Objective Biochemical indicators such as N-terminal pro-brain type natriuretic peptide（NT pro-BNP）and high-sensitivity Creactive protein（hsCRP）predict mortality in acute coronary syndrome（ACS）.However,little is ...Objective Biochemical indicators such as N-terminal pro-brain type natriuretic peptide（NT pro-BNP）and high-sensitivity Creactive protein（hsCRP）predict mortality in acute coronary syndrome（ACS）.However,little is known about the relationship of these factors with severity of coronary artery stenosis in patients with.Methods Three hundred and thirty-one subjects including 246 unstable angina pectoris patients and 85 myocardial infarction patients were recruited and classified into two groups：single-vessel disease group（1-vessel disease,n=93）and multiple-vessel disease group（≥2-vessels disease,n=238）according to selective coronary angiography.Plasma levels of NT pro-BNP and hsCRP were measured and severity of coronary stenosis was determined by Gensini score.Results NT pro-BNP but not hsCRP level was higher in patients with myocardial infarction than in patients with unstable angina pectoris.The patients with multiple-vessel disease had significantly higher NT pro-BNP level but not hsCRP compared with those with single-vessel disease.NT pro-BNP levels increased significantly as left ventricle（LV）function decreased,and only NT proBNP but not hsCRP level was related to Gensini score of severity of coronary stenosis in ACS.Conclusion NT proBNP but not hsCRP level is related to severity of coronary artery stenosis in patients in ACS.展开更多
1 Introduction Inflammation is one of the main mechanisms in the pathogenesis of atherosclerosis,and the interest to the evaluation of inflammatory biomarkers in coronary artery disease(CAD)has been increasing over th...1 Introduction Inflammation is one of the main mechanisms in the pathogenesis of atherosclerosis,and the interest to the evaluation of inflammatory biomarkers in coronary artery disease(CAD)has been increasing over the last decade.[1,2]Destabilization of chronic artery plaques,which leads to acute coronary syndromes,has been associated with inflammatory status.[1,3]。展开更多
Objectives To investigate the morphologic characteristics of intramural hematoma(IMH)on CT angiography(CTA),and evaluate the possible correlation of serum C-reactive protein(CRP)with morphologic characteristics of IMH...Objectives To investigate the morphologic characteristics of intramural hematoma(IMH)on CT angiography(CTA),and evaluate the possible correlation of serum C-reactive protein(CRP)with morphologic characteristics of IMH.Material and Methods Forty-two patients who were initially diagnosed as IMH by aortic CTA and also had serum CRP examination on the same day of CTA were enrolled in this retrospective study,including 30 males and 12 females,with the mean age of 61±14 years old.The volumetric CT data were retrospectively processed and analyzed on post-processing workstation.Based on the thickness of IMH and the length-area curve,the crosssectional area of true lumen and total vessel were measured,the hematoma-vessel ratio(HVR)was calculated.Imaging characteristics were compared between patients who had pathological elevated CRP(>0.8 mg/dl)and those did not.Spearman correlation analyses of CRP level and morphological characteristics of IMH were performed,and the receiver operating characteristic(ROC)curve was used to evaluate the diagnostic validity of CRP.Results Of all 42 IMH patients,the mean serum CRP was 3.94±4.71 mg/dl,and the mean HVR was 46.7%±14.2%.HVR in patients with elevated CRP was significantly higher than those with normal CRP(49.7%±15.0%vs.40.7%±10.5%,P=0.030).HVR was mildly correlated with CRP in all patients(r=0.48,P<0.001).CRP levels differed neither between patients with Stanford type A and B(P=0.207),nor between patients with and without intimal disruption(P=0.230).To discriminate HVR>47%(the mean value),the area under curve(AUC)were 0.700(95%CI:0.535-0.865)for CRP at a cutoff point of 3.55 mg/dl,with a sensitivity of 54.5%and a specificity of 90.0%.Conclusion CRP was mildly correlated with the severity of cross-sectional hematoma area of IMH,but not with Stanford types and the presence of intimal disruption.展开更多
Background Atrial fibrillation （AF） is associated with inflammation and endothelial dysfunction. However, the association between inflammation （as indexed by high-sensitivity C-reactive protein, hs-CRP） and endoth...Background Atrial fibrillation （AF） is associated with inflammation and endothelial dysfunction. However, the association between inflammation （as indexed by high-sensitivity C-reactive protein, hs-CRP） and endothelial function [as indexed by big endothelin-1 （ET-1）] in AF patients remains unclear. Methods We enrolled 128 patients with lone AF, among which 83 had paroxysmal AF, and 45 had persistent AF. Eighty-two age- and gender-matched controls of paroxysmal supraventricular tachycardia without AF history were evaluated. Plasma hs-CRP, big ET-1 levels and other clinical characteristics were compared among the groups. Results Patients with persistent AF had higher hs-CRP concentrations than those with paroxysmal AF （P 〈 0.05）, both groups had higher hs-CRP level than controls （P 〈 0.05）. Patients with persistent AF had higher big ET-1 level than those with paroxysmal AF, although the difference did not reach the statistical significance （P 〉 0.05）, and both groups had higher big ET-1 levels than controls （P 〈 0.05）. Multiple regression analyses revealed hs-CRP as an inde- pendent determinant of AF （P 〈 0.001）. Further adjusted for big ET-1, both big ET-1 and hs-CRP were independent predictors for AF （P 〈 0.001）, but the odds ratio for hs-CRP in predicting AF attenuated from 8.043 to 3.241. There was a positive relation between hs-CRP level and big ET-1 level in paroxysmal AF patients （r = 0.563, P 〈 0.05）, however, the relationship in persistent AF patients was poor （r = 0.094, P 〈 0.05）. Conclusions Both plasma hs-CRP and big ET-1 levels are elevated in lone AF patients, and are associated with AF. In paroxysmal lone AF patients, there were significant positive correlations between plasma hs-CRP level and big ET- 1 level.展开更多
