术前sCD40L预测冠脉支架后再狭窄的临床价值研究

目的探讨冠心病患者支架植入术前sCD40L对再狭窄的诊断预测价值。方法选择成功接受普通支架置入术的稳定型心绞痛和不稳定型心绞痛患者共92例,分别于支架术前,术后第1、5、15天和180天取外周静脉血测定血清sCD40L。所有患者随访6个月。结果支架内再狭窄率23.9%(22/92)。再狭窄患者支架术前和术后血清sCD40L浓度均显著高于无再狭窄患者术前sCD40L浓度;再狭窄患者支架术后高水平sCD40L持续至术后6个月,而无再狭窄患者术后5天恢复至正常。根据受试者工作特征曲线确定术前血清sCD40L>3.96μg/L为截断值,计算术前sCD40L诊断再狭窄的敏感性、特异性、阳性预测值(PPV)、阴性预测值(NPV)、准确度和阳性似然比分别为72.7%、90%、69.6%、91.3%、85.9%和7.27。多变量Logistic回归分析发现,在校正混杂因素后,术前sCD40L是术后再狭窄独立预测因子,OR1.92(95%CI1.39～2.64,P=0.013)。结论再狭窄患者支架术前、术后血清sCD40L水平增加提示可能与支架内再狭窄有关。支架术前血清sCD40L是术后再狭窄的独立预测因子,术前sCD40L有...     

Preprocedural C-reactive protein levels and cardiovascular events after coronary stent implantation.

OBJECTIVES: This study assessed the predictive value of preprocedural C-reactive protein (CRP) levels on six-month clinical and angiographic outcome in patients undergoing coronary stent implantation. BACKGROUND: Recent data indicate that low-grade inflammation as detected by elevated CRP serum levels predicts the risk of recurrent coronary events. METHODS: We prospectively investigated the predictive value of preprocedural CRP-levels on restenosis and six-month clinical outcome in 276 patients after coronary stent implantation. The primary combined end point was death due to cardiac causes, myocardial infarction related to the target vessel and repeat intervention of the stented vessel. RESULTS: Grouping patients into tertiles according to preprocedural CRP-levels revealed that, despite identical angiographic and clinical characteristics at baseline and after stent implantation, a primary end point event occurred in 24 (26%) patients of the lowest tertile, in 42 (45.6%) of the middle tertile and in 38 (41.3%) of the highest CRP tertile, p = 0.01. On multivariate analysis, tertiles of CRP levels were independently associated with a higher risk of adverse coronary events (relative risk = 2.0 [1.1 to 3.5], tertile I vs. II and III, p = 0.01) in addition to the minimal lumen diameter after stent (p = 0.04). In addition, restenosis rates were significantly higher in the two upper tertiles compared with CRP levels in the lowest tertile (45.5% vs. 38.3% vs. 18.5%, respectively, p = 0.002). CONCLUSIONS: Low-grade inflammation as evidenced by elevated preprocedural serum CRP-levels is an independent predictor of adverse outcome after coronary stent implantation, suggesting that a systemically detectable inflammatory activity is associated with proliferative responses within successfully implanted stents.     

Association between plasma pregnancy-associated plasma protein a and restenosis after percutaneous coronary angioplasty

