Chlamydia pneumoniae, herpes simplex virus and cytomegalovirus in symptomatic and asymptomatic high-grade internal carotid artery stenosis. Does infection influence plaque stability?

BACKGROUND: Current debates are focused on inflammatory processes in atherosclerotic lesions as a possible pathomechanism for destabilization and thrombembolism. In this prospective study the role of systemic and local infection in patients with high-grade internal carotid artery stenosis (ICA) was evaluated. PATIENTS AND METHODS: Serum antibody titers of 109 consecutive patients, who underwent surgery for ICA stenosis (asymptomatic n = 40, symptomatic n = 69) were prospectively measured for Chlamydia pneumoniae (Cpn) (IgA and IgG), Herpes simplex virus (HSV) (IgG, IgM) and Cytomegalovirus (CMV) (IgG, IgM) respectively. 53 carotis plaques of this group (asymptomatic n = 17, symptomatic n = 36) could be analyzed by polymerase chain reaction (PCR) for Cpn-, HSV- and CMV-DNA presence. RESULTS: Seropositivity was found in 61,5% for Cpn, 91,7% for HSV and 72,5% CMV respectively. No significant relation was found between symptomatic and asymptomatic patients as well as no difference was seen for presence of IgA antibodies against Cpn comparing both groups. Plaque-PCR revealed Cpn in 7 cases (13,2%), HSV in 2 cases (3,8%) and no CMV had been detected. Again, no significant relationship was found concerning symptomatic and asymptomatic patients. All 9 PCR-positive plaques displayed lesions of "complicated atherosclerosis" as central fibrous necrosis and calcification or plaque bleeding and surface thrombosis. CONCLUSIONS: Our results do not support the hypothesis that systemic Cpn, HSV or CMV- infection or evidence of Cpn-, HSV- or CMV-DNA in carotid plaques causes plaque destabilization and cerebral thromboembolism. Plaque infection could only be observed in cases with advanced atherosclerosis.     

Relation between plasma adiponectin, high-sensitivity C-reactive protein, and coronary plaque components in patients with acute coronary syndrome

The present study investigated the relation between plasma high-sensitivity C-reactive protein (hs-CRP) and adiponectin and coronary plaque components in patients with acute coronary syndrome (ACS). Previous studies showed a pivotal role of inflammation in the progression of atherosclerosis and the prognostic value of several biomarkers. However, relations among inflammatory biomarkers and plaque characteristics were unknown. Ninety-three culprit plaques (ACS n = 50, non-ACS n = 43) and 56 nonculprit plaques (ACS n = 28, non-ACS n = 28) were analyzed using Virtual Histology intravascular ultrasound to examine relations among plasma hs-CRP, adiponectin, and ratios of each coronary plaque component. Plasma adiponectin was significantly lower and plasma hs-CRP was significantly higher in patients with than without ACS. Culprit plaques in patients with ACS had greater amounts of necrotic core plaque than those in patients without ACS. There was an inverse relation between serum hs-CRP and adiponectin with regard to necrotic core ratio in both culprit and nonculprit lesions in patients with ACS, but not those without ACS. In conclusion, increased plasma hs-CRP and hypoadiponectinemia might be related to the progression of ACS.     

Evaluation by multislice computed tomography of atherosclerotic coronary artery plaques in non-culprit, remote coronary arteries of patients with acute coronary syndrome.

BACKGROUND: Patients with acute coronary syndrome (ACS) frequently have vulnerable plaques in the remote coronary arteries, suggesting that ACS is part of the pan-coronary process. In the present study the computed tomography (CT) plaque density in non-culprit atherosclerotic coronary artery lesions was evaluated by multislice computed tomography (MSCT) in patients with ACS and non-ACS. METHODS AND RESULTS: MSCT was performed in 21 patients with ACS and 53 patients with non-ACS: 16 of the 21 ACS patients (76%) and 30 of the non-ACS 53 patients (57 %) had non-calcified plaques in the non-culprit coronary arteries (p=0.18). CT-low-density plaques (CT density <68 Hounsfield units (HU)) were more frequent in the ACS group (13/16 patients, 81%) than in the non-ACS group (13/30 patients, 43%, p=0.03). In addition, the CT density of the non-culprit lesion was significantly lower in patients with ACS than in those with non-ACS (44.1+/-22.9 and 77.3+/-33.7 HU, respectively). CONCLUSION: Patients with ACS more frequently had CT-low-density plaques in the non-culprit, remote arteries than those with non-ACS, which suggests that ACS treatment should focus not only on stabilizing the culprit lesion but also on systemic stabilization of non-culprit lesions.     