Background The data on the prognostic values of high sensitivity C-reactive protein （hsCRP） levels in patients with advanced symp-tomatic heart failure （HF） receiving cardiac resynchronization therapy （CRT） are ...Background The data on the prognostic values of high sensitivity C-reactive protein （hsCRP） levels in patients with advanced symp-tomatic heart failure （HF） receiving cardiac resynchronization therapy （CRT） are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP （〉3 mg/L） prior to CRT was associated with a significant 2.39-fold increase （P=0.006） in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels （–0.5 ± 4.1 mg/L reduction） compared with non-responders （1.7 ± 6.1 mg/L increase, P=0.018）. Com-pared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations （Log-rank P〈0.001）. The echocardio-graphic improvement was also better among patients in whom 6-month hsCRP levels were reduced or remained low compared to those in whom 6-month hsCRP levels were raised or maintained high. Conclusions Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.展开更多
Objective To investigate whether C-reactive protein (CRP) is a biomarker of malignant ventricular arrhythmias (MVA) occurring in non-ST elevation myocardial infarction (NSTEMI) patients with Global Registry of Acute C...Objective To investigate whether C-reactive protein (CRP) is a biomarker of malignant ventricular arrhythmias (MVA) occurring in non-ST elevation myocardial infarction (NSTEMI) patients with Global Registry of Acute Coronary events (GRACE) scores < 140. Methods A total of 1450 NSTEMI patients were included in this study. Hs-CRP blood levels were measured via a turbidimetric immunoassay after confirming the diagnosis of NSTEMI with GRACE scores < 140. Results Consistent with prior studies, the MVA occurrence rate in our cohort was 6.7%, and patients with MVA exhibited a reduced left ventricular ejection fraction (46.1%± 6.9% vs. 61.5%± 8.7%, P = 0.032), a higher incidence of Killip classification > 1 (34.1% vs. 24.2%, P < 0.001), an increased surgical revascularization rate (34.1% vs. 9.7%, P < 0.001), and increased mortality (16.5% vs. 5.8%, P < 0.001). Serum hs-CRP levels were higher (P = 0.003) in NSTEMI patients with MVA, and this increase appeared unrelated to other clinical parameters. The C-statistic to discriminate MVA was 0.82 (95% CI: 0.74–0.89). Using receiver operating characteristics analysis, we optimized a cutoff point of 16 mL/L, and the sensitivity and specificity were 95% and 61%, respectively;the positive predictive value was 20% and the negative predictive value was 99%. Conclusions An hs-CRP assay is a potential MVA biomarker in low-risk NSTEMI patients with GRACE scores < 140. If validated in prospective studies, hs-CRP may offer a low-cost supplementary strategy for risk stratification for NSTEMI patients.展开更多
Background Ischemia/reperfusion injury （IRI） is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein （CRP）...Background Ischemia/reperfusion injury （IRI） is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein （CRP） might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation （OGD/R） in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase （LDH） leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester （TMRE） and mitochondrial permeability transition pore （mPTP） opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 pg/mL CRP, cell viability decreased markedly （82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007）, and the LDH leakage significantly increased （145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122）. CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 pM atorvastatin （Ator） before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase （ERK） 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group （170.4% ± 3.00% v.v. 93.53% ± 1.94%, P 〈 0.0001）. Western blot analysis revealed that Akt expression was markedly activated （184.2% ± 6.96% vs. 122.7% ± 5.30%, P = 0.0003） and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. Conclusions Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP- sensitive potassium （mitoKATp） channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.展开更多
Psychological depression is considered a major determinant of health status in patients with heart failure （HF）. The incidence of depression in HF is four to five times higher than that in the general population.
Background Coronary artery disease(CAD)remains a leading cause of morbidity and mortality.Cytokines play a potential role in atherosclerosis pathogenesis and progression.We investigated the association between high se...Background Coronary artery disease(CAD)remains a leading cause of morbidity and mortality.Cytokines play a potential role in atherosclerosis pathogenesis and progression.We investigated the association between high sensitive C-reactive protein(hs CRP)and severity of CAD.Methods CAD patients were stratified according to hs CRP cut-off value into high levels hs CRP group(≥8.4 mg/L)and low levels hs CRP group(<8.4 mg/L).Severity of CAD was assessed according to artery stenosis degree and the number of vessel involved.Statistical analysis was performed using Statistical Package for the Social Sciences(SPSS,version 23.0).Results The mean age was 60.3±11.0 years.The level of hs CRP was increased and ranged from 0.2 to 1020.0 mg/L.Biochemical risk factors and severity of CAD didn’t show significant differences between the two groups.In multivariate linear analysis,cardiac troponin I(c Tn I)and serum amyloid A(SAA)were predictors of hs CRP.As shown in receiver operating characteristic(ROC)curve analysis performed in patients with ST-segment elevation myocardial infarction(STEMI)and compared to myonecrosis biomarkers,hs CRP(area under the curve(AUC):0.905;95%CI:0.844-0.966;P<0.001)could be a powerful predictor marker in evaluating the infarct size after myocardial infarction but not better than c Tn I.Conclusions Hs CRP levels were not associated with the severity of CAD but could be useful in the evaluation of myocardial necrosis in patients with STEMI.展开更多
