Infection with Chlamydia pneumoniae but not Helicobacter pylori is related to elevated apolipoprotein B levels

OBJECTIVE: Results of many studies show that apolipoprotein B (apo B) is a better marker of risk of vascular disease than other lipid markers including LDL and HDL-cholesterol and triglycerides. We investigated the association between two infectious agents: C. pneumoniae and H. pylori, known to have an atherogenic effect, and apo B, to evaluate the effects of chronic infections on apo B levels. METHODS AND RESULTS: The study group consisted of 257 patients in whom diagnostic coronary angiography was performed. C. pneumoniae IgG and IgM and H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and apo B levels were measured by the nephelometry method. Established risk factors of atherosclerosis were recorded. Of 257 patients recruited, 104 had normal vessels, 88 had 3 or more vessels obstructed and 65 had ectatic vessels without atherosclerosis. Mean apo B concentration was significantly higher in C. pneumoniae IgG and IgM positive healthy subjects compared with C. pneumoniae negatives (0.954 vs. 0.722 and 0.973 vs. 0.851, p < 0.001 and p = 0.007, respectively). Apo B levels were significantly higher in severe atherosclerotic patients (0.985 +/- 0.234 g/l) compared with control subjects (0.892 +/- 0.244 g/l) (p = 0.008), but the difference was not significant in ectatic subjects (0.946 +/- 0.272 g/l) when compared with controls (p = 0.18). Apo B levels were higher but not statistically significant in H. pylori antibody positive cases when compared with negatives. CONCLUSIONS: Apo B levels increased with C. pneumoniae infection. This finding supports the hypothesis that lipid profiles change to atherogenic lipid profile in chronic infections.     

Detection of Chlamydia pneumoniae and Helicobacter pylori in atherosclerotic plaques of carotid artery by polymerase chain reaction.

OBJECTIVES: A possible role of some microorganisms has been proposed in the pathogenesis of atherosclerosis, but it is still an unresolved issue. We investigated the presence of Chlamydia pneumoniae and Helicobacter pylori DNA in carotid artery atherosclerotic plaques by using PCR. METHODS: One hundred and four patients with atherosclerotic diseases were included. The study group consisted of 52 atherosclerotic plaque specimens obtained from the carotid arteries of patients who had carotid endarterectomy and the control group consisted of 52 specimens obtained from the macroscopically healthy regions of ascending aorta in patients who had undergone coronary artery bypass grafting. The presence of C. pneumoniae and H. pylori DNA in endarterectomy specimens were demonstrated by PCR. RESULTS: C. pneumoniae DNA was detected in 16 of 52 (30.8%) atherosclerotic plaques and 1 of 52 (1.9%) macroscopically healthy ascending aorta wall specimens (P < 0.001). H. pylori DNA was detected in 9 of 52 (17.3%) atherosclerotic plaques and none of the controls (P = 0.003). CONCLUSIONS: The higher incidence of C. pneumoniae and H. pylori DNA in atherosclerotic plaques suggests that these microorganisms may play a role in the pathogenesis of atherogenesis.     

Gastroduodenal Helicobacter pylori infection diagnosed by Helicobacter pylori stool antigen is related to atherosclerosis

OBJECTIVE: The causative relation between Helicobacter pylori (H. pylori) and atherosclerosis has been determined as seropositivity or determination of H. pylori from atherome plaques by molecular methods. The site of entrance and the reservoir of the bacteria in the body is still a subject of discussion. In this study Helicobacter pylori stool antigen (HpSA) which shows gastrointestinal system colonization and infection with high specificity and sensitivity was determined in atherosclerotic, ectatic and angiographically normal groups. METHODS AND RESULTS: A total of 62 patients was categorized according to diagnostic coronary angiography as 12 had normal coronary arteries, eight had one, 18 had two, and 12 had three atherosclerotic coronary arteries. Twelve patients had ectatic vessels. There were 27 (44%) HpSA positive and 35 (56%) HpSA negative patients. There was a statistically significant relation between HpSA positivity and the degree of vessel involvement in coronary artery disease (CAD) patients, essentially between the group with three vessels (83%) obstructed and the normal group (25%). Ectatic vessel group had a higher incidence (50%) of HpSA positivity compared to the control group but not enough for statistical significance. CONCLUSIONS: The results indicate that gastrointestinal system H. pylori colonization increases the risk of atherosclerosis. We may speculate that the reservoir and spread of H. pylori is via gastrointestinal tract. Studies may be performed to detect whether gastrointestinal tract H. pylori infection treatment will decrease the risk of coronary artery damage caused by H. pylori.     