Relationship between high sensitive C-reactive protein and coronary plaque component in patients with acute coronary syndrome: Virtual Histology study

OBJECTIVES: Elevated circulating C-reactive protein (CRP)is commonly observed in patients with acute coronary syndrome(ACS), suggesting enhanced inflammation in vulnerable plaques. However, few data are available on the relationship between the levels of CRP and the histological composition of coronary plaque. We investigated the relationship between plasma high sensitive CRP level and coronary plaque component with Virtual Histology intravascular ultrasound (VH-IVUS). METHODS: Twenty eight patients with ACS and 37 patients with non-ACS were enrolled in the study. Plasma high sensitve CRP levels were measured before catheterization. A total of 125 lesions (ACS; 24 culprit lesions, 30 non-culprit lesions, non-ACS; 34 culprit lesions, 37 non-culprit lesions)underwent IVUS volumetric investigation, and the volume of plaque and media were calculated. Spectral analysis of IVUS radiofrequency data was performed with VH software, and plaque and media were classified into fibrous, fibro-fatty, dense calcium, and necrotic core elements. RESULTS: Although the plasma high sensitive CRP level in patients with ACS was higher than that in those with non-ACS (0.26 +/- 0.2 vs 0.15 +/- 0.17 mg/dl, p < 0.05), necrotic core volume was not different between the two groups(11.7 +/- 7.3 vs 12.3 +/- 7.2mm3/cm, p = 0.71). There was a positive correlation between high sensitve CRP and necrotic core volume in patients with ACS, not only in culprit lesions (p = 0.0004, r2 = 0.564) but also in non-culprit lesions (p = 0.0008, r2 = 0.473), whereas patients with non-ACS showed no correlations. CONCLUSIONS: IVUS spectral analysis revealed that elevated plasma high sensitve CRP level was correlated with necrotic core volume in patients with ACS, both in culprit and non-culprit lesions, suggesting enhanced vascular inflammation.     

Endothelial progenitor cell mobilization after percutaneous coronary intervention

BACKGROUND: In animal models, circulating endothelial progenitor cells (EPC) have been shown to participate in repair of damaged or degenerating vascular surfaces. In humans, reduced EPC counts correlate with cardiovascular risk and disease outcome; yet it has been difficult to establish that EPC are in fact mobilized in response to vascular injury as a physiologic response. We therefore studied early (<12h) mobilization of EPCs into the peripheral circulation after a defined vascular manipulation, percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) and non-ACS patients. METHODS AND RESULTS: CD34/CD31 positive EPC colony forming units (EPC-CFU) were quantified by a blinded observer in peripheral blood samples from eight control patients with angiographically normal coronary arteries, and in 30 patients with coronary artery lesions before and 12h after PCI. All patients (n=38) had one or more CV risk factors. Ten patients presented with acute coronary syndrome (PCI(ACS)), and the rest (n=20) underwent elective PCI (PCI(Elect)). Despite the presence of an acute coronary syndrome, patients in the PCI(ACS) group did not present with increased EPC-CFU compared with either the PCI(Elect) or control groups (P>0.05). In addition, EPC-CFU (colonies/ml blood) increased significantly in the PCI(Elect) group after stent placement (11.8+1.6 before versus 16.5+1.9 after, P=0.0009), while in contrast, PCI did not stimulate EPC mobilization in patients in the PCI(ACS) group (9.6+3.2 before versus 6.5+1.8, P=0.20). We found a higher presenting vascular endothelial growth factor (VEGF) level in the PCI(Elect) group compared to PCI(ACS) (78.7+25.2 versus 15.3+7.9 pg/ml blood, P=0.02). However, VEGF levels increased after PCI only in the PCI(ACS) group (15.3+7.9 to 133.3+27.5 pg/ml, P=0.003) and not in the PCI(Elect) group (78.7+25.2 to 79.7+12.2 pg/ml, P=0.97). CONCLUSION: Our findings suggest that focal coronary endothelial injury as a result of PCI triggers early mobilization of EPC into the peripheral circulation in patients presenting for an elective PCI, without a corresponding rise in VEGF levels. In contrast, patients with an acute coronary syndrome fail to respond to PCI with early EPC mobilization despite a significant rise in VEGF. The results of the present study may suggest a novel mechanism for early EPC augmentation after PCI.     