Objective To evaluate the effects of simvastatin combined with omega-3 fatty acids on high sensitive C-reactive protein(HsCRP), lipidemia, and fibrinolysis in coronary heart disease (CHD) and CHD risk equivalent patie...Objective To evaluate the effects of simvastatin combined with omega-3 fatty acids on high sensitive C-reactive protein(HsCRP), lipidemia, and fibrinolysis in coronary heart disease (CHD) and CHD risk equivalent patients with mixed dyslipi-demia. Methods A randomized, double-blind placebo controlled and parallel group trial was conducted. Patients with CHD and CHD risk equivalents with mixed dyslipidemia were treated with 10 or 20 mg simvastatin for 6-12 weeks. Following with the treatment of patients whose low-density lipoprotein cholesterol (LDL-ch) reaching goal level (< 100 mg/dL) or close to the goal (< 130 mg/dL), while triglyceride (TG) ≥200 mg/dL and < 500 mg/dL, was combined with omega-3 fatty acids (3 g/d) or a placebo for 2 months. The effects of the treatment on HsCRP, total cholesterol (TC), LDL-ch, high-density lipoprotein cholesterol (HDL-ch), TG, lipoprotein (a) [LP (a)], apolipoprotein A1 (apoA1), apolipoprotein B (apoB), plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (tPA) were investigated. Forty patients finished the study with each group consisting of twenty patients. Results (1) There were significant reductions of HsCRP, TG, TC, and TC/HDL-ch, which decreased by 2.16 ±2.77 mg/L (38.5%), 94.0 ±65.4 mg/dL (31.1%), 13.3 ±22.3 mg/dL (6.3%), 0.78 ±1.60 respectively in the omega-3 fatty acids group (P< 0.01, < 0.001, < 0.05, < 0.05) compared to the baseline. HsCRP and triglyceride reduction were more significant in omega-3 fatty acids group compared to the placebo group (P=0.021 and 0.011 respectively). (2) In the omega-3 fatty acids group, the values and percentage of TG reduction had a significantly positive relation with HsCRP reduction (r=0.51 and 0.45, P=0.021 and 0.047 respectively). Conclusion In CHD and CHD risk equivalent patients with mixed dyslipidemia, dyslipidemia’s therapeutic effect using simvastatin and omega-3 fatty acids may result from not only the combination of lipid adjustment, but also enhancement of their own nonlipid influences.展开更多
Recently many new disease markers and risk factors have been proposed, but it is not yet clear how far the new markers are validated as predictive risk factors enable us to increase accuracy as well as enhancing our a...Recently many new disease markers and risk factors have been proposed, but it is not yet clear how far the new markers are validated as predictive risk factors enable us to increase accuracy as well as enhancing our ability to predict cardiovascular (CV) events and to plan prevention and therapy.展开更多
Inflammation is an important component of active atherosclerotic disease. C-reactive protein (CRP)is a non-specific inflammatory marker that is increased in inflammatory conditions. Newer more sensitive assays (high s...Inflammation is an important component of active atherosclerotic disease. C-reactive protein (CRP)is a non-specific inflammatory marker that is increased in inflammatory conditions. Newer more sensitive assays (high sensitivity CRP) can detect the low levels of inflammation associated with vascular disease. CRP levels can give further risk assessment to individuals beyond predictions from traditional risk factors. This measurement is most useful in helping to discriminate risk in intermediate risk patients such as metabolic syndrome patients. Exercise and weight loss have been shown to significantly lower CRP levels. Lipid lowering therapies, especially with the statin class of medications, also lower CRP levels. A reduction in inflammation may be an important component of plaque stabilization and contribute to cardiovascular risk reduction.展开更多
Objective: To explore the relationship between C-reactive protein(CRP) concentration and severity of coronary artery lesion. Methods: The plasma CRP concentration were tested in 166 cases who underwent coronary angiog...Objective: To explore the relationship between C-reactive protein(CRP) concentration and severity of coronary artery lesion. Methods: The plasma CRP concentration were tested in 166 cases who underwent coronary angiography(CAG),coronary heart disease(CHD) was presented in 86 patients and absent in 80 cases as normal control group, and results of the two groups and different numbers of diseased coronary vessels in CHD group were analyzed. Results: The plasma CRP concentration were 2293±198, 5126±508, 12969±1076 μg/L, respectively,for the normal control group, the stable angina group and the unstable angina group. The CRP concentration in the stable angina group and unstable angina group were significantly higher than those of the normal control group (P<0.05, P<0.01, respectively). In the CHD group, the plasma CRP concentration were 5131±513, 7024±689, 11970±2075 μg/L, respectively,for the 1-vessel-disease-group, the 2-vessel-disease-group and the 3-vessel-disease-group. The CRP concentration of the three groups were significantly higher than those of the normal control group (P<0.01). Conclusion: CRP concentration is closely associated with severity of coronary artery lesion.展开更多
BACKGROUND: Inappropriate antibiotic treatment for patients with viral infections has led to a surge in antimicrobial resistance, increasing mortality and healthcare costs. Viral and bacterial infections are often dif...BACKGROUND: Inappropriate antibiotic treatment for patients with viral infections has led to a surge in antimicrobial resistance, increasing mortality and healthcare costs. Viral and bacterial infections are often difficult to distinguish. Myxovirus resistance protein A(MxA), an essential antiviral factor induced by interferon after viral infection, holds promise for distinguishing between viral and bacterial infections. This study aimed to determine the ability of Mx A to distinguish viral from bacterial infections.METHODS: We quantified MxA in 121 infected patients via dry immunofluorescence chromatography. The Kruskal-Wallis test and receiver operating characteristic(ROC) curve analysis were used to determine the diagnostic value of Mx A, either alone or in combination with C-reactive protein(CRP) or procalcitonin(PCT), in patients with viral, bacterial, or co-infections.RESULTS: The value of MxA(ng/mL) was significantly higher in patients with viral infections than in those with bacterial and co-infections(82.3 [24.5–182.9] vs. 16.4 [10.8–26.5], P<0.0001)(82.3 [24.5–182.9] vs. 28.5 [10.2–106.8], P=0.0237). The area under the curve(AUC) of the ROC curve for distinguishing between viral and bacterial infections was 0.799(95% confidence interval [95% CI] 0.696–0.903), with a sensitivity of 68.9%(95% CI 54.3%–80.5%) and specificity of 90.0%(95% CI 74.4%–96.5%) at the threshold of 50.3 ng/mL. Combining the MxA level with the CRP or PCT level improved its ability. MxA expression was low in cytomegalovirus(15.8 [9.6–47.6] ng/mL) and Epstein-Barr virus(12.9 [8.5–21.0] ng/mL) infections.CONCLUSION: Our study showed the diagnostic efficacy of Mx A in distinguishing between viral and bacterial infections, with further enhancement when it was combined with CRP or PCT. Moreover, EpsteinBarr virus and human cytomegalovirus infections did not elicit elevated Mx A expression.展开更多