BACKGROUND: Restenosis after percutaneous coronary angioplasty remains an important limitation of this procedure. This study evaluates the association between plasma pregnancy-associated plasma protein A (PAPP-A) levels and restenosis after coronary angioplasty. METHODS AND RESULTS: Blood samples were collected from all patients at baseline, and their levels of PAPP-A, inflammation (high-sensitivity C-reactive protein (hsCRP)) and platelet activation (soluble CD40 ligand (sCD40L)) were determined. Those patients whose PCI was successful underwent a repeat angiography at a median of 6.4 months (interquartile range 6-9.8 months). Their baseline and follow-up angiograms were compared by quantitative coronary angiography to assess the incidence of restenosis. Endpoints were restenosis (> or =50%) and a composite of major adverse cardiac events. Of the 184 patients, 162 patients underwent an angiographic follow up at 6 months. Patients with restenosis had significantly higher PAPP-A levels than those without (19.24+/-2.56 vs 11.95+/-2.32 mIu/L; p<0.001). The PAPP-A levels were significantly correlated to follow up diameter stenosis (r=0.54, p=0.01). Late lumen loss at follow-up was significantly smaller when PAPP-A levels were <12.51 mIu/L (0.55+/-0.61 vs 0.90+/-0.57 mm; p<0.001). The rates for restenosis (28.4 vs 50.6%; p<0.001) and major advent cardiac events (15.6 vs 51.1%, p<0.001) were significantly lower in patients with PAPP-A levels <12.51 mIu/L. Univariate analysis revealed that PAPP-A (p<0.001), hsCRP (p=0.009) and sCD40L (p=0.03) were significantly related to restenosis. However, only PAPP-A could predict restenosis (odds ratio 0.95; 95% confidence interval 0.84-1.13; p=0.02) in multivariate analysis. CONCLUSIONS: The PAPP-A level is a strong independent predictor of restenosis in patients who have undergone coronary angioplasty.     

Plasma levels of C-reactive protein after coronary stent implantation.

AIMS: This study was designed to investigate the role of inflammation on the occurrence of angiographic restenosis 6 months after coronary stent implantation and the influence of different kinds of antithrombotic and antiplatelet strategies on inflammation. METHODS AND RESULTS: In an open randomized trial, 40 consecutive patients were treated with aspirin (100 mg. day(-1)) and either ticlopidine (2x250 mg. day(-1)) (n=17), or phenprocoumon (INR 2.0-3.0) and dipyridamole (3x160 mg. day(-1)) (n=23) after successful elective coronary stent implantation. Plasma levels of C-reactive protein were determined one day before stent implantation and serially thereafter twice daily up to 120 h. C-reactive protein plasma levels increased significantly (P<0.0001) after stent implantation. Phenprocoumon and dipyridamole or ticlopidine had no effect on C-reactive protein plasma levels (P=0.51) or the occurrence of angiographic restenosis (P=0.48). C-reactive protein plasma levels were significantly higher in patients with lesion type C compared to types A or B (P=0.035), respectively. C-reactive protein plasma levels were significantly higher and mean shoulder levels occurred 48 h later in patients with restenosis compared to patients without restenosis after 6 months (P=0.038). CONCLUSIONS: Elevated C-reactive protein plasma levels still persisting 96 h after stent implantation might reflect a prolonged inflammatory reaction to coronary stent implantation which might causally be involved in pathophysiological mechanisms leading to restenosis.     

Relationship between plasma inflammatory markers and platelet aggregation in patients with clopidogrel resistance after angioplasty

We evaluated the relationship between plasma inflammation markers and clopidogrel resistance in patients after stent implantation. The plasma levels of C-reactive protein (CRP), P-selectin, platelet soluble CD40 ligand (sCD40L), interleukin 6 (IL-6) and platelet aggregation were measured in 352 patients undergoing percutaneous coronary intervention (PCI) at baseline and after 6 months. The plasma levels of CRP, P-selectin, sCD40L, IL-6 was higher in 65 (18.5%) patients with clopidogrel resistance than in those with normal responsiveness at 6 months after PCI. There was a significant positive correlation between soluble CD40L levels and platelet aggregation (r = .28, P < .05). Diabetes (DM) and sCD40L level were independent predictors for unresponsiveness after stent implantation according to stepwise multivariate analyses. The hazard ratio (HR) for sCD40L level was 3.02 (95% CI = 1.28 to 3.25; P = .036) and for DM 2.53 (95% CI = 1.28 to 6.55, P = .03). We conclude that sCD40L and DM may influence clopidogrel resistance.     