Prior cytomegalovirus infection and the risk of restenosis after percutaneous transluminal coronary balloon angioplasty

BACKGROUND: Restenosis is a common problem after all revascularization procedures in atherosclerotic coronary arteries. Reactivated human cytomegalovirus (CMV) has been detected in tissues of restenotic vascular lesions and was hypothesized to be a contributing pathogenic factor. Recent data suggest an association of restenosis after optimal coronary atherectomy with CMV serostatus, and a possible role of antiviral therapy was discussed. We therefore tested the hypothesis that prior CMV infection might be a risk factor for restenosis after conventional coronary balloon angioplasty (PTCA). METHODS AND RESULTS: We analyzed 92 consecutive patients who had been admitted for control angiography after previous PTCA within a mean interval of 6 months. Anti-CMV antibodies were measured as an indicator of prior CMV infection and latency. The coronary angiograms before PTCA, directly after, and 6 months later were analyzed quantitatively. Sixty-five percent of the patients were CMV-positive. Before PTCA, the degree (mean+/-SD) of stenosis was 69+/-10% in CMV-positive and 68+/-8.3% in CMV-negative subjects. PTCA resulted in a residual stenosis of 39% in both groups. After 6 months, the late losses of luminal diameter in the CMV-positive and -negative groups were 11+/-13% and 12+/-15%, respectively (P=0.658). In an ANCOVA with 25 potential risk factors for restenosis, CMV serostatus was not significantly associated with restenosis development. CONCLUSIONS: Our data indicate that prior CMV infection, in contrast to optimal atherectomy, is not associated with chronic restenosis after conventional coronary balloon angioplasty. The results do not support a possible benefit from antiviral therapy.     

多层螺旋计算机断层扫描血管造影对冠状动脉易损斑块的检测作用

目的 评价多层螺旋计算机断层扫描（computed tomography,CT）血管造影（multislice computed tomography angiography,MSCTA）检测冠状动脉易损斑块的可靠性,建立急性冠脉综合征积分（score system of acute coronary syndromes,SACS）,用于评估冠状动脉粥样硬化性心脏病（冠心病）患者危险分层.方法 研究20例非急性冠脉综合征及41例急性冠脉综合征且冠状动脉MSCTA发现斑块的患者,比较两组斑块CT值、重构指数（RI）等指标,进而构建急性冠脉综合征发病风险预测模型.结果 两组病变血管99支,可分析斑块1 17个,非急性冠脉综合征组36个,以钙化斑块为主（88.9％,32/36）;急性冠脉综合征组81个,以脂质斑块为主（37.0％,30/81）.两组正性重构比例比较,差异有统计学意义（61.1％ vs.32.1％,P＜0.01）;负性重构比例比较,差异有统计学意义（25.0％vs.19.8％,P＜0.01）.由RI建立SACS,所得模型为：SACS=0.003PA＋2.255RI-4.22,预测准确率为76.9％（P＜0.01）,受试者工作曲线下面积为0.815（P＜0.01）.结论 急性冠脉综合征患者冠状动脉斑块多为脂质斑块,以正性重构为主,SACS对急性冠脉综合征发病具有较高的预测价值,有助于临床指导冠心病危险分层及早期干预.     