The systemic response to tissue injury, regardless of cause is characterized by a cytokine-mediated alteration in the hepatic synthesis of a number of different plasma proteins,known collectively as 'acute pha... The systemic response to tissue injury, regardless of cause is characterized by a cytokine-mediated alteration in the hepatic synthesis of a number of different plasma proteins,known collectively as 'acute phase reactants'. These proteins include C-reactive protein, serum amyloid A protein, alphal glycoprotein, ceruloplasmin, alpha macroglobulins, complement components (C1-C4, factor B, C9, C11), alpha1antitrypsin, alpha1 antichymotrypsin, fibrinogen, prothrombin,factor Ⅷ, plasminogen, haptoglobin, ferritin, immunoglobulins and lipoproteins. The initiation of the acute phase response is linked to the production of hormone-like polypeptide mediators now called cytokines, namedly, interleukin 1(IL-1),tumor necrosis factor, interferon gamma, interleukin 6 (IL-6),leukemia inhibitory factor, ciliary neurotropic factor, oncostatin M, and interleukin 11 (IL- 11).……展开更多
Objective To investigate the relationship between CRP, plasminogen activator inhibitor type 1 （PAI-1） levels, PAI-1 gene promoter 4G/5G polymorphism and the type of acute myocardial infarction （ST elevation myocard...Objective To investigate the relationship between CRP, plasminogen activator inhibitor type 1 （PAI-1） levels, PAI-1 gene promoter 4G/5G polymorphism and the type of acute myocardial infarction （ST elevation myocardial infarction, STEMI vs the non-ST elevation Myocardial infarction, NSTEMI）. Methods One hundred seventy-six consecutive patients with AMI were included for the study, of whom 60 had STEMI and 56 had NSTEMI, and 60 adults without cardiovascular and cerebrovascular disease were selected as controls. Blood samples were obtained from patients within 6 h of AMI and the plasma PAI-1, CRP, and the gene polymorphism were measured. Results Plasma levels of PAI- 1 and CRP were higher in AMI groups, compared those in the control group, and plasma levels of PAI-1 were significantly higher in patients with STEMI compared to those with NSTEMI （80.12ng/ml VS.73.01ng/ml, P 〈0.01）, while CRP levels were not significantly different between patient with STEMI and NSTEMI （3.87 ± 0.79 mg/ml VS.4.01 ±0.69mg/ml, P〉0.05）. PAI-1 levels presented a significant correlation with CRP levels in the NSTEMI subjects. However, PAI-1 and CRP levels could explain the lack of a significant relationship between them in control and STEMI subjects.The frequencies of 4G/4G genotype in the AMI group were higher than those in the control group and higher in patient with STEMI than in patient with NSTEMI. Plasma levels of PAI-1 in subjects with 4G/4G genotype were significantly increased as compared to those in subjects with 4G/5G and 5G/5G genotype. Conclusions Plasma PAI-1 levels were associated with different myocardial infarction type, and PAI-1 promoter 4G/5G polymorphisms and CRP may be related to plasma PAI-1 levels展开更多
Background Coronary artery calcification （CAC） is a predictor of cardiovascular events and plaque burden and is closely associatedwith chronic inflammation. Intedeukin （IL）-37 is a newly discovered member of the I...Background Coronary artery calcification （CAC） is a predictor of cardiovascular events and plaque burden and is closely associatedwith chronic inflammation. Intedeukin （IL）-37 is a newly discovered member of the IL-1 family and is considered an anti-inflammatorycytokine. Our recent study on mice indicated that IL-37 could attenuate atherosclerosis and vascular calcification, which suggests that IL-37could be associated with the development of atherosclerosis and related diseases. The aim of this study was to investigate if IL-37 plays arole in the progression of CAC in patients. Methods Two hundred participants with suspected cardiovascular disease were recruited. Thelevels of plasma IL-37, osteoprotegerin （OPG）, hypersensitive C-reactive protein （hsCRP） together with other biochemical parameters weremeasured, and a coronary calcium assessment was carried out by multi-detector row CT. A score of 〈 10 AU （Agatston units） denotes anabsence of CAC, a score of 11-100 AU denotes mild CAC, 101-400 denotes moderate CAC, and 〉 400 AU denotes severe CAC. ResultsOur initial data showed that there were no apparent differences in plasma IL-37 levels among patients with or without mild or moderate CAC.However, IL-37 levels were significantly increased in patients with severe CAC （P 〈 0.001）. Similar results were observed for plasma OPGand hsCRP levels. When IL-37 levels in patients with severe calcification were compared with that in all of the other non-severe CAC groups,it became apparent that there was a significant positive correlation between IL-37 level and severe CAC （r = 0.360, P 〈 0.001; OR = 1.033）using Spearrnan＇s correlation and binary logistic regression analysis. Conclusions This study demonstrates that the anti-inflammatory cy-tokine IL-37 is associated with high coronary calcium levels, suggesting that IL-37 expression may be caused by the activation ofinf/amma-tion and that IL-37 might become a predictor of severe CAC in the future, which requires further investigation.展开更多
BACKGROUND：Biomarkers may be helpful in risk stratification and prediction of mortality in septic patients. This study aimed to investigate the diagnostic role of soluble triggering receptor expressed on myeloid cel...BACKGROUND：Biomarkers may be helpful in risk stratification and prediction of mortality in septic patients. This study aimed to investigate the diagnostic role of soluble triggering receptor expressed on myeloid celI-I（sTREM-1）, procalcitonin （PCT）, C-reactive protein （CRP） and other inflammatory markers in patients with sepsis. METHODS：A total of 56 patients with systemic inflammation response syndrome （SIRS） who had been admitted to the ICU department of the Second Hospital of Tianjin Medical University between May 2009 and July 2010 were enrolled. They were divided into a sepsis group （n=32） and a SIRS group （n=24）. Twenty-five non-SIRS patients served as controls. The sepsis group was sub-divided into a survival group and a death group according to 28-day prognosis. The values of sTREM-1, PCT, CRP, white blood cell （WBC）, and neutrophil count percentage （N） were measured. Acute physiology and chronic health evaluation II （APACHE II） score were determined within 24 hours. The correlation between sTREM-1 and APACHE II score was analyzed. Quantitative data were analyzed by the F test or the KruskaI-Wallis test. RESULTS： The plasma level of sTREM-1 in the sepsis group was significantly higher than that in the SIRS group and control group. The plasma level of sTREM-1 in the non-survival group was significantly higher than that in the survival group. In the sepsis group, the plasma sTREM-1 level was positively correlated with APACHE II score （rs=0.426, P= 0.032）. The area under the ROC curve of sTREM-1 was 0.935, larger than that of PCT and CRP. CONCLUSION：Plasma sTREM-1 is useful in the diagnosis of sepsis at early stage. The increased level of sTREM-1 during the first 24 hours may be correlated with poor outcome of patients with sepsis.展开更多