Sustained elevation of serum CD40 ligand levels one month after coronary angioplasty predicts angiographic restenosis

BACKGROUND: Percutaneous coronary intervention induces an early inflammatory reaction. The intensity of such a reaction as measured by high-sensitivity C-reactive protein has been correlated with recurrent ischemic events, but its association with restenosis remains uncertain. OBJECTIVES: To characterize the type and duration of the postangioplasty inflammatory reaction and to identify new inflammatory markers correlating with restenosis. METHODS: Fifty-three consecutive patients who underwent successful balloon angioplasty were studied. Levels of specific inflammatory markers were measured before intervention, and at one-month and six-month follow-up. Six-month clinical and angiographic follow-up was conducted in all patients, and quantitative coronary analysis was systematically performed. RESULTS: Levels of soluble CD40 ligand (sCD40L) and matrix metalloproteinase-2 showed a rise and fall pattern over six months, with peak levels measured at one month (P < 0.0001), while levels of soluble vascular cell adhesion molecule-1 increased after angioplasty and remained elevated at six months (P = 0.07). Plasma levels of sCD40L at one month correlated with angiographic late loss (r = 0.48, P = 0.001) and were predictive of six-month restenosis (area under receiver operating characteristic curve 0.75 [95% CI 0.61 to 0.88]). CONCLUSIONS: The results imply that inflammation persists for at least one month following angioplasty and that future therapeutic interventions targeting inflammation to prevent restenosis should be active during this period. Furthermore, the ability of sCD40L levels to predict restenosis at six months may indicate the relevance of this pathway as a therapeutic target for restenosis prevention.     

Predictive value of preintervention C-reactive protein on clinical outcome after directional coronary atherectomy followed by stent implantation.

BACKGROUND: Preprocedural C-reactive protein (CRP) serum levels have been shown to predict the recurrence of angina or major adverse cardiac events after percutaneous coronary intervention. Directional coronary atherectomy (DCA), by reducing residual plaque burden and restenosis, has been shown to improve clinical outcome after coronary stenting. Thus, we assessed the influence of preprocedural CRP serum levels on the recurrence of cardiac events after DCA followed by bare metal stent implantation. METHODS: We enrolled 40 consecutive patients (34 males; 61+/-10 years old) with single-vessel disease who were undergoing DCA. In all patients, preprocedural CRP serum levels were measured by an ultrasensitive nephelometric method. The endpoint of the study was defined as the composite incidence of death, myocardial infarction, and recurrence of angina requiring repeat revascularization at 6-month follow-up. RESULTS: CRP serum levels were a significant independent predictor of the composite endpoint at multiple regression analysis [odds ratio=1.69; 95% confidence interval (95% CI)=1.04-2.75; P=.033]. Patients with recurrence of cardiac events had CRP serum levels higher than those of patients not having events on follow-up [3.95 (2.2-5.7) vs. 2 (1.3-3.3); P=.05]. CONCLUSION: In conclusion, our study shows that baseline CRP serum levels predict cardiac events after coronary bare metal stenting despite plaque debulking with directional atherectomy.     

Comparison of effects of drug-eluting stents versus bare metal stents on plasma C-reactive protein levels

After coronary stenting, inflammatory mechanisms play a crucial role in the pathogenesis of neointimal proliferation and in-stent restenosis. Drug-eluting stents (DESs) have been shown to decrease in-stent restenosis in different studies. We compared plasma C-reactive protein (CRP) levels after DES implantation with levels after bare metal stent (BMS) implantation. We performed percutaneous coronary intervention with a single stent in 67 patients (54 men; 59 +/- 9 years of age; n = 21 in the BMS group, n = 46 in the DES group) who had stable angina. Plasma CRP levels were determined before intervention and at 48 hours, 72 hours, and 2 weeks after coronary stenting. There was no difference in clinical and angiographic baseline characteristics except that the DES group had more patients with diabetes (34.8% vs 9.5%, p = 0.04), smaller reference vessels (2.95 +/- 0.53 vs 3.29 +/- 0.53 mm, p = 0.02), and smaller stent diameters (3.0 +/- 0.4 mm vs 3.4 +/- 0.5 mm, p <0.01). Plasma CRP levels at 48 hours (13.4 +/- 14.7 vs 5.9 +/- 4.9 mg/L, p <0.01) and 72 hours (16.7 +/- 19.8 vs 5.4 +/- 3.9 mg/L, p <0.01) after stent implantation were significantly higher in the BMS than in the DES group. In conclusion, DESs showed significantly lower plasma CRP levels after coronary stenting compared with BMSs. This may reflect the potent effects of DESs on acute inflammatory reactions induced by coronary intervention.     