高敏C反应蛋白与急性冠脉综合征的相关性

目的：探讨高敏C反应蛋白（hsCRP）与急性冠脉综合征（ACS）病变严重程度及预后之间的关系。方法：选择95例ACS患者,其中急性心肌梗塞（AMI）50例、不稳定型心绞痛（UAP）45例,并根据冠脉病变程度分单支血管病变（SVL）组48例和多支血管病变（MVL）组47例。另选40例非ACS患者作为非ACS对照组,测定各组hsCRP、纤维蛋白原、血脂等指标,进行比较。结果：与非ACS对照组比较,UAP组、AMI组hsCRP水平明显升高[（0.85±0.49）mg/L比（10.01±1.73）mg/L比（52.73±2.39）mg/L,P〈0.01],AMI组明显高于UAP组（P〈0.01）;MVL组hsCRP水平明显高于SVL组[（69.11±1.98）mg/L比（10.12±2.01）mg/L,P〈0.05]。Spearman相关分析显示,hsCRP与冠脉狭窄呈正相关（r=0.210,P=0.042）,与纤维蛋白原（r=0.516,P〈0.0001）、血脂水平呈明显正相关（r=0.100～0.159,P〈0.001～〈0.0001）。结论：高敏C反应蛋白与冠脉病变严重程度呈正相关,是冠心病的独立危险因素;测定高敏C反应蛋白水平对急性冠脉综合征的危险分层和预测病变严重程度具有较高的临床参考价值。     

High prevalence of seropositivity for antibodies to Chlamydia-specific lipopolysaccharide in patients with acute coronary syndrome

BACKGROUND: Results of recent studies have demonstrated that there is an association between infection with Chlamydia pneumoniae and coronary artery disease (CAD). Inflammatory response caused by chlamydial infection has been considered to contribute to the development of atherosclerosis in coronary arteries. OBJECTIVE: The aim of this study was to investigate the specific relations between chlamydial infection and coronary events in patients with CAD. METHODS: We measured serum levels of immunoglobulin A and G antibodies against Chlamydia spp.-specific lipopolysaccharide in 155 patients with CAD and 60 age-matched and sex-matched healthy controls by enzyme-linked immunosorbent assay. CAD patients were divided into groups of the patients with acute coronary syndrome [(ACS), n = 35], old myocardial infarction [(OMI), n = 60] and chronic coronary heart disease [(CCHD), n = 60]. RESULTS: Prevalence of both seropositive antibodies in the control group and CCHD group were not different. In contrast, in ACS group there were significantly higher prevalences of seropositive immunoglobulin A (46 versus 12%, P = 0.0001) and G (74 versus 45%, P = 0.005) antibodies and in OMI group there was a significantly higher prevalence of seropositive immunoglobulin A antibodies (28 versus 12%, P = 0.02). Furthermore, compared with CCHD group, in ACS group there were significantly higher prevalences of seropositive immunoglobulin A (P = 0.00006) and G (P = 0.002) antibodies and in OMI group there was a higher prevalence of seropositive immunoglobulin A (P = 0.01). Adjustment for confounding factors did not change these findings. CONCLUSIONS: Infection with Chlamydia is significantly associated with ACS and OMI, but not with CCHD. These findings suggest that chronic and reactive infection with Chlamydia can lead to disruption of vulnerable plaque in patients with ACS.     

Number of yellow plaques detected in a coronary artery is associated with future risk of acute coronary syndrome: detection of vulnerable patients by angioscopy.

OBJECTIVES: We sought to test whether the risk of acute coronary syndrome (ACS) can be estimated by angioscopy. BACKGROUND: Disruption of vulnerable plaque and subsequent thrombosis is regarded as a major mechanism of ACS. Although yellow plaques are supposedly vulnerable, the association between angioscopically determined extent of coronary atherosclerosis and risk of ACS events has not been reported. METHODS: Patients (n = 552) who received catheterization and angioscopic examination for the diagnosis of coronary artery diseases were prospectively included and followed up for new onset of ACS events. Yellow color intensities of all detected yellow plaques were graded as 1, 2, or 3 according to the standard colors. Number of yellow plaques (NYP) in a coronary artery and maximum color grade of detected yellow plaques (maxYP) were determined. Association between the incidence of ACS events and angioscopic findings were analyzed. RESULTS: Follow-up interval was 57.3 +/- 22.1 months. Acute coronary syndrome events were detected in 39 patients (7.1%). Although maxYP was not statistically different (2.0 +/- 0.7 vs. 1.8 +/- 0.9; p = 0.18), NYP was higher in the patients with an ACS event than those without the event (3.1 +/- 1.8 vs. 2.2 +/- 1.5; p = 0.008). Patients with NYP > or =2 and those with NYP > or =5 had 2.2- and 3.8-fold higher event rates, respectively, than those with NYP 0 or 1 (9.0% and 15.6%, respectively, vs. 4.1%; p = 0.02). Multivariate logistic regression analysis revealed NYP and multivessel disease as the independent risk factors of ACS events. CONCLUSIONS: Patients with multiple yellow plaques per vessel have a higher risk of suffering ACS events than those with NYP 0 or 1. Angioscopy would be useful to detect vulnerable patients.     