文摘Objective Biochemical indicators such as N-terminal pro-brain type natriuretic peptide（NT pro-BNP）and high-sensitivity Creactive protein（hsCRP）predict mortality in acute coronary syndrome（ACS）.However,little is known about the relationship of these factors with severity of coronary artery stenosis in patients with.Methods Three hundred and thirty-one subjects including 246 unstable angina pectoris patients and 85 myocardial infarction patients were recruited and classified into two groups：single-vessel disease group（1-vessel disease,n=93）and multiple-vessel disease group（≥2-vessels disease,n=238）according to selective coronary angiography.Plasma levels of NT pro-BNP and hsCRP were measured and severity of coronary stenosis was determined by Gensini score.Results NT pro-BNP but not hsCRP level was higher in patients with myocardial infarction than in patients with unstable angina pectoris.The patients with multiple-vessel disease had significantly higher NT pro-BNP level but not hsCRP compared with those with single-vessel disease.NT pro-BNP levels increased significantly as left ventricle（LV）function decreased,and only NT proBNP but not hsCRP level was related to Gensini score of severity of coronary stenosis in ACS.Conclusion NT proBNP but not hsCRP level is related to severity of coronary artery stenosis in patients in ACS.
基金Supported by the Ministry of Science and Higher Education grant(#MD-2314.2020.7).The authors declare no conflict of interest.
文摘1 Introduction Inflammation is one of the main mechanisms in the pathogenesis of atherosclerosis,and the interest to the evaluation of inflammatory biomarkers in coronary artery disease(CAD)has been increasing over the last decade.[1,2]Destabilization of chronic artery plaques,which leads to acute coronary syndromes,has been associated with inflammatory status.[1,3]。
基金Fund supported by the Clinical Research Supporting Fund of Chinese PLA General Hospital(2016FC-TSYS-1039)~~
文摘Objectives To investigate the morphologic characteristics of intramural hematoma(IMH)on CT angiography(CTA),and evaluate the possible correlation of serum C-reactive protein(CRP)with morphologic characteristics of IMH.Material and Methods Forty-two patients who were initially diagnosed as IMH by aortic CTA and also had serum CRP examination on the same day of CTA were enrolled in this retrospective study,including 30 males and 12 females,with the mean age of 61±14 years old.The volumetric CT data were retrospectively processed and analyzed on post-processing workstation.Based on the thickness of IMH and the length-area curve,the crosssectional area of true lumen and total vessel were measured,the hematoma-vessel ratio(HVR)was calculated.Imaging characteristics were compared between patients who had pathological elevated CRP(>0.8 mg/dl)and those did not.Spearman correlation analyses of CRP level and morphological characteristics of IMH were performed,and the receiver operating characteristic(ROC)curve was used to evaluate the diagnostic validity of CRP.Results Of all 42 IMH patients,the mean serum CRP was 3.94±4.71 mg/dl,and the mean HVR was 46.7%±14.2%.HVR in patients with elevated CRP was significantly higher than those with normal CRP(49.7%±15.0%vs.40.7%±10.5%,P=0.030).HVR was mildly correlated with CRP in all patients(r=0.48,P<0.001).CRP levels differed neither between patients with Stanford type A and B(P=0.207),nor between patients with and without intimal disruption(P=0.230).To discriminate HVR>47%(the mean value),the area under curve(AUC)were 0.700(95%CI:0.535-0.865)for CRP at a cutoff point of 3.55 mg/dl,with a sensitivity of 54.5%and a specificity of 90.0%.Conclusion CRP was mildly correlated with the severity of cross-sectional hematoma area of IMH,but not with Stanford types and the presence of intimal disruption.
文摘Background Atrial fibrillation （AF） is associated with inflammation and endothelial dysfunction. However, the association between inflammation （as indexed by high-sensitivity C-reactive protein, hs-CRP） and endothelial function [as indexed by big endothelin-1 （ET-1）] in AF patients remains unclear. Methods We enrolled 128 patients with lone AF, among which 83 had paroxysmal AF, and 45 had persistent AF. Eighty-two age- and gender-matched controls of paroxysmal supraventricular tachycardia without AF history were evaluated. Plasma hs-CRP, big ET-1 levels and other clinical characteristics were compared among the groups. Results Patients with persistent AF had higher hs-CRP concentrations than those with paroxysmal AF （P 〈 0.05）, both groups had higher hs-CRP level than controls （P 〈 0.05）. Patients with persistent AF had higher big ET-1 level than those with paroxysmal AF, although the difference did not reach the statistical significance （P 〉 0.05）, and both groups had higher big ET-1 levels than controls （P 〈 0.05）. Multiple regression analyses revealed hs-CRP as an inde- pendent determinant of AF （P 〈 0.001）. Further adjusted for big ET-1, both big ET-1 and hs-CRP were independent predictors for AF （P 〈 0.001）, but the odds ratio for hs-CRP in predicting AF attenuated from 8.043 to 3.241. There was a positive relation between hs-CRP level and big ET-1 level in paroxysmal AF patients （r = 0.563, P 〈 0.05）, however, the relationship in persistent AF patients was poor （r = 0.094, P 〈 0.05）. Conclusions Both plasma hs-CRP and big ET-1 levels are elevated in lone AF patients, and are associated with AF. In paroxysmal lone AF patients, there were significant positive correlations between plasma hs-CRP level and big ET- 1 level.
