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High Sensitivity C-reactive Protein (high + sensitivity_c-reactive_protein)
Selected AbstractsBrachial-ankle pulse wave velocity and cardiovascular risk factors in the non-diabetic and newly diagnosed diabetic Chinese: Guangzhou Biobank Cohort Study-CVDDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2010Lin Xu Abstract Background Increased arterial stiffness is an important cause of cardiovascular disease (CVD). We examined determinants of arterial stiffness in subjects across strata of glycaemic status. Methods A total of 1249 subjects from a sub-study of the Guangzhou Biobank Cohort Study (GBCS-CVD) had brachial-ankle pulse wave velocity (baPWV) measured by automatic oscillometric method. Major cardiovascular risk factors including glycosylated haemoglobin A1c (HbA1c), high sensitivity C-reactive protein (hsCRP), fasting triglyceride, low- and high-density lipoprotein cholesterol and both fasting and post 2-h oral glucose-load glucose, systolic and diastolic blood pressure were assessed. Results In all, 649, 479 and 121 subjects were classified into normoglycaemia, impaired glucose metabolism (IGM) and newly diagnosed diabetes groups, respectively. Both age and systolic blood pressure were significantly associated with increased baPWV in all three groups (all p < 0.001). In both normoglycaemic and IGM groups, hsCRP and HbA1c were positively associated with baPWV (p from 0.04 to < 0.001), whereas current smoking and triglyceride were associated with baPWV in the normoglycaemic and IGM group, respectively (p = 0.04 and 0.001). No gender difference in baPWV was observed in the normoglycaemic or IGM groups. However, in the newly diagnosed diabetes group, men had higher baPWV than women (p = 0.01). Conclusions In the normoglycaemic and IGM subjects, after adjusting for age, blood pressure and other confounders, increasing HbA1c was associated with increased baPWV, suggesting a pathophysiological role of chronic glycaemia that can contribute to vascular disease risk in persons without diabetes. Copyright © 2010 John Wiley & Sons, Ltd. [source] Association of components of the metabolic syndrome with the appearance of aggregated red blood cells in the peripheral blood.DIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 2 2005An unfavorable hemorheological finding Abstract Background Components of the metabolic syndrome are associated with low-grade inflammation. This can be accompanied by the synthesis of sticky proteins and erythrocyte aggregation. Methods The degree of erythrocyte aggregation was evaluated by a simple slide test and image analysis along with other markers of the acute-phase response, including the white blood cell count (WBCC), erythrocyte sedimentation rate (ESR), fibrinogen and high sensitivity C-reactive protein (hs-CRP) concentrations. Patients were categorized in four groups according to the absence or presence of 1, 2 and 3 or more components of the metabolic syndrome. Results We examined a total of 1447 individuals (576 women and 871 men) who gave their informed consent for participation. A significant cardiovascular risk factors, age and hemoglobin adjusted correlation was noted between the degree of erythrocyte aggregation and the number of components of the metabolic syndrome (r = 0.17, p < 0.0005). This correlation was better than that observed for clottable fibrinogen (r = 0.13 p < 0.0005), for ESR (r = 0.11 p < 0.0005) or WBCC (r = 0.13 p < 0.0005). A somewhat better correlation was noted for hs-CRP (r = 0.26 p < 0.0005). Conclusions The multiplicity of components of the metabolic syndrome is associated with enhanced erythrocyte aggregation, probably related to the presence of multiple adhesive macromolecules in the peripheral blood. The enhanced aggregation might contribute to capillary slow flow, tissue deoxygenation as well as vasomotor tone changes in the presence of multiple components of this syndrome. Copyright © 2004 John Wiley & Sons, Ltd. [source] Plasma matrix metalloproteinase-3 level is an independent prognostic factor in stable coronary artery diseaseEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2005T. C. Wu Abstract Background, Recent evidence suggests the important role of matrix metalloproteinases (MMPs) in the progression of atherosclerosis and development of clinical events. We