, respectively) and triglyceride (143 +/- 60 and 112 +/- 63 mg/dl, respectively) in serum were significantly higher in patients with CAD than in controls (both p < 0.04). There were no significant differences between the two groups in serum high-density lipoprotein cholesterol (34 +/- 13 and 32 +/- 14 mg/dl, respectively) and lipoprotein (a) (Lp(a):241 +/- 247 and 223 +/- 263 mg/l, respectively) levels. The rate of IgG seropositivity was 52% (28/54) in patients with stable CAD, 41% (23/56) in patients with unstable CAD, and 35% in controls (p = NS). The rate of IgA seropositivity was 25% (14/54) in patients with stable CAD, 12% (6/49) in patients with unstable angina, and 12% (6/49) in controls (all p = NS). CONCLUSIONS: Only a small percentage of patients with CAD demonstrate seropositivity against Chlamydia pneumoniae. Antibiotic therapy in these selected patients, but not in the remaining patients, may be considered rational. These considerations may underlie the failure to see consistent benefits of antibiotic therapy in patients with CAD.