文摘Background The data on the prognostic values of high sensitivity C-reactive protein （hsCRP） levels in patients with advanced symp-tomatic heart failure （HF） receiving cardiac resynchronization therapy （CRT） are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP （〉3 mg/L） prior to CRT was associated with a significant 2.39-fold increase （P=0.006） in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels （–0.5 ± 4.1 mg/L reduction） compared with non-responders （1.7 ± 6.1 mg/L increase, P=0.018）. Com-pared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations （Log-rank P〈0.001）. The echocardio-graphic improvement was also better among patients in whom 6-month hsCRP levels were reduced or remained low compared to those in whom 6-month hsCRP levels were raised or maintained high. Conclusions Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.
基金supported by the Capital Health Research and Development of Special Foundation (2018-1-2061)
文摘Objective To investigate whether C-reactive protein (CRP) is a biomarker of malignant ventricular arrhythmias (MVA) occurring in non-ST elevation myocardial infarction (NSTEMI) patients with Global Registry of Acute Coronary events (GRACE) scores < 140. Methods A total of 1450 NSTEMI patients were included in this study. Hs-CRP blood levels were measured via a turbidimetric immunoassay after confirming the diagnosis of NSTEMI with GRACE scores < 140. Results Consistent with prior studies, the MVA occurrence rate in our cohort was 6.7%, and patients with MVA exhibited a reduced left ventricular ejection fraction (46.1%± 6.9% vs. 61.5%± 8.7%, P = 0.032), a higher incidence of Killip classification > 1 (34.1% vs. 24.2%, P < 0.001), an increased surgical revascularization rate (34.1% vs. 9.7%, P < 0.001), and increased mortality (16.5% vs. 5.8%, P < 0.001). Serum hs-CRP levels were higher (P = 0.003) in NSTEMI patients with MVA, and this increase appeared unrelated to other clinical parameters. The C-statistic to discriminate MVA was 0.82 (95% CI: 0.74–0.89). Using receiver operating characteristics analysis, we optimized a cutoff point of 16 mL/L, and the sensitivity and specificity were 95% and 61%, respectively;the positive predictive value was 20% and the negative predictive value was 99%. Conclusions An hs-CRP assay is a potential MVA biomarker in low-risk NSTEMI patients with GRACE scores < 140. If validated in prospective studies, hs-CRP may offer a low-cost supplementary strategy for risk stratification for NSTEMI patients.
文摘Background Ischemia/reperfusion injury （IRI） is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein （CRP） might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation （OGD/R） in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase （LDH） leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester （TMRE） and mitochondrial permeability transition pore （mPTP） opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 pg/mL CRP, cell viability decreased markedly （82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007）, and the LDH leakage significantly increased （145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122）. CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 pM atorvastatin （Ator） before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase （ERK） 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group （170.4% ± 3.00% v.v. 93.53% ± 1.94%, P 〈 0.0001）. Western blot analysis revealed that Akt expression was markedly activated （184.2% ± 6.96% vs. 122.7% ± 5.30%, P = 0.0003） and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. Conclusions Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP- sensitive potassium （mitoKATp） channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.
文摘Psychological depression is considered a major determinant of health status in patients with heart failure （HF）. The incidence of depression in HF is four to five times higher than that in the general population.
基金funded by research organizations in Tunisia(Ministry of Public Health and Ministry of Higher Education and Scientific Research)。
文摘Background Coronary artery disease(CAD)remains a leading cause of morbidity and mortality.Cytokines play a potential role in atherosclerosis pathogenesis and progression.We investigated the association between high sensitive C-reactive protein(hs CRP)and severity of CAD.Methods CAD patients were stratified according to hs CRP cut-off value into high levels hs CRP group(≥8.4 mg/L)and low levels hs CRP group(<8.4 mg/L).Severity of CAD was assessed according to artery stenosis degree and the number of vessel involved.Statistical analysis was performed using Statistical Package for the Social Sciences(SPSS,version 23.0).Results The mean age was 60.3±11.0 years.The level of hs CRP was increased and ranged from 0.2 to 1020.0 mg/L.Biochemical risk factors and severity of CAD didn’t show significant differences between the two groups.In multivariate linear analysis,cardiac troponin I(c Tn I)and serum amyloid A(SAA)were predictors of hs CRP.As shown in receiver operating characteristic(ROC)curve analysis performed in patients with ST-segment elevation myocardial infarction(STEMI)and compared to myonecrosis biomarkers,hs CRP(area under the curve(AUC):0.905;95%CI:0.844-0.966;P<0.001)could be a powerful predictor marker in evaluating the infarct size after myocardial infarction but not better than c Tn I.Conclusions Hs CRP levels were not associated with the severity of CAD but could be useful in the evaluation of myocardial necrosis in patients with STEMI.