Chlamydia pneumoniae exposure and inflammatory markers in acute coronary syndrome (CIMACS)

Previous studies have shown higher levels of Chlamydia pneumoniae (C. pneumoniae, CP) antibody titers (CPIgG), C-reactive protein (CRP), and fibrinogen in patients with coronary artery disease. The role of these infectious and inflammatory markers in precipitating acute coronary syndrome (ACS) is unclear. We conducted a cross-sectional study on patients (n = 830, mean age 63 +/- 15 years, 57% male) admitted to the chest pain center of our institution. The differences in the CPIgG, CRP, and fibrinogen levels in patients who were diagnosed with ACS versus those who were not (non-ACS) were evaluated. CPIgG titers tended to be higher in the ACS group than in the non-ACS group. However, when different titers were used to define seropositivity, the difference achieved statistical significance only at the titer of > or =1:1,024 (35% vs 26%, p = 0.004). CRP (median 0.48 vs 0.33 mg/dl, p <0.0001), fibrinogen (median 317 vs 293 mg/dl, p <0.0001), and leukocyte count (median 7.7 vs 6.9 10(9)/L, p <0.0001) were higher in the ACS group. On multivariate analysis, CPIgG > or =1:1,024 (odds ratio [OR] 1.62), diabetes (OR 1.91), hypertension (OR 1.46), prior myocardial infarction (OR 1.78), smoking (OR 1.70), Caucasian race (OR 1.7), high-density lipoprotein (OR 0.98), and elevated troponin-T (OR 12.44) were the only factors independently associated with ACS. Thus, we found a strong association between high level seropositivity to CP and ACS. This may indicate recent re-infection or an exaggerated immune response to CP as an etiologic factor for ACS. This study also suggests that therapeutic interventions may need to be specifically targeted to these patients.     

肺炎衣原体感染与急性冠脉综合征的相互关系

目的探讨肺炎衣原体(CP)感染与急性冠脉综合征(ACS)的相互关系。方法应用固相酶联免疫吸附(ELISA)方法定量检测130例ACS患者、40例非ACS患者和50例健康者血清CP特异性抗体IgG,并同时应用乳胶颗粒凝集试验进行CRP测定。结果CP抗体和CRP阳性率在ACS组明显高于非ACS组和健康组,和健康组比较,P<0.01和P<0.05。结论CP感染可能通过影响动脉粥样硬化斑块的稳定性而增加ACS的危险性。     

Does chronic Chlamydia pneumoniae infection increase the risk of myocardial injury? Insights from patients with non-ST-elevation acute coronary syndromes