Detection of Helicobacter pylori specific DNA in human atheromatous coronary arteries and its association to prior myocardial infarction and unstable angina

BACKGROUND: Chronic infections have been proposed to play a role in the aetiology or progression of atherosclerotic plaques. Increased risk of coronary artery disease has been suggested in patients seropositive for Helicobacter pylori. AIM: To analyse coronary specimens in patients with severe (coronary artery disease) for Helicobacter pylori specific DNA. PATIENTS AND METHODS: Atherosclerotic plaques were obtained in 46 consecutive patients (9 female, 37 male, mean age 62.7+/-9.17 years) during coronary bypass procedures. Serum was analysed for IgG -/cagA-antibodies specific for Helicobacter pylori. Polymerase chain reaction and sequence analysis were used to identify bacterial DNA. Coronary artery biopsies from 19 autopsies without coronary artery disease were examined as a control group. RESULTS: Of the 46 coronary artery disease patients, 32 (69.6%) were Helicobacter pylori seropositive. Positive results for Helicobacter pylori DNA showed 18 seropositive and 4 seronegative (with anamnesis of eradication therapy). A total of 22 patients (47.8%) of the coronary artery disease group but none of controls revealed positive DNA. In the coronary artery disease group, a correlation between DNA presence and prior myocardial infarction (p=0.008) and unstable angina (p<0.001) was found. CONCLUSION: Identification of DNA in atherosclerotic plaques of patients with severe coronary artery disease supports the hypothesis that Helicobacter pylori infection may influence the development of atherosclerosis. Our results may indicate an direct involvement of Helicobacter pylori in the progression and instability of plaques in these patients.     

Detection of Chlamydia pneumoniae but not of Helicobacter pylori in symptomatic atherosclerotic carotids associated with enhanced serum antibodies,inflammation and apoptosis rate

BACKGROUND AND PURPOSE: Numerous seroepidemiological and pathological studies linked Chlamydia pneumoniae and Helicobacter pylori with atherosclerosis. However, analyses of these infectious agents in the pathogenesis of stroke are either lacking or contradictory. Therefore, we evaluated the detection rate of C. pneumoniae and H. pylori in normal carotids vs. atherosclerotic carotids and compared these findings with serology, plaque morphology, inflammatory cell infiltrates and apoptosis rate. METHODS: The study was performed on 40 morphological normal carotids from autopsy and 20 advanced atherosclerotic carotids from endarterectomy after stroke. Serum IgG antibody titre was measured by enzyme immunoassay (H. pylori) and microimmunofluorescence (MIF) technique (C. pneumoniae). Immunohistochemistry (IHC) and Western blotting were performed to identify C. pneumoniae, H. pylori, to characterize plaque morphology (macrophages and smooth muscle cells) and the inflammatory infiltrate (T- and B cells) and to detect apoptosis (TUNEL staining). RESULTS: C. pneumoniae was found significantly more frequently in atherosclerotic than in normal carotids (P=0.001), which correlated with elevated C. pneumoniae IgG-antibody titres (P=0.048). Although H. pylori was not detected in carotids, elevated H. pylori antibody titres were significantly associated with the degree of atherosclerosis (P=0.001). The C. pneumoniae infected carotids displayed a slightly enhanced infiltrate of T cells and apoptosis rate, but no morphological changes. CONCLUSION: C. pneumoniae but not H. pylori, was detected by IHC primarily in symptomatic carotids, without specific morphological differences. Correlation of C. pneumoniae in-situ-detection and IgG antibodies suggested a possible connection between respiratory-tract and endovascular infection. The C. pneumoniae associated T-lymphocytes and apoptosis rate indicate an immune-mediated inflammatory process, involving vascular walls.     