assessed the prognostic value of different plasma MMPs in patients with stable coronary artery disease (CAD). Materials and methods, A total of 165 consecutive nondiabetic patients with angiographically significant CAD (n = 150) or normal coronary angiograms despite exercise-induced myocardial ischemia (cardiac syndrome X, n = 15) and 17 normal subjects were evaluated. In each subject, plasma inflammatory markers including high sensitivity C-reactive protein (hsCRP) and MMP-2, 3 and 9 were measured. In CAD patients, major cardiovascular events including cardiac death, nonfatal myocardial infarction, unscheduled coronary revascularization and hospitalization as a result of unstable angina were prospectively followed up for more than 6 months. Results, Plasma levels of MMPs were significantly higher in CAD patients than in those with cardiac syndrome X and in normal subjects (MMP-2: 914·76 ± 13·20 vs. 830·79 ± 31·95 vs. 783·08 ± 28·40 ng mL,1, P = 0·002; MMP-3: 129·59 ± 4·21 vs. 116·86 ± 8·09 vs. 91·71 ± 9·55 ng mL,1, P = 0·011; MMP-9: 31·42 ± 2·84 vs. 11·40 ± 5·49 vs. 6·71 ± 2·89 ng mL,1, P = 0·006). In CAD patients, there were 48 major cardiovascular events during a mean follow-up period of 17·74 ± 0·85 months. The numbers of diseased vessels (HR = 2·19, 95% CI 1·20,1·02, P = 0·011), plasma hsCRP (HR = 2·21, 95% CI 1·18,4·11, P = 0·013) and MMP-3 level (HR = 2·46, 95% CI = 1·15,5·28, P = 0·021) were associated with the development of cardiovascular events. However, only the plasma MMP-3 level was an independent predictor of the adverse events in CAD patients (HR = 2·47, 95% CI 1·10,5·54, P = 0·028). Conclusions, Plasma MMP levels were increased in CAD patients. Plasma MMP-3 level, rather than hsCRP, was an independent prognostic marker for future cardiovascular events, suggesting its potential role in risk stratification and clinical management of stable CAD. [source] Increased strength of erythrocyte aggregates in blood of patients with inflammatory bowel diseaseINFLAMMATORY BOWEL DISEASES, Issue 5 2009Nitsan Maharshak MD Abstract Background: Increased strength of red blood cell (RBC) aggregates are present during the acute inflammatory response and contribute to erythrocyte aggregation and may lead to microvascular dysfunction. Inflammatory bowel diseases (IBDs) are characterized by damage to the bowel wall. This damage may be at least partially attributed to microvascular ischemia caused by enhanced erythrocyte aggregation. The aim of this study was to evaluate the strength of RBC aggregates in the blood of patients with IBD. Methods: The strengths of RBC aggregates were characterized by integrative RBC aggregation parameters, determined by measuring of RBC aggregation as a function of shear stress. The results are represented as the area under the curve (AUC) of aggregate size plotted against shear stress. For each patient, dynamic aggregation and disaggregation of RBC were recorded and analyzed according to the RBC aggregate size distribution at the different shear stresses. Aggregation indices were correlated with disease activity and inflammatory biomarkers. Results: We examined 53 IBD patients and 63 controls. IBD patients had significantly elevated concentrations of inflammation-sensitive proteins and aggregation parameters. The strength of large aggregates, represented by AUC for large fraction aggregates, among patients (15.2 ± 18.6) was double that of controls (7 ± 10.9) (P = 0.006). The strength of large aggregates correlated with disease activity (r = 0.340; P < 0.001) with concentration of fibrinogen (r = 0.575; P < 0.001) and with concentration of high sensitivity C-reactive protein (r = 0.386; P < 0.001). Conclusions: The strength of RBC aggregates is increased in patients with IBD and correlates with the intensity of the acute phase response. This could contribute to bowel damage in these diseases. (Inflamm Bowel Dis 2009) [source] Relationship of serum homocysteine and high sensitivity C-reactive protein in elderly people with essential hypertensionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 9 2010L. Yan-Yan No abstract is available for this article. [source] Vulnerable Plaque: The Pathology of Unstable Coronary LesionsJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 6 2002RENU VIRMANI M.D. Vulnerable plagues have been defined as precursors to lesions that