Background Cumulative evidence suggests a positive association between Chlamydia pneumoniae (Cpn) infection and risk of future coronary events among patients with stable coronary artery disease. However, its prognostic role in unstable coronary syndromes is less well defined. Because Cpn immunoglobulin A (IgA) may be a more reliable indicator of chronic infection than immunoglobulin G (IgG), we speculated that in patients with non-ST-elevation acute coronary syndromes (ACS), this marker might serve as a more useful prognostic tool. Accordingly, we evaluated plasma samples acquired at presentation in 178 patients with ACS for a possible association between Cpn IgA titer and biochemical evidence of myocardial injury. Methods Cpn IgG (positive if ≥1:32), and IgA titers (positive if ≥1:16) were measured by use of the microimmunofluorescence technique in 70 patients with ACS in whom myocardial injury developed associated with their presenting events (elevated CK-MB and/or troponin I); and in 108 patients with ACS without such injury. The odds ratios (ORs) for myocardial injury associated with consecutive antibody titers were determined for each of Cpn IgG and IgA. Multiple logistic regression was applied to adjust for key baseline characteristics. Results Median age of subjects was 64 years; 63% were male and 33% were smokers. The median antibody titers among those with and without myocardial injury respectively were as follows: IgG (1:128 vs 1:128), IgA (1:32 vs <1:16, P = .2). The adjusted ORs for myocardial injury associated with consecutive IgA titers were as follows: IgA ≥1:16, adjusted OR 1.49 (P = .22); ≥1:32, OR 1.95 (P = .04); ≥1:64, OR 1.37 (P = .38); ≥1:128, OR 0.77 (P = .55). No significant trend was found for any IgG titer. Conclusions Among patients with non-ST-elevation ACS, a Cpn IgA ≥1:32 at presentation was associated with a significantly higher risk of myocardial injury complicating the presenting event. (Am Heart J 2002;144:987-94.)     

Cytomegalovirus infection in ulcerative colitis

OBJECTIVE: Cytomegalovirus (CMV) infection has been reported as an exacerbating factor in inflammatory bowel disease but the relationship between CMV infection and ulcerative colitis (UC) remains unclear. There has been no detailed research to elucidate the clinicopathologic features of CMV infection in UC using surgical specimens. The aim of this study was to investigate the clinicopathologic features of CMV infection in UC patients who had undergone colectomy. MATERIAL AND METHODS: Surgical specimens taken from UC patients were examined for CMV infection. The patients were divided into three groups: severe, refractory, and UC-associated dysplasia or cancer according to the operative indications. CMV infection rates were evaluated and a comparison of clinical parameters was made between CMV-positive and CMV-negative patients, and the risk factors for CMV infection were analyzed using multivariate analyses. RESULTS: It was found that 25% of 32 patients were positive for CMV in the severe UC group; 8.3% of 72 patients were positive for CMV in the refractory UC group. None of the 22 patients was positive for CMV in the UC-associated dysplasia or cancer group. The CMV-positive rate in the severe UC group was significantly higher than that in the other groups (p<0.05). Patients' age at the time of operation was higher in the CMV-positive group than in the CMV-negative group among the patients with severe UC (p<0.01), and age at operation was an independent risk factor for CMV infection. CONCLUSIONS: CMV is found more frequently in severe UC than refractory UC and UC-associated cancer or dysplasia. Higher age can be a risk factor for CMV infection in patients with severe UC. However, a high steroid dose may not always be a risk factor for CMV infection.     

血清新碟呤与急性冠脉综合征患者冠脉病变程度的相关性

目的:分析血清新碟呤(neopterin,Npt)对评估急性冠脉综合征(ACS)冠状动脉病变的临床价值。方法:经冠状动脉造影(CAG)确诊的126例ACS患者,依据临床类型分为:ST段抬高型心肌梗死(STEMI)组45例,非ST段抬高型心肌梗死(NSTEMI)组40例,不稳定型心绞痛(UAP)组41例。采用ELISA法测定并比较各组血清Npt、白细胞介素-8(IL-8)及超敏C反应蛋白(hs-CRP)水平,分析其与冠状动脉病变类型及斑块类型的关系。结果:血清Npt浓度在STEMI组中高于NSTEMI及UAP组(P<0.05),而IL-8及hs-CRP在3组中无显著差异。血清Npt浓度在冠脉复杂病变中显著高于冠脉简单病变与冠脉临界病变(P<0.05),而IL 8及hs CRP在3种病变中无显著差异。Ⅱ型、Ⅲ型斑块患者中血清Npt浓度高于Ⅰ型斑块患者(P<0.05),而IL-8及hs-CRP在3种斑块类型中无显著差异。结论:血清Npt与冠脉综合征患者冠脉病变程度相关,可能成为有效评估ACS患者冠脉病变程度的一个指标。     

Mid-Term Clinical Outcomes of ACS and Non-ACS Patients Treated With Everolimus-Eluting Stents