The relationship between preprocedural platelet size and subsequent in-stent restenosis

OBJECTIVE: Elevated mean platelet volume predicts restenosis after percutaneous transluminal coronary angioplasty but its effect on the development of in-stent restenosis is not known. We assessed the effect of mean platelet volume measured before coronary stent implantation for stable angina pectoris on subsequent development of in-stent restenosis. METHODS AND RESULTS: We retrospectively analysed the data of 60 patients who had stent implantation on one native coronary artery for stable angina pectoris and control angiographies for clinically suspected restenosis within 6 months. Mean platelet volume was measured by auto analyzer one day before stent implantation. Clinical and demographic data and laboratory results were obtained from the hospital charts of the patients. In-stent restenosis was evaluated visually from control angiograms. Angiographic in-stent restenosis was present in 35 (58%) of 60 patients and 25 (42%) patients had no restenosis. Mean platelet volume in the in-stent restenosis group was 8.28 +/- 0.71 fl compared to 7.63 +/- 0.74 fl in the no-restenosis group (p = 0.001). There was a positive correlation between preprocedural mean platelet volume and development of in-stent restenosis (r = 0.44; p < 0.001). A mean platelet volume value of > or = 8.4 fl was associated with an odds ratio of 16.0 for development of in-stent restenosis, with high specificity and positive predictivity but poor sensitivity and negative predictivity (96%, 93%, 40% and 53%, respectively). CONCLUSIONS: Mean platelet volume measured before stent implantation is correlated with subsequent development of in-stent restenosis. If preprocedural mean platelet volume is greater than 8.4 fl, in-stent restenosis is more probable to occur.     

Predictive value of preprocedural fibrinogen concerning coronary stenting

Elevated fibrinogen levels after coronary balloon angioplasty have been reported to be useful in predicting restenosis. Therefore, we sought to evaluate the relationship between preprocedural fibrinogen levels and the 6-12-month outcomes of patients undergoing coronary stenting. Plasma levels of fibrinogen were measured in 390 consecutive patients prior to coronary stenting. The primary end point was binary restenosis (percent diameter stenosis of >/=50%). The secondary combined end point was death due to cardiac causes, myocardial infarction related to the target vessel and target lesion revascularization. Patients were grouped into tertiles according to fibrinogen levels. Both at baseline and immediately after procedure, clinical and angiographic characteristics were almost identical in the fibrinogen tertiles. An increase in restenosis rate was observed across the tertiles (18.6, 23.9, 38.1%, P<0.001, respectively). In addition, the frequency of the secondary end point increased in the highest tertile (14.9, 21.5, 37.2%, P<0.001, respectively). Multivariate analysis revealed that high levels of fibrinogen (per 100 mg/dl, OR 1.82, P<0.001) and stent length (P=0.034) were independent predictors for restenosis. An elevated preprocedural fibrinogen level should be considered as a stronger predictor for restenosis after coronary stenting, which might be associated with coagulation and inflammation.     

Increased secretion of insulin during oral glucose tolerance test can be a predictor of stent restenosis in nondiabetic patients.