文摘Objective To evaluate the effects of simvastatin combined with omega-3 fatty acids on high sensitive C-reactive protein(HsCRP), lipidemia, and fibrinolysis in coronary heart disease (CHD) and CHD risk equivalent patients with mixed dyslipi-demia. Methods A randomized, double-blind placebo controlled and parallel group trial was conducted. Patients with CHD and CHD risk equivalents with mixed dyslipidemia were treated with 10 or 20 mg simvastatin for 6-12 weeks. Following with the treatment of patients whose low-density lipoprotein cholesterol (LDL-ch) reaching goal level (< 100 mg/dL) or close to the goal (< 130 mg/dL), while triglyceride (TG) ≥200 mg/dL and < 500 mg/dL, was combined with omega-3 fatty acids (3 g/d) or a placebo for 2 months. The effects of the treatment on HsCRP, total cholesterol (TC), LDL-ch, high-density lipoprotein cholesterol (HDL-ch), TG, lipoprotein (a) [LP (a)], apolipoprotein A1 (apoA1), apolipoprotein B (apoB), plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (tPA) were investigated. Forty patients finished the study with each group consisting of twenty patients. Results (1) There were significant reductions of HsCRP, TG, TC, and TC/HDL-ch, which decreased by 2.16 ±2.77 mg/L (38.5%), 94.0 ±65.4 mg/dL (31.1%), 13.3 ±22.3 mg/dL (6.3%), 0.78 ±1.60 respectively in the omega-3 fatty acids group (P< 0.01, < 0.001, < 0.05, < 0.05) compared to the baseline. HsCRP and triglyceride reduction were more significant in omega-3 fatty acids group compared to the placebo group (P=0.021 and 0.011 respectively). (2) In the omega-3 fatty acids group, the values and percentage of TG reduction had a significantly positive relation with HsCRP reduction (r=0.51 and 0.45, P=0.021 and 0.047 respectively). Conclusion In CHD and CHD risk equivalent patients with mixed dyslipidemia, dyslipidemia’s therapeutic effect using simvastatin and omega-3 fatty acids may result from not only the combination of lipid adjustment, but also enhancement of their own nonlipid influences.
文摘Recently many new disease markers and risk factors have been proposed, but it is not yet clear how far the new markers are validated as predictive risk factors enable us to increase accuracy as well as enhancing our ability to predict cardiovascular (CV) events and to plan prevention and therapy.
文摘Inflammation is an important component of active atherosclerotic disease. C-reactive protein (CRP)is a non-specific inflammatory marker that is increased in inflammatory conditions. Newer more sensitive assays (high sensitivity CRP) can detect the low levels of inflammation associated with vascular disease. CRP levels can give further risk assessment to individuals beyond predictions from traditional risk factors. This measurement is most useful in helping to discriminate risk in intermediate risk patients such as metabolic syndrome patients. Exercise and weight loss have been shown to significantly lower CRP levels. Lipid lowering therapies, especially with the statin class of medications, also lower CRP levels. A reduction in inflammation may be an important component of plaque stabilization and contribute to cardiovascular risk reduction.
文摘Objective: To explore the relationship between C-reactive protein(CRP) concentration and severity of coronary artery lesion. Methods: The plasma CRP concentration were tested in 166 cases who underwent coronary angiography(CAG),coronary heart disease(CHD) was presented in 86 patients and absent in 80 cases as normal control group, and results of the two groups and different numbers of diseased coronary vessels in CHD group were analyzed. Results: The plasma CRP concentration were 2293±198, 5126±508, 12969±1076 μg/L, respectively,for the normal control group, the stable angina group and the unstable angina group. The CRP concentration in the stable angina group and unstable angina group were significantly higher than those of the normal control group (P<0.05, P<0.01, respectively). In the CHD group, the plasma CRP concentration were 5131±513, 7024±689, 11970±2075 μg/L, respectively,for the 1-vessel-disease-group, the 2-vessel-disease-group and the 3-vessel-disease-group. The CRP concentration of the three groups were significantly higher than those of the normal control group (P<0.01). Conclusion: CRP concentration is closely associated with severity of coronary artery lesion.
基金supported by the National Natural Science Foundation of China (82272196 and 82272220)。
文摘BACKGROUND: Inappropriate antibiotic treatment for patients with viral infections has led to a surge in antimicrobial resistance, increasing mortality and healthcare costs. Viral and bacterial infections are often difficult to distinguish. Myxovirus resistance protein A(MxA), an essential antiviral factor induced by interferon after viral infection, holds promise for distinguishing between viral and bacterial infections. This study aimed to determine the ability of Mx A to distinguish viral from bacterial infections.METHODS: We quantified MxA in 121 infected patients via dry immunofluorescence chromatography. The Kruskal-Wallis test and receiver operating characteristic(ROC) curve analysis were used to determine the diagnostic value of Mx A, either alone or in combination with C-reactive protein(CRP) or procalcitonin(PCT), in patients with viral, bacterial, or co-infections.RESULTS: The value of MxA(ng/mL) was significantly higher in patients with viral infections than in those with bacterial and co-infections(82.3 [24.5–182.9] vs. 16.4 [10.8–26.5], P<0.0001)(82.3 [24.5–182.9] vs. 28.5 [10.2–106.8], P=0.0237). The area under the curve(AUC) of the ROC curve for distinguishing between viral and bacterial infections was 0.799(95% confidence interval [95% CI] 0.696–0.903), with a sensitivity of 68.9%(95% CI 54.3%–80.5%) and specificity of 90.0%(95% CI 74.4%–96.5%) at the threshold of 50.3 ng/mL. Combining the MxA level with the CRP or PCT level improved its ability. MxA expression was low in cytomegalovirus(15.8 [9.6–47.6] ng/mL) and Epstein-Barr virus(12.9 [8.5–21.0] ng/mL) infections.CONCLUSION: Our study showed the diagnostic efficacy of Mx A in distinguishing between viral and bacterial infections, with further enhancement when it was combined with CRP or PCT. Moreover, EpsteinBarr virus and human cytomegalovirus infections did not elicit elevated Mx A expression.