Drug-eluting stents (DES) have proven to be effective for reducing the rate of restenosis, whereas stent thrombosis (ST) after DES implantation has raised safety concerns. Everolimus-eluting stents (EES) are a new generation of DES that have demonstrated safety and efficacy compared with first-generation DES. However, the use of EES in patients presenting with acute coronary syndrome (ACS) has not been adequately investigated. We compared the clinical outcomes between the ACS and non-ACS groups treated with EES. A total of 335 consecutive patients who received EES implantation between January 2010 and January 2011 were investigated (ACS; n = 172, non-ACS; n = 163). Clinical outcome data were obtained for 94.3% of the patients. Follow-up angiography was performed in 58.5% of all patients. The median follow-up period was 8 months in both groups. Clinical outcomes were not statistically different between the groups. The rate of target lesion revascularization (TLR) was 2.5% in the ACS group and 3.8% in the non-ACS group (P = 0.37). MACE occurred in 8.2% of the ACS group and 10.2% of the non-ACS group (P = 0.54). A definite ST was identified in one patient in each group (P = 0.75). The unadjusted cumulative event rates estimated by the Kaplan-Meier method and the log-rank test showed no significant difference between the groups for TLR, target vessel revascularization (TVR), all-cause death, or MACE. In conclusion, EES was safe and efficacious for patients presenting with ACS, as well as for those with non-ACS during a mid-term follow-up period.     

髓过氧化物酶早期识别急性冠状动脉综合征的临床价值

目的:探讨髓过氧化物酶(MPO)浓度与急性冠状动脉综合征(ACS)的关系及其早期识别ACS的临床价值。方法: 采用酶联免疫吸附法测定血浆MPO浓度。 结果: ACS组患者血浆MPO浓度明显升高,与正常对照组、稳定型心绞痛（SAP）组比较差异有统计学意义（P<0.05）。SAP组血浆MPO浓度高于正常对照组（P<0.05）。血浆MPO浓度与中性粒细胞、肌酸激酶同工酶及受试组呈正相关,与年龄、高敏感C反应蛋白、总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、三酰甘油、天冬氨酸氨基转移酶、空腹血糖、乳酸脱氢酶、红细胞计数、血小板计数无相关性。依据临床表现和冠状动脉造影,临床诊断ACS 41例, 非ACS组37例,绘制ROC曲线（A=0.927,P=0.000）。MPO诊断界值为212.59 μg/L,MPO≥212.59 μg/L为阳性,诊断为ACS,MPO<212.59 μg/L为阴性,诊断非ACS。临床诊断ACS 41例中,MPO阳性39例,阴性2例,非ACS组37例中,MPO阳性5例,阴性32例,MPO诊断ACS灵敏度为95%,特异度为86%,准确度为91%,假阴性率(漏诊率)为5%,假阳性率(误诊率)为14%,阳性预测值为89%,阴性预测值为94%。本法与临床诊断ACS方法进行Kappa一致性检验,Kappa系数值为0.819,P=0.000,说明两种方法的吻合程度具有统计学意义,两法一致性较好。采用Logistic逐步回归,筛选出有统计学意义的影响因素为MPO 、低密度脂蛋白胆固醇和肌酸激酶同工酶,建立预测模型,MPO预测ACS总正确率为95%,提示MPO对ACS具有较高的预测价值。结论: MPO能有效地早期识别ACS。     

Serologic markers for cytomegalovirus in acute coronary syndromes.