Inflammatory-destructive biomarkers of atherosclerotic plaques instability. Study of arterial wall and blood

Concentrations of tumor necrosis factor, interleukin 1- and its receptor antagonist, IL-6, IL-8, IL-18, IL-2, ligand of CD40 receptor (CD40L), high sensitive C-reactive protein (hsCRP), monocyte chemotactic protein -1, endothelial monocyte activating protein II, adhesive molecules (sICAM-1 and sVCAM-1), matrix metalloproteinase (MMP-3, MMP-7, MMP-9), tissue inhibitor of metalloproteinase (TIMP-1) and endothelin-1 were studied in blood and in coronary artery intima/media of men with coronary atherosclerosis without acute coronary syndrome. Blood levels of hsCRP, IL-8, IL-6 and CD40L were higher, while blood levels of sVCAM and TIMP-1 were lower in men with prevalence of unstable atherosclerotic plaques compared to men with prevalence of stable atherosclerotic plaques in coronary arteries. Blood levels of hsCRP, IL-6 and IL-8 correlated with characteristics of coronary artery atherosclerotic plaques instability. Correlation between hsCRP blood level and hsCRP concentration in coronary artery intima/media material was also revealed.     

Effect of Chlamydia pneumoniae infection on coronary flow reserve and intimal hyperplasia after stent implantation in patients with angina pectoris.

OBJECTIVES: Chlamydia pneumoniae (C. pneumoniae) has been detected in tissue from coronary atherosclerotic vascular lesions and may be involved in the pathogenesis of atherosclerosis. However, the effect of prior C. pneumoniae infection on coronary intimal hyperplasia after stent implantation and on coronary microvascular function is unknown. METHODS: Seventy-three patients with stable angina pectoris and a single de novo coronary lesion were studied prospectively. All patients underwent successful coronary angioplasty and stent implantation for the stenotic lesion. Blood samples were tested for prior C. pneumoniae infection before the procedure, and patients were divided into two groups: Seropositive and seronegative. Coronary flow reserve was measured in the non-stenotic coronary vessel before angioplasty, and quantitative coronary arteriography was performed at the stent implantation site before angioplasty and 6 months later in all patients. RESULTS: Coronary flow reserve in the non-stenotic vessel was significantly lower in the seropositive group than in the seronegative group (2.51 +/- 0.35 vs 2.76 +/- 0.43, p < 0.05). The minimum luminal diameter was smaller and late loss was greater in the seropositive group than in the seronegative group (minimum luminal diameter: 1.52 +/- 0.59 vs 1.91 +/- 0.79 mm, p < 0.05, late loss: 1.17 +/- 0.55 vs 0.76 +/- 0.67, p < 0.05). However, there was no significant difference in the restenosis rate or target lesion revascularization rate between the two groups. CONCLUSIONS: Prior C. pneumoniae infection may accelerate intimal hyperplasia after stent implantation and impair coronary microvascular function in the non-stenotic coronary vessels.     

C-reactive protein, atherosclerosis and kidney function in hypertensive patients

Previous studies have shown a relationship between coronary or carotid atherosclerosis and C-reactive protein (CRP) concentrations. In the present investigation, we evaluated the relationship between high-sensitivity CRP (hsCRP) concentrations and the presence of atherosclerotic lesions in the renal arteries and/or abdominal aorta. In 95 hypertensive patients who underwent intra-arterial DSA on suspicion of renovascular disease, blood was sampled during the procedure for measurement of hsCRP. The presence of atherosclerotic lesions was assessed at the level of the renal arteries and the abdominal aorta. Haemodynamically significant renal artery stenosis was diagnosed when 50% or more stenosis was observed. Patients with fibromuscular disease (n = 8) or incomplete data (n = 4) were excluded from analysis. The results revealed that the median hsCRP concentrations were significantly higher among the 57 patients with atherosclerosis of the aorta and/or renal arteries compared to those in the 26 patients without any angiographic lesions (4.6 vs 1.7 mg/l; P < 0.005). Moreover, in patients with renal artery stenosis, levels of hsCRP were higher when the degree of stenosis exceeded 50%. However, the association between hsCRP and the presence of atherosclerosis appeared to be confounded by serum creatinine, creatinine clearance, age and gender. In the whole group a significant inverse relationship was found between creatinine clearance and hsCRP (P < 0.05). In conclusion, hsCRP concentrations are related to atherosclerotic lesions in the renal arteries and the abdominal aorta. While this supports the view that atherosclerotic renal artery stenosis is part of a systemic inflammatory vascular disease, increased concentrations of CRP may also coincide with decreased renal function.     