rupture. However, coronary thrombosis may occur from other lesions like plaque erosion and calcified nodules, although to a lesser frequency than rupture. Therefore, the definition of vulnerable plaque should be all-inclusive. Using descriptive terminology, the authors define the precursor lesion of plaque rupture as "thin-cap fibroatheroma" (TCFA). Morphologically, TCFAs have a necrotic core with an overlying thin fibrous cap (< 65 mm) consisting of collagen type I, which is infiltrated by macrophages. These lesions are most frequent in the coronary tree of patients dying with acme myocardial infarction and least common in those with plaque erosion. TCFAs are more common in patients with high serum total cholesterol (TC) and a high TC to high density cholesterol ratio, in women >50 years, and in those patients with elevated levels of high sensitivity C-reactive protein. TCFAs are mostly found in the proximal left anterior descending coronary arteries and less commonly in the proximal right or the proximal left circumflex coronary arteries. In TCFAs, necrotic core length is , 2,17 mm (mean 8 mm) and the underlying cross-sectional luminal narrowing in over 75% of cases is < 75% (< 50% diameter stenosis). The area of the necrotic core in at least 75% of cases is ,3 mm2. Clinical studies of TCFAs are limited as angiography and intravascular ultrasound (TVUS) catheters cannot precisely identify these lesions. Newer catheters and other techniques are at various stages of development and will play a significant role in the understanding of plaque progression and the development of symptomatic coronary artery disease. [source] Emerging concepts in cardiovascular disease risk assessment: Where do women fit in?JOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 9 2009Adjunct Instructor, CRNP Cardiovascular Nurse Practitioner, Deborah Gleeson MSN Abstract Purpose: To highlight the current limitations in the assessment of cardiovascular disease (CVD) risk for women. This article will offer the reader information on the current process for assessing CVD risk in women, the pitfalls associated with this current strategy, and the role of novel risk factors. Data sources: Extensive review of the medical literature in the area of women's cardiovascular health. Conclusions: The assessment of CVD risk for women is currently an evolving science. Limitations in the ability of the Framingham score to accurately estimate risk in women from diverse populations are increasingly recognized. Vastly different treatment goals between the genders for similar levels of risk factors have led to a re-evaluation of this strategy in women. While the Framingham score is still useful for guiding cholesterol treatment goals, the current preventive guidelines for women emphasize assessing a woman's risk throughout her lifetime. The future development of tools for improved risk stratification that incorporate novel risk factors may in fact improve our ability to appropriately risk stratify women to evidence-based therapies. Implications for practice: Utilizing the Framingham Risk Assessment Tool and further CVD risk stratification using novel markers such as high sensitivity C-reactive protein, family history, and functional capacity may identify unique subsets of women at higher risk for CVD. Nurse practitioners can be instrumental in this assessment, education, and treatment of women at risk for CVD. [source] Inflammation in end-stage renal disease: The hidden enemy (Review Article)NEPHROLOGY, Issue 1 2006PETER STENVINKEL SUMMARY: Cardiovascular disease (CVD) remains the major cause of morbidity and mortality in end-stage renal disease (ESRD) patients. As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of CVD in this high-risk population, inflammation (interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor. Indeed, several different inflammatory biomarkers, such as high sensitivity C-reactive protein (hs-CRP), have been shown to independently predict mortality in ESRD patients. As CRP is so strongly associated with vascular disease it has been suggested that this hepatic-derived protein is not only a marker, but also a mediator, of vascular disease. Although in vitro data from studies on endothelial cells, monocytes-macrophages and smooth muscle cells support a direct role for CRP in atherogenesis, data from studies