BACKGROUND: Several studies relate cytomegalovirus (CMV) infection to the development of atherosclerosis. Its influence in triggering acute coronary syndromes (ACS) is not known. OBJECTIVES: We set out to identify a relationship between CMV infection, occurrence of ACS and prognosis. METHODS: Serologic markers (IgM and IgG) for CMV were tested prospectively at admission and at 30 days, in patients (pts) admitted to our CCU for ACS. Serologic markers for CMV were also tested in a group of pts with stable coronary artery disease admitted for elective coronary angiography. A greater than two-fold elevation of IgG titer at 30 days was defined as reactivation/reinfection. At 30 days and six months, the composite endpoint of death, myocardial (re)infarction and re-admission for unstable angina was evaluated. RESULTS: There were 60 pts with ACS in the study group (age 63 +/- 10 years, 75% male) and 31 pts in the control group (age 64 +/- 10 years, 71% male). On admission, 95% of the pts with ACS and 81% in the control group presented a positive IgG (p = 0.029). In the study group, at 30 days, the only pt with a 3-fold titer elevation had an endpoint. The percentage was 17% for the group with a > or = 2- and < 3-fold elevation and 11% in the group without reactivation (p = 0.034). At six months, 50% of the patients with a greater than 2-fold titer elevation and 15% of the remaining patients had an endpoint (p = 0.017). In the control group, at 30 days, 3 pts (10%) had a significant elevation in IgG titer, > or = 2- and < 3-fold, without endpoint. CONCLUSIONS: In pts with ACS, we found a higher prevalence of serologic markers for CMV than in pts with stable coronary disease. An elevation in IgG titer for CMV was associated with a worse outcome at 30 days and six months.     

CD14 C(-260)T promoter polymorphism and prevalence of acute coronary syndromes

BACKGROUND: Inflammation and infection have been implicated in atherosclerosis and its complications. The CD14 receptor mediates monocyte activation by lipopolysaccharide (LPS) of Gram-negative bacteria. The aim of this study was to assess whether the C(-260)T polymorphism in the promoter of the CD14 receptor gene is associated with a higher prevalence of acute coronary syndromes (ACS) and severity of coronary atherosclerosis. METHODS: We studied 428 patients (mean age: 63+/-10 years, 67% men) consisting of 334 patients with coronary artery disease (CAD) and 94 patients with normal coronary arteriogram. Patients with CAD were subdivided in two groups: (1) no previous history of ACS (n=140; 64+/-9 years; 79% men) and (2) patients with a history of ACS (n=194; 64+/-10 years; 80% men). CD14 genotypes were determined by a Polymerase Chain Reaction (PCR)-Restriction Fragment Length Polymorphism Analysis (RFLP) technique. RESULTS: Patients with a prior ACS had a significantly higher frequency of the T/T genotype than CAD patients without prior ACS (33% vs. 20%; P=0.009), even after multivariate analysis (odd ratio [OR] 1.8 [1.1-3.1]; confidence intervals [CI] 95%; P=0.023). T/T genotype was not significantly different in CAD patients without prior ACS compared to controls (20% vs. 22.3%; P=0.67), and there was no significant association between genotypes, or allele frequencies, and severity of CAD. CONCLUSIONS: The CD14 C(-260)T polymorphism is associated with a history of ACS and it may represent a genetically determined risk factor for the development of ACS and atheromatous plaque vulnerability in angina patients.     

Cytomegalovirus infection is associated with elevated interleukin-10 in coronary artery disease

Previous studies show that cytomegalovirus (CMV) infection could increase the production of inflammatory cytokines in coronary artery disease (CAD). However, little is known about the influence of CMV infection on interleukin-10 (IL-10) levels in CAD. We attempted to investigate the relationships between CMV infection and serum IL-10 levels in patients with CAD. CMV IgG and serum levels of IL-10 were measured with ELISA in patients with CAD (n=463) and smooth coronary artery controls documented by coronary arteriography (n=125). Subjects were dichotomized according to calculated median level of IL-10 (6.84 pg/ml) in different groups or subgroups. The seropositivity of CMV IgG was more frequently found in the high IL-10 group than the low IL-10 group (46.8% versus 30.4%, P<0.001). The prevalence of CMV infection was significantly higher in the high IL-10 group than the low IL-10 group among the patients with CAD (48.1% versus 28.6%, P<0.001), but among the controls (40.4% versus 35.6%, P=0.588). On multiple logistic regression analysis, the adjusted odds ratio (95% confidence intervals) of high IL-10 associated with CMV infection was 2.3 (1.6-3.4, P<0.001) in the patients with CAD, and 1.1 (0.5-2.5, P=0.83) in the controls. We found a significant association of CMV infection with elevated IL-10 in the patients with CAD; therefore, we propose that changes in the immune response to CMV are a compounding factor in CAD.