Lack of association between seropositivity to Chlamydia pneumoniae and carotid atherosclerosis.

Since the Chlamydia pneumoniae (C. pneumoniae)-specific antibody was shown to be associated with acute myocardial infarction and chronic coronary heart disease, the role of C. pneumoniae in the etiology of cardiovascular disease has been studied by a number of groups. We investigated the association between the C. pneumoniae-specific antibody, measured by microimmunofluorescence, risk factors for cardiovascular disease, and atherosclerosis in a randomly selected urban population. Overall, immunoglobulin-G (IgG) seroprevalence to C. pneumoniae in this sample of 1,034 subjects was 58%, whereas IgA seroprevalence was 32%. There was a decline in seropositivity with age for IgG but not IgA. Men were more likely than women to be IgG (66% vs 51%, chi-square p = 0.001) and IgA seropositive (36% vs 28%, chi-square p = 0.005). Current smokers had higher IgA seropositivity than nonsmokers (43% vs 30%). Those patients with a family history of cerebrovascular disease were more likely to have IgG antibody than those without (75% vs 57%, chi-square p= 0.007). Neither IgG nor IgA seropositivity was associated with the standard risk factors of hypertension, hyperlipidemia, or family history of ischemic heart disease, nor was seropositivity associated with carotid intima medial thickening (IMT) or atherosclerotic plaque as measured by carotid B-mode ultrasound. There was no difference between those participants who were IgG or IgA seropositive and seronegative in measurements of mean IMT, prevalence of abnormal IMT, and percentage with atherosclerotic plaque. In conclusion, although C. pneumoniae was associated with several risk factors for cardiovascular disease in a large cross-sectional population, we found no independent association between seroprevalence to C. pneumoniae and carotid atherosclerosis as measured by carotid IMT.     

Serological evidence of Chlamydia pneumoniae lipopolysaccharide antibodies in atherosclerosis of various vascular regions

BACKGROUND: The role of Chlamydia pneumoniae in the pathogenesis of atherosclerosis has so far mainly been investigated in patients suffering from coronary heart disease; the other vascular regions have virtually been ignored. The aim of this study was to carry out a statistical survey of serological markers of a C. pneumoniae infection in patients with different patterns of atherosclerosis manifestation. PATIENTS AND METHODS: 340 patients were examined for the atherosclerotic alteration of peripheral arteries of the lower limbs, carotid arteries and coronary arteries by ultrasound scan and/or angiography. Immunoglobulin(Ig)G and IgA-rELISA were used to measure chlamydial lipopolysaccharide antibodies. Species determination was performed using the IgG micro-immunofluorescence test. RESULTS: 24.0% of atherosclerotic cases (A) and 52.3% of controls (C) were negative for C. pneumoniae lipopolysaccharide antibodies (p = 0.00002). By contrast, 45.1% of atherosclerotic cases and 16.9% of controls were positive for both IgG and IgA (p = 0.00002). The mean antibody titers of the atherosclerosis group were higher than in the control group (IgG positive xAIgG = 344, xCIgG = 272; IgG and IgA positive xAIgG = 576, xCIgG = 486 and xAIgA = 120, xCIgA = 91). Concerning atherosclerosis manifestation in various vascular regions, no significant differences were found between IgG and IgA antibody titers and prevalence. CONCLUSIONS: The results show that a persistent C, pneumoniae infection with evidence of lipopolysaccharide immunoglobulin G and A is equally associated with the atherosclerotic alteration of coronary arteries, carotid arteries and peripheral arterial occlusive disease, irrespective of the severity of atherosclerosis and with no predisposition to any particular vascular region.     