performed in vivo have been controversial. The causes of the highly prevalent state of inflammation in ESRD are multiple, including inflammatory signals associated with the dialysis procedure, decreased renal function, volume overload, comorbidity and intercurrent clinical events. As the prevalence of inflammation varies considerably between continents and races, dietary and/or genetic factors may have an impact on inflammation in ESRD. Elevated CRP in dialysis patients could be evaluated at three different levels: (i) national/regional level; (ii) dialysis unit level; and (iii) individual patient level. [source] Proinflammatory Cytokines, Hepatocyte Growth Factor and Adipokines in Peritoneal Dialysis PatientsARTIFICIAL ORGANS, Issue 7 2010Chien-Te Lee Abstract Chronic inflammation is a well-recognized complication in dialysis patients and a potential role of the adipose tissue as an important tissue of origin contributing to inflammation has been proposed. Stable peritoneal dialysis (PD) patients were enrolled to investigate the relationship between serum levels of proinflammatory cytokines and adipokines. Our results revealed that there was a strong association between high sensitivity C-reactive protein and interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-,) but not with IL-10 and IL-18. IL-6 correlated with TNF-,, IL-10, and IL-18. No association was found between IL-10 and IL-18. Adiponectin was positively correlated with all proinflammatory cytokines, except IL-10. No significant association was found between resistin and proinflammatory cytokines. Hepatocyte growth factor (HGF) was directly related to proinflammatory cytokines but not with adipokines. The presence of residual kidney function (RKF) affected IL-6, TNF-,, and HGF levels. The peritoneal transport property did not influence inflammatory cytokine and adipokine levels. In conclusion, there was a close relationship between proinflammatory cytokines and adipokines. HGF correlated with proinflammatory cytokines but not with adipokines. The PD-related factors such as RKF, peritoneal property and dialysis glucose load affected levels of proinflammatory cytokines. Body mass index was an important determinant of leptin and adiponectin in PD patients. [source] Effects of the angiotensin II receptor blocker losartan on the monocyte expression of biglycan in hypertensive patientsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2010Maria A Sardo Summary 1.,Recently, we demonstrated that biglycan (BGN) is increased in circulating monocyte cells from hypertensive patients and that angiotensin (Ang) II is able to increase BGN expression. The present study was designed to investigate the effects of treatment with the angiotensin AT1 receptor antagonist losartan on monocyte BGN mRNA and protein expression in essential hypertension. 2.,One hundred and twenty-six newly diagnosed hypertensive patients without additional risk factors for atherosclerosis and cardiovascular disease were treated with 100 mg losartan once daily for 6 months. Biglycan mRNA and protein expression was determined in monocytes isolated from peripheral blood before (T0) and after (T1) therapy. Plasma levels of interleukin (IL)-6, tumour necrosis factor (TNF)-, and high sensitivity C-reactive protein (hs-CRP) were also determined. In addition, BGN mRNA and protein expression was determined after the ex vivo addition of 1 ,mol/L AngII to monocytes isolated from 20 randomly selected hypertensive patients. 3.,Biglycan mRNA and protein expression, blood pressure and plasma levels of fibrinogen, IL-6, TNF-, and CRP were significantly lower at T1 than at T0. Variations in BGN expression were associated with inflammatory markers, but not directly with blood pressure. In AngII-stimulated monocytes, BGN mRNA and protein expression was significantly lower at T1 that at T0. Moreover, mean BGN mRNA expression in AngII-stimulated monocytes isolated from losartan-treated patients was similar to baseline expression in unstimulated monocytes from untreated patients. 4.,The results of the present study show that losartan can reduce BGN expression in monocytes from hypertensive patients, without any linear association with blood pressure, suggesting that the effects of AngII on BGN expression in monocytes may be modulated, in part, by an AT1 receptor blocker. [source] | ||||||||||