Insulin is known to stimulate proliferation and migration of vascular smooth muscle cells. As the predominant mechanism of restenosis after stent implantation is neointimal tissue proliferation, one can expect a relationship between hyperinsulinemia and restenosis in these patients. The aim of this study was to determine whether hyperinsulinemia during oral glucose tolerance test is a predictor of the development of restenosis after stent implantation in nondiabetic patients. We prospectively studied 52 nondiabetic patients with effort angina who underwent elective stent implantation for single-vessel coronary artery disease. In order to increase the statistical power of the study, numerous exclusion criteria were applied. All patients were subjected to a 75 g oral glucose tolerance test a day before the stent implantation and underwent follow-up angiography 6 months later. Plasma insulin levels in fasting (6.77 +/- 1.57 vs. 5.36 +/- 1.35 micro U/ml; P = 0.005), at 30 min (102.48 +/- 10.6 vs. 47.74 +/- 12.75 micro U/ml; P = 0.001), 1 hr after (120.23 +/- 14.1 vs. 63.08 +/- 12.62 micro /ml; P = 0.001), 2 hr after (63.58 +/- 8.64 vs. 34.88 +/- 6.82 micro /ml; P = 0.001), and 3 hr after (25.71 +/- 5.65 vs. 23.02 +/- 4.61 micro /ml; P = 0.04) loading were significantly higher in patients with stent restenosis than in patients without stent restenosis. Insulin area and insulin area/glucose area were also significantly higher in patients with stent restenosis than in patients without (219.5 +/- 23.8 vs. 118.9 +/- 21.8, P = 0.001, and 0.62 +/- 0.09 vs. 0.33 +/- 0.06, P = 0.001, respectively). By multiple logistic regression analysis, insulin area during oral glucose tolerance test was found to be an independent predictor of stent restenosis (OR = 1.12; 95% CI = 1.01-1.25; P = 0.031). In conclusion, nondiabetic patients with hyperinsulinemia during oral glucose tolerance test have a high risk for restenosis after stent implantation, and performing this simple test before intervention may be useful for the prediction of stent restenosis.     

Preprocedural high-sensitivity C-reactive protein predicts death or myocardial infarction but not target vessel revascularization or stent thrombosis after percutaneous coronary intervention

BackgroundHigh-sensitivity C-reactive protein (hs-CRP) elevation is associated with poor clinical outcome in patients with coronary artery disease (CAD). However, the prognostic value of preprocedural hs-CRP elevation before coronary stent implantation remains debated especially regarding restenosis and target vessel revascularization (TVR). Furthermore, whether hs-CRP elevation may predict stent thrombosis (ST) is unknown.MethodsWe included 560 consecutive patients, who underwent coronary stent implantation in our institution. Blood samples for hs-CRP determination were obtained immediately before the procedure. During a median follow-up of 12.5 months, cardiovascular events including death, myocardial infarction (MI), TVR, and ST were systematically included.ResultsMedian hs-CRP was 3.10 [25–75th percentile: 1.36-8.63] mg/l. There were 27 (4.8%) deaths, 17 (3.1%) nonfatal MI, 58 (10.5%) TVR, and 12 (2.1%) ST. The composite criteria death–MI occurred in 44 (7.9%) patients. Independent predictors of the composite death–MI were hs-CRP level [hazard ratio (HR)=1.33 (95% CI: 1.05-1.70); P=.021], diabetes (P=.003), and multivessel CAD (P=.011). The composite death–MI occurred in 31 (13.3%) of the 233 patients with hs-CRP >4.63 mg/l vs. 13 (4.0%) of the 327 patients with hs-CRP <4.63 mg/L (P<.001). By contrast, hs-CRP predicted neither TVR [HR=0.88 (0.73-1.08); P=.23] nor ST [HR=1.15 (0.77-1.71); P=.49].ConclusionHigh hs-CRP levels before coronary stent implantation are associated with risk of death or MI, but are not related to TVR or ST. These data suggest that preprocedural hs-CRP is more a predictor of global cardiovascular risk than a predictor of stent-related complications.     

Association between plasma lipoprotein(a) concentration and restenosis after stent implantation.