Aortic distensibility associates with increased ascending thoracic aorta diameter and left ventricular diastolic dysfunction in patients with coronary artery ectasia

Coronary artery ectasia is usually linked to coronary atherosclerosis. Its primary defect is a destruction of vascular media, which leads to coronary dilatation. The aim of the present study is to evaluate whether ascending aorta present anatomical and functional wall changes in patients with coronary ectasia compared with patients without ectasia. Forty patients with known coronary ectasia (group A) underwent echocardiography in order to study aortic lumen diameter and wall properties (distensibility and stiffness index). Twenty-five patients with coronary artery disease (group B) and 40 individuals with normal coronary arteries (group C) served as control groups. Both ascending aorta diameter and ascending aorta index were significantly increased in group A compared with groups B and C (P < 0.05 and P < 0.001, respectively). Furthermore, in patients with ectatic coronary arteries ascending aorta index, systolic blood pressure and diastolic dysfunction independently associate with aortic distensibility. In patients with coronary artery ectasia, ascending aortic diameter could be enlarged while aortic stiffness is related to diastolic dysfunction. We suggest that coronary ectasia is not an isolated lesion but a reflection of a generalized vascular media defect, and should not be recognized as a benign entity.     

Chlamydial lipopolysaccharide is present in serum during acute coronary syndrome and correlates with CRP levels

Infections, Chlamydia pneumoniae as a major candidate, have been suggested to participate in inflammatory processes ultimately leading to atherosclerosis. In the present study we measured serum levels of chlamydial lipopolysaccharide (cLPS) and highly sensitive C-reactive protein (hsCRP) in the acute coronary syndrome (ACS) patients (n=145). During ACS, both cLPS and hsCRP were elevated and significant correlation (P=0.003, r=0.25) between them was observed. Both cLPS and hsCRP levels decreased after the event and correlation remained significant during the follow-up period. Our results suggest that cLPS is liberated from the damaged tissue persistently infected with C. pneumoniae during the ACS event. The significant correlation between cLPS and hsCRP levels further point to the possibility that both levels reflect the magnitude of tissue damage.     

Detection of cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae DNA in carotid atherosclerotic plaques by the polymerase chain reaction

OBJECTIVE: Cytomegalovirus (CMV), Helicobacter pylori (H. pylori) and Chlamydia pneumoniae (C. pneumoniae) have been associated with human atherosclerosis. The reported rates of detection within atherosclerotic lesions by PCR vary widely for all of these pathogens.We investigated their presence in carotid atherosclerotic plaques. METHODS AND RESULTS: Eighty-three carotid atherosclerotic specimens were available for examination. The highly sensitive polymerase chain reaction method was employed with primers specific for each agent. The presence of CMV DNA was not detected in any of the examined samples (0%), whereas the presence of H. pylori DNA was observed in two out of eighty-three cases (2.4%). C. pneumoniae DNA was found in eighteen (21.6%) of the plaques studied. CONCLUSIONS: H. pylori DNA was detected in a very small subset of atherosclerotic plaques, whereas CMV DNA was not detected in any of the plaques studied. C. pneumoniae DNA was found in a significant number of our atherosclerotic plaques. Further studies are needed to clarify the possible causal relation between infection by these organisms and atherosclerosis.     

Anatomical and functional characteristics of ectatic coronary arteries. An intracoronary ultrasound study

OBJECTIVE: Using intracoronary ultrasound we studied the anatomical characteristics and the pulsatile changes of the coronary arterial wall of ectatic coronary arteries in patients with atherosclerotic coronary artery disease who underwent percutaneous transluminal coronary angioplasty. METHODS AND RESULTS: Three study groups were formed according to the characteristics of the coronary segments, (a) group CES, coronary segments with ectasia, n = 10, (b) group NES, normal coronary segments adjacent to ectatic sites, n = 10 and (c) group NAS, normal coronary segments adjacent to atherosclerotic sites, n = 30. Pulsatile changes was defined as CSLA(syst)-CSLA(dia)/CSLA(dia) x 100. Coronary segments with ectasia (CES group) had significantly thinner media than the NAS group. Furthermore, increased vessel wall pulsatile changes were found in the ectatic segments. CONCLUSIONS: Atherosclerotic ectatic coronary segments reveal diminished media thickness and increased coronary arterial wall pulsatile changes, which may be indicative of a mechanically and structurally weak artery prone to aneurysm formation.     