文摘 The systemic response to tissue injury, regardless of cause is characterized by a cytokine-mediated alteration in the hepatic synthesis of a number of different plasma proteins,known collectively as 'acute phase reactants'. These proteins include C-reactive protein, serum amyloid A protein, alphal glycoprotein, ceruloplasmin, alpha macroglobulins, complement components (C1-C4, factor B, C9, C11), alpha1antitrypsin, alpha1 antichymotrypsin, fibrinogen, prothrombin,factor Ⅷ, plasminogen, haptoglobin, ferritin, immunoglobulins and lipoproteins. The initiation of the acute phase response is linked to the production of hormone-like polypeptide mediators now called cytokines, namedly, interleukin 1(IL-1),tumor necrosis factor, interferon gamma, interleukin 6 (IL-6),leukemia inhibitory factor, ciliary neurotropic factor, oncostatin M, and interleukin 11 (IL- 11).……
文摘Objective To investigate the relationship between CRP, plasminogen activator inhibitor type 1 （PAI-1） levels, PAI-1 gene promoter 4G/5G polymorphism and the type of acute myocardial infarction （ST elevation myocardial infarction, STEMI vs the non-ST elevation Myocardial infarction, NSTEMI）. Methods One hundred seventy-six consecutive patients with AMI were included for the study, of whom 60 had STEMI and 56 had NSTEMI, and 60 adults without cardiovascular and cerebrovascular disease were selected as controls. Blood samples were obtained from patients within 6 h of AMI and the plasma PAI-1, CRP, and the gene polymorphism were measured. Results Plasma levels of PAI- 1 and CRP were higher in AMI groups, compared those in the control group, and plasma levels of PAI-1 were significantly higher in patients with STEMI compared to those with NSTEMI （80.12ng/ml VS.73.01ng/ml, P 〈0.01）, while CRP levels were not significantly different between patient with STEMI and NSTEMI （3.87 ± 0.79 mg/ml VS.4.01 ±0.69mg/ml, P〉0.05）. PAI-1 levels presented a significant correlation with CRP levels in the NSTEMI subjects. However, PAI-1 and CRP levels could explain the lack of a significant relationship between them in control and STEMI subjects.The frequencies of 4G/4G genotype in the AMI group were higher than those in the control group and higher in patient with STEMI than in patient with NSTEMI. Plasma levels of PAI-1 in subjects with 4G/4G genotype were significantly increased as compared to those in subjects with 4G/5G and 5G/5G genotype. Conclusions Plasma PAI-1 levels were associated with different myocardial infarction type, and PAI-1 promoter 4G/5G polymorphisms and CRP may be related to plasma PAI-1 levels
文摘Background Coronary artery calcification （CAC） is a predictor of cardiovascular events and plaque burden and is closely associatedwith chronic inflammation. Intedeukin （IL）-37 is a newly discovered member of the IL-1 family and is considered an anti-inflammatorycytokine. Our recent study on mice indicated that IL-37 could attenuate atherosclerosis and vascular calcification, which suggests that IL-37could be associated with the development of atherosclerosis and related diseases. The aim of this study was to investigate if IL-37 plays arole in the progression of CAC in patients. Methods Two hundred participants with suspected cardiovascular disease were recruited. Thelevels of plasma IL-37, osteoprotegerin （OPG）, hypersensitive C-reactive protein （hsCRP） together with other biochemical parameters weremeasured, and a coronary calcium assessment was carried out by multi-detector row CT. A score of 〈 10 AU （Agatston units） denotes anabsence of CAC, a score of 11-100 AU denotes mild CAC, 101-400 denotes moderate CAC, and 〉 400 AU denotes severe CAC. ResultsOur initial data showed that there were no apparent differences in plasma IL-37 levels among patients with or without mild or moderate CAC.However, IL-37 levels were significantly increased in patients with severe CAC （P 〈 0.001）. Similar results were observed for plasma OPGand hsCRP levels. When IL-37 levels in patients with severe calcification were compared with that in all of the other non-severe CAC groups,it became apparent that there was a significant positive correlation between IL-37 level and severe CAC （r = 0.360, P 〈 0.001; OR = 1.033）using Spearrnan＇s correlation and binary logistic regression analysis. Conclusions This study demonstrates that the anti-inflammatory cy-tokine IL-37 is associated with high coronary calcium levels, suggesting that IL-37 expression may be caused by the activation ofinf/amma-tion and that IL-37 might become a predictor of severe CAC in the future, which requires further investigation.
文摘BACKGROUND：Biomarkers may be helpful in risk stratification and prediction of mortality in septic patients. This study aimed to investigate the diagnostic role of soluble triggering receptor expressed on myeloid celI-I（sTREM-1）, procalcitonin （PCT）, C-reactive protein （CRP） and other inflammatory markers in patients with sepsis. METHODS：A total of 56 patients with systemic inflammation response syndrome （SIRS） who had been admitted to the ICU department of the Second Hospital of Tianjin Medical University between May 2009 and July 2010 were enrolled. They were divided into a sepsis group （n=32） and a SIRS group （n=24）. Twenty-five non-SIRS patients served as controls. The sepsis group was sub-divided into a survival group and a death group according to 28-day prognosis. The values of sTREM-1, PCT, CRP, white blood cell （WBC）, and neutrophil count percentage （N） were measured. Acute physiology and chronic health evaluation II （APACHE II） score were determined within 24 hours. The correlation between sTREM-1 and APACHE II score was analyzed. Quantitative data were analyzed by the F test or the KruskaI-Wallis test. RESULTS： The plasma level of sTREM-1 in the sepsis group was significantly higher than that in the SIRS group and control group. The plasma level of sTREM-1 in the non-survival group was significantly higher than that in the survival group. In the sepsis group, the plasma sTREM-1 level was positively correlated with APACHE II score （rs=0.426, P= 0.032）. The area under the ROC curve of sTREM-1 was 0.935, larger than that of PCT and CRP. CONCLUSION：Plasma sTREM-1 is useful in the diagnosis of sepsis at early stage. The increased level of sTREM-1 during the first 24 hours may be correlated with poor outcome of patients with sepsis.