BACKGROUND: The plasma concentration of lipoprotein (a) [Lp(a)] is associated with atherosclerotic and thrombotic vascular diseases. The aim of the present study was to evaluate the association between plasma Lp(a) concentration and in-stent restenosis. METHODS AND RESULTS: One hundred and 9 patients with successful elective coronary stent implantation underwent follow-up angiography at 24+/-6 weeks. Restenosis after stent implantation occurred in 38 patients. Univariate analysis showed that the reference diameter of the lesion was smaller in the restenosis group (2.93+/-0.29 mm) than in the no-restenosis group (3.21+/-0.43 mm) (p < 0.05). The lesion was longer in the restenosis group (14.2+/-5.3 mm) than in the no-restenosis group (11.6+/-4.9 mm) (p < 0.05). Plasma Lp(a) concentrations in the restenosis group (30.5+/-23.9 mg/dl) were higher than in the no-restenosis group (16.9+/-11.1 mg/dl) (p < 0.01). Other lipid concentrations were similar in both groups. Among the plasma Lp(a) concentrations, the rate of restenosis (71.4%) in the high Lp(a) group (> 40 mg/dl) (n = 14) was greater compared with the other groups: 33.3% in the intermediate Lp(a) group (10-40 mg/dl) (n = 54), and 24.4% in the low Lp(a) group (< 10 mg/dl) (n = 41) (p < 0.01). The late loss (0.57+/-0.53 mm) in the low Lp(a) group was significantly less than the other groups: 0.88+/-0.47 mm in the intermediate Lp(a) group, and 1.08+/-0.56 mm in the high Lp(a) group (p < 0.05). In a multivariate regression model, plasma Lp(a) concentration remained significant as an independent predictor of restenosis in patients undergoing stent implantation (p = 0.020 odds ratio (OR) 1.37 95%conficence interval (CI) 1.050-1.793), although the reference diameter (p = 0.025 OR 0.23 95%CI 0.061-0.830) and lesion length (p = 0.021 OR 1.12 95%CI 1.017-1.232) were related to stent restenosis. CONCLUSIONS: Plasma Lp(a) concentration is an independent predictor of stent restenosis.     

Plasma monocyte chemoattractant protein-1 antigen levels and the risk of restenosis after coronary stent implantation

Monocyte chemoattractant protein-1 (MCP-1) plays a fundamental role in monocyte recruitment and has been implicated in atherosclerosis. The present study tested the hypothesis that increased levels of MCP-1 are associated with an increased risk for restenosis post stent implantation. The plasma MCP-1 antigen levels were measured pre-stenting, and at 24 and 48 h and 6 months post stenting in 41 patients with stable exertional angina (SEA) who had undergone successful stent implantation. Nineteen patients with chest pain syndrome were selected as a control group. Initial plasma MCP-1 antigen levels (mean +/- SE, pg/ml) in the patients with SEA were significantly higher than those in the control group (852.3+/-51.4 vs 418.2+/-26.7, p<0.001). The patients with SEA were divided into 2 groups based on follow-up angiographic findings: 17 patients with restenosis (R group); 24 patients without restenosis (N group). The lesion was significantly longer in the R group than in the N group (p<0.03). Plasma MCP-1 antigen levels at pre-stenting were not significantly different between the 2 groups (820.6+/-69.1 in the R group vs 874.7+/-73.8 in the N group). Serial changes of plasma MCP-1 levels were plotted as percent changes from the initial levels (mean +/- SE, %) and were significantly higher in the R group than in the N group at 48 h and at 6 months post stent implantation (104.6+/-4.8 vs 89.2+/-3.4, p<0.01, 109.6+/-11.2 vs 98.5+/-5.0, p<0.05). The study concludes that MCP-1 production at stented coronary arterial sites is associated with an increased risk for restenosis post stent implantation.     

Serial changes in circulating concentrations of soluble CD40 ligand and C-reactive protein in patients with unstable angina undergoing coronary stenting.

BACKGROUND: This study tested the hypothesis that serum concentrations of high-sensitivity C-reactive protein (hs-CRP) and soluble CD40 ligand (sCD40L) significantly reflect serial changes in patients with unstable angina, and thus the serum concentrations of these inflammatory biomarkers may be good candidates for predicting late restenosis after coronary stenting. METHODS AND RESULTS: The circulating concentrations of sCD40L and hs-CRP were prospectively measured (both pre-procedure, and on days 21, 90, and 180 after the procedure) in 77 consecutive patients with unstable angina undergoing coronary stenting. These inflammatory mediators were also evaluated in 30 healthy volunteers. The serum concentrations of sCD40L and hs-CRP were significantly higher pre-procedure in study patients than in normal control subjects (all p values < 0.0001). These inflammatory markers then declined to a substantially lower concentration by day 21 (all p values < 0.05). Circulating concentrations of hs-CRP in each patient then differed little from each other afterwards. However, the sCD40L concentration was once again raised significantly on days 90 and 180 as compared to day 21 (both p values < 0.05). This study found no significant link between raised circulating concentrations of sCD40L and hs-CRP and late restenosis. CONCLUSIONS: Circulating concentrations of sCD40L and hs-CRP were significantly increased in unstable angina patients pre-procedure and declined substantially thereafter. However, the circulating concentrations of these 2 inflammatory mediators were not useful in predicting late restenosis following coronary stenting.     