Effect of ectasia size or the ectasia ratio on the thrombosis in myocardial infarction frame count in patients with isolated coronary artery ectasia

Coronary blood flow was quantified using the thrombosis in myocardial infarction (TIMI) frame-count method. This measurement has been significantly correlated with flow velocity measured invasively by use of a Doppler flow wire. Coronary artery ectasia or aneurysm (CEA) is thought to be present in patients with a slow blood flow. In this study, we aimed to assess the relationship between the ectasia size or ectasia ratio and TIMI frame count in patients with CEA. The study population included 58 patients with isolated CEA of the right coronary artery. In patients with CEA, an ectasia ratio was calculated as diameter of the ectatic segment/diameter of the adjacent normal segment. According to the ectasia ratio, ectatic vessels were divided into two groups: ectasias with a 1.5- to 2.0-fold increase (group A) and more than 2.0-fold increase (group B) in normal vessel diameter. Patients with a significant stenotic lesion (>50%) in the ectatic vessel were excluded. The control group was formed from a matched population of 35 patients with angiographically proven normal coronary arteries. Characteristics of the ectasia and control groups are similar. The TIMI frame counts for the right coronary artery (RCA) were significantly higher in the ectasia group as compared with the control group (43 ± 12 vs 23 ± 8, P < 0.001). The ectasia group had 38 patients in group A and 20 patients in group B. The TIMI frame counts were significantly higher in group B than in group A (43 ± 10 vs 51 ± 15, P < 0.05). The TIMI frame count of the RCA showed a significant correlation with the ectasia ratio and the maximum diameter of the ectatic segment (r = 0.578, P < 0.001 and r = 0.435, P < 0.001, respectively). Our data suggest that TIMI frame count measurement depends on the ectasia size or ectasia ratio, and an increased ectasia ratio is markedly associated with decreased TIMI frame counts in patients with CEA.     

Coronary artery ectasia--a variant of occlusive coronary arteriosclerosis.

In a study of 1000 consecutive coronary arteriograms, 12 patients (all men) had coronary artery ectasia. Ectasia was found most frequently in the circumflex or right coronary artery. Only 1 patient had ectasia in the left anterior descending coronary artery. In 11 patients, ectasia of one artery was associated with severe stenosis or occlusion of other vessels, typical of arteriosclerosis. Histology from an ectatic segment in one of this group showed changes of severe arteriosclerosis with extensive intimal fibrosis and destruction of the media. One patient had a mixed collagen vascular disease. Measurement of coronary sinus flow in 2 patients with coronary artery ectasia showed flows in the range of patients with non-ectatic coronary artery disease. At cardiac surgery flows down the graft to ectatic arteries were in the same range as in grafts to non-ectatic vessels. Patients with coronary artery ectasia should be anticoagulated.     

Associations of plasma C-reactive protein levels with the presence and extent of coronary stenosis in patients with stable coronary artery disease

Prospective studies showed plasma high sensitivity C-reactive protein (hsCRP) levels to be a powerful predictor of cardiac events. However, the association between hsCRP levels and the extent of coronary stenosis in patients with coronary artery disease (CAD) remains controversial. We investigated the association between hsCRP levels and the extent of coronary stenosis in 273 patients undergoing elective coronary angiography. Plasma hsCRP levels were higher in patients with CAD than in those without CAD (0.70 mg/l versus 0.56 mg/l, P < 0.02), but hsCRP levels did not correlate with the number of >50% stenotic vessels and were not a significant factor for CAD. However, after the exclusion of 76 patients taking statins, a step-wise increase in hsCRP levels was found depending on the number of >50% stenotic vessels: 0.50 in CAD(-), 0.68 in 1-vessel, 0.77 in 2-vessel, and 0.88 mg/l in 3-vessel disease (P < 0.01). The hsCRP levels also correlated with the numbers of >50% and >25% stenotic segments (r = 0.30 and 0.32, P < 0.001). Multivariate analysis revealed the hsCRP levels to be a significant factor for CAD. Thus, after the exclusion of patients with statins, plasma hsCRP levels were found to be associated with the presence and extent of coronary stenosis in patients with stable CAD.     