Plasma, serum, and platelet expression of CD40 ligand in adults with cardiovascular disease

The application of soluble CD40 ligand (sCD40L) as a biomarker has garnered great scientific and clinical interest. However, there are many uncertainties with regard to the biology of sCD40L. Although presumed to be a marker of platelet activation, relative levels in plasma, serum, and platelet expression are unknown, as is the optimal method for its measurement. We measured CD40L from serum, platelet-poor plasma, and platelet surface in adults who had stable cardiovascular disease (CVD) and those who had unstable CVD (n = 40). Plasma sCD40L did not differ significantly between groups. Serum sCD40L was significantly lower (1.4 +/- 1.3 vs 5.2 +/- 3.7 ng/ml, p <0.001) and platelet membrane CD40L expression was higher (1.4 +/- 0.7% vs 0.9 +/- 0.6%, p = 0.03) in unstable compared with stable CVD. When the 2 groups were considered together, there was a significant correlation between plasma and serum sCD40L levels (rho = 0.4, p = 0.02) and negative correlations between plasma (rho = -0.3, p = 0.04) and serum (rho = -0.4, p = 0.01) sCD40L levels with platelet membrane CD40L expression. In unstable CVD, the correlation between sCD40L measurements was poor. Consistent with enhanced platelet activation, there was a positive correlation between platelet aggregation and surface CD40L expression (rho = 0.5, p = 0.02) and between platelet expression of CD40L and P-selectin (rho = 0.4, p = 0.05) in unstable CVD. There was no correlation between CD40L and platelet count or C-reactive protein. Only surface expression of CD40L compared with platelet-derived (plasma) or total (serum) CD40L level proved a reliable marker of platelet function in patients who had stable CVD and those who had unstable CVD. In conclusion, our data demonstrate the complex nature of CD40L and highlight the distinct processes of expression, shedding, and clearance of this ligand in patient populations.     

Drug-eluting stent-supported percutaneous coronary intervention for chronic total coronary occlusion.

OBJECTIVES: This study sought to determine the clinical and angiographic outcomes after drug-eluting stent (DES)-supported percutaneous coronary intervention (PCI) for chronic total coronary occlusion (CTO). BACKGROUND: There are few data about the efficacy of DES-supported PCI for CTO. METHODS: All consecutive patients who had a sirolimus-eluting stent or a paclitaxel-eluting stent implanted for CTO from December 2003 to December 2004 were analyzed. Clinical and angiographic outcomes of patients treated with DES were compared with a case-matched control group of patients treated with bare metal stents (BMS) in the 12 months before the routine use of DES. RESULTS: Successful DES-supported PCI was performed in 92 patients and 104 CTO. The case-matched control group consisted of 26 patients and 27 CTO successfully treated with BMS. There were no differences between groups in baseline clinical and angiographic characteristics. Stent length in the DES group was higher as compared with that of BMS group (51+/-28 mm vs. 40+/-19 mm, P=0.073). The 6-month major adverse cardiac event (MACE) rate was lower in the DES group as compared with that of BMS group (9.8% vs. 23%, P=0.072). The angiographic follow-rate was 80% in the DES group and 81% in the BMS group. The 6-month restenosis rate was 19% in the DES group and 45% in the BMS group (P<0.001). By multivariate analysis, it was found that in the DES group, the only predictors of restenosis were stented segment length (OR 1.031, 95% CI 1.01-1.06, P=0.009) and a target vessel reference diameter<2.5 mm (OR 6.48, 95% CI 1.51-27.83, P=0.012), while the only predictor of MACE was stent length (OR 1.04, 95% CI 1.01-1.08, P=0.006). CONCLUSIONS: DES implantation for CTO decreases the risk of mid-term restenosis and MACE. Small vessels and diffuse disease requiring the implantation of multiple stents and very long stents for full coverage of the target lesion are still associated with a relatively high risk of restenosis.     

老年动脉粥样硬化不稳定斑块患者多种生化指标的变化及意义

目的通过对入选病例行氧化应激、炎症、免疫及血栓形成等方面的多种生化指标的检测,评价这些指标在老年动脉粥样硬化不稳定斑块患者中的变化情况及临床意义。方法选取105例经64层螺旋CT(64-MSCT)颈动脉成像确诊为颈动脉粥样硬化斑块的老年患者,根据CT结果分为稳定斑块组(55例)、不稳定斑块组(50例),分别测定血浆C反应蛋白(CRP)、丙二醛(MDA)、可溶性CD40配体(sCD40L)、同型半胱氨酸(HCY)、纤维蛋白原(FIB)水平。结果不稳定斑块组的CRP、MDA,sCD40L,FIB及HCY水平均显著高于稳定斑块组(P<0.05);不稳定斑块组与稳定斑块组的Logistic回归分析表明仅sCD40、CRP、吸烟是显著影响动脉粥样硬化不稳定斑块病变的因素(P<0.05)。结论血浆生化指标CRP、HCY、FIB、MDA、sCD40L水平的升高与老年动脉粥样硬化不稳定斑块病变显著相关,其中血浆高水平的CRP、sCD40L是影响不稳定斑块病变的独立因素,CRP及sCD40L水平的变化可能更能预测老年动脉粥样硬化不稳定斑块病变,尤其是特异性较高的sCD40L。     

Association between circulating level of CD40 ligand and angiographic morphologic features indicating high-burden thrombus formation in patients with acute myocardial infarction undergoing primary coronary intervention.

BACKGROUND: This study tested the hypothesis that in the acute phase of myocardial infarction (MI), the circulating level of soluble CD40 ligand (sCD40L), an index of platelet activation, is predictive of angiographic morphologic features that indicate high-burden thrombus formation (HBTF) in the infarct-related artery (IRA). METHODS AND RESULTS: This prospective study included 162 consecutive patients: 64 with HBTF and 98 with low-burden thrombus formation (LBTF). All patients had a Killip's classification相似文献   

Plasma levels of soluble CD40 ligand are elevated in inflammatory bowel diseases

BACKGROUND AND AIMS: CD40/CD40 ligand (CD40L) interaction is important for induction of T cell dependent antibody production and cell-mediated immune responses. Overexpression of CD40/CD40L in the intestinal mucosa is likely to be involved in the pathogenesis of inflammatory bowel disease (IBD). A soluble form of CD40L (sCD40L) exists in the circulation. This study investigated whether plasma levels of sCD40L are higher in patients with IBD than in healthy controls. PATIENTS AND METHODS: Plasma levels of sCD40L were measured in 89 patients with Crohn's disease (CD), 56 patients with ulcerative colitis (UC), 17 patients with infectious diarrhea, and 42 healthy controls, using a specific enzyme-linked immunosorbent assay. RESULTS: In CD patients plasma levels of sCD40L were significantly higher than in healthy controls. Patients with UC and infectious diarrhea had higher sCD40L levels than healthy controls, but the differences were not significant. CD patients with fistulas and/or abscesses (n=38) had significantly higher levels of sCD40L than patients with uncomplicated CD (n=51). Only in patients with uncomplicated CD plasma levels of sCD40L correlated significantly with C-reactive protein and alpha(1)-glycoprotein. In UC patients there was a significant correlation of sCD40L with C-reactive protein. However, there was no significant correlation between plasma sCD40L levels and Crohn's disease activity index or Rachmilewitz score. CONCLUSION: Elevated plasma levels of sCD40L in CD patients supposedly reflect activation of functional CD40L in the intestine and might be a marker of intestinal inflammation.