冠状动脉瘤样扩张与电子束CT检测的冠状动脉钙化

为探讨冠状动脉瘤样扩张患者电子束CT检测的冠状动脉钙化的特点及其临床和病理意义 ,将 2 7例经选择性冠状动脉造影确诊的冠状动脉瘤样扩张患者行电子束CT检查以计算钙化积分 ,并与 2 7例年龄和性别匹配的冠状动脉造影正常者进行比较。结果发现 ,冠状动脉瘤样扩张组钙化阳性率、钙化积分中位数及钙化积分的自然对数转换值均显著高于正常对照组 (P <0 .0 1或 0 .0 0 1)。冠状动脉瘤样扩张组中 2 1例粥样硬化性瘤样扩张患者钙化阳性率为 81.0 % ;弥漫性扩张动脉的钙化积分对数转换值显著低于局限性扩张动脉 (1.2 2± 1.79比 2 .86± 1.85 ,P <0 .0 5 )。结果提示 ,粥样硬化性冠状动脉瘤样扩张患者多数存在较为广泛的冠状动脉钙化 ,且钙化程度与病变类型有关。     

血浆尾加压素Ⅱ水平与冠状动脉病变程度的关系

目的探讨血浆尾加压素Ⅱ(UⅡ)与冠状动脉粥样硬化病变程度的关系。方法采用放射免疫法测定经冠状动脉(冠脉)造影证实的20例冠脉正常者(A组)与20例冠脉狭窄患者(冠脉狭窄＜50%,B组)53例冠心病患者(冠脉狭窄≥50％,C组)动脉血浆UⅡ水平。结果C组及B组的UⅡ水平均显著低于A组(P＜0．001),同时C组UⅡ水平显著低于B组(P＜0．001),而且C组中急性冠脉综合征患者(ACS组)UⅡ水平显著低于稳定性心绞痛患者(SAP组,P＜0．001),相关分析示血浆UⅡ水平与血管病变支数呈负相关(r=-0．449,P＜0．001),与Gensini积分呈负相关(相关系数r=-0．634,P＜0．001)。结论UⅡ水平与冠脉的病变程度呈显著负相关,提示UⅡ可能参与冠脉粥样硬化发生与发展。     

Internal mammary artery atherosclerosis in segments removed during coronary artery bypass grafting surgery and C.pneumoniae infection.

OBJECTIVE: Recent studies suggest the association of atherosclerotic cardiovascular disease with Chlamydia pneumoniae infection. We investigated C. pneumoniae DNA in internal mammarian artery (IMA) (used as a coronary bypass conduit) and its relationship with atherosclerosis. METHODS: Sixty-six consecutive patients who underwent coronary artery bypass grafting (CABG) during an eight-month period were included in this study. From all patients, we attempted to obtain surplus segments of harvested IMA grafts. The vessels were examined histopathologically, and presence of C. pneumoniae DNA in IMA grafts was assessed by polymerase chain reaction (PCR). RESULTS: C. pneumoniae DNA was found in 7 (10.6%) of 66 IMA specimens. The light microscopic examinations of IMA segments from the C. pneumonia positive group showed atherosclerotic intimal changes in four of the seven patients. These atherosclerotic changes were type II in three patients and type III in one patient according to the AHA classification. The rest of the IMA segments from 62 patients did not show any discernible atherosclerotic lesion. CONCLUSION: The IMA graft examination by PCR and histopathology may be helpful in the determination of future graft patency for IMA bypass surgery.