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      Club Cell-16 and RelB as Novel Determinants of Arterial Stiffness in Exacerbating COPD Patients

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          Abstract

          Background

          Exacerbations of chronic obstructive pulmonary disease (COPD) are acute events of worsened respiratory symptoms that may increase the risk of cardiovascular disease (CVD), a leading cause of mortality amongst COPD patients. The utility of lung-specific inflammatory mediators such as club cell protein-16 (CC-16) and surfactant protein D (SPD) and that of a novel marker of CV outcomes in COPD- RelB- in predicting adverse cardiovascular events during exacerbation is not known.

          Methods

          Thirty-eight subjects with COPD admitted to the hospital for severe exacerbation were included in this analysis. Clinical, physiological and arterial stiffness measurements were performed within 72 hours of admission; this was followed by measurements taken every 3 days until hospital discharge, then once a week until 30 days after discharge, and then again at 90 and 180 days. Plasma concentrations of inflammatory mediators were measured from peripheral venous blood taken at admission, and at days 15, 30, 90 and 180.

          Results

          CC-16 and RelB concentrations were increased at day 15 of exacerbations whereas SPD concentrations were decreased. The course of change in CC-16 and RelB levels over time was inversely associated with that of carotid-femoral pulse wave velocity, the gold-standard measure of arterial stiffness. Increases in CC-16 could predict a decreased number of subsequent exacerbations during follow-up.

          Conclusions

          Lung-specific (CC-16) and novel (RelB) biomarkers are associated with systemic cardiovascular changes over time. CC-16 can predict subsequent exacerbations in subjects with severe COPD and may be an important biomarker of pulmonary and systemic stress in COPD.

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          Most cited references38

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          2007 Guidelines for the management of arterial hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).

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            Aortic pulse-wave velocity and its relationship to mortality in diabetes and glucose intolerance: an integrated index of vascular function?

            Arterial distensibility measures, generally from pulse-wave velocity (PWV), are widely used with little knowledge of relationships to patient outcome. We tested whether aortic PWV predicts cardiovascular and all-cause mortality in type 2 diabetes and glucose-tolerance-tested (GTT) multiethnic population samples. Participants were randomly sampled from (1) a type 2 diabetes outpatient clinic and (2) primary care population registers, from which nondiabetic control subjects were given a GTT. Brachial blood pressures and Doppler-derived aortic PWV were measured. Mortality data over 10 years' follow-up were obtained. At any level of systolic blood pressure (SBP), aortic PWV was greater in subjects with diabetes than in controls. Mortality risk doubled in subjects with diabetes (hazard ratio 2.34, 95% CI 1.5 to 3.74) and in those with glucose intolerance (2.12, 95% CI 1.11 to 4.0) compared with controls. For all groups combined, age, sex, and SBP predicted mortality; the addition of PWV independently predicted all-cause and cardiovascular mortality (hazard ratio 1.08, 95% CI 1.03 to 1.14 for each 1 m/s increase) but displaced SBP. Glucose tolerance status and smoking were other independent contributors, with African-Caribbeans experiencing reduced mortality risk (hazard ratio 0.41, 95% CI 0.25 to 0.69). Aortic PWV is a powerful independent predictor of mortality in both diabetes and GTT population samples. In displacing SBP as a prognostic factor, aortic PWV is probably further along the causal pathway for arterial disease and may represent a useful integrated index of vascular status and hence cardiovascular risk.
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              Aortic stiffness is an independent predictor of primary coronary events in hypertensive patients: a longitudinal study.

              Arterial stiffness may predict coronary heart disease beyond classic risk factors. In a longitudinal study, we assessed the predictive value of arterial stiffness on coronary heart disease in patients with essential hypertension and without known clinical cardiovascular disease. Aortic stiffness was determined from carotid-femoral pulse wave velocity at baseline in 1045 hypertensives. The risk assessment of coronary heart disease was made by calculating the Framingham risk score according to the categories of gender, age, blood pressure, cholesterol, diabetes, and smoking. Mean age at entry was 51 years, and mean follow-up was 5.7 years. Coronary events (fatal and nonfatal myocardial infarction, coronary revascularization, and angina pectoris) and all cardiovascular events served as outcome variables in Cox proportional-hazard regression models. Fifty-three coronary events and 97 total cardiovascular events occurred. In univariate analysis, the relative risk of follow-up coronary event or any cardiovascular event increased with increasing level of pulse wave velocity; for 1 SD, ie, 3.5 m/s, relatives risks were 1.42 (95% confidence interval [CI], 1.10 to 1.82; P<0.01) and 1.41 (95% CI, 1.17 to 1.70; P<0.001), respectively. Framingham score significantly predicted the occurrence of coronary and all cardiovascular events in this population (P<0.01 and P<0.0001, respectively). In multivariate analysis, pulse wave velocity remained significantly associated with the occurrence of coronary event after adjustment either of Framingham score (for 3.5 m/s: relative risk, 1.34; 95% CI, 1.01 to 1.79; P=0.039) or classic risk factors (for 3.5 m/s: relative risk, 1.39; 95% CI, 1.08 to 1.79; P=0.01). Parallel results were observed for all cardiovascular events. This study provides the first direct evidence in a longitudinal study that aortic stiffness is an independent predictor of primary coronary events in patients with essential hypertension.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, CA USA )
                1932-6203
                25 February 2016
                2016
                : 11
                : 2
                : e0149974
                Affiliations
                [1 ]Department of Medicine, McGill University, Montreal, Quebec, Canada
                [2 ]Department of Pathology, McGill University, Montreal, Quebec, Canada
                [3 ]Department of Pharmacology & Therapeutics, McGill University, Montreal, Québec, Canada
                [4 ]Respiratory Epidemiology and Clinical Research Unit, Research Institute of the McGill University Health Center, Montreal, Québec, Canada
                [5 ]Meakins Christie Laboratories, McGill University, Montreal, Québec, Canada
                University of Rochester Medical Center, UNITED STATES
                Author notes

                Competing Interests: JB reports grants from the Canadian Institute of Health Research, CanCOLD Operating grant Collaborative Program Rx&D (Almirall, Astra Zeneca, Boehringer Ingelheim, GSK, Merck, Novartis, Takeda) and the Canadian Respiratory Research Network (CRRN), grants from Fonds de Recherche du Quebec-Sante (FRQ-S) RHN COPD, research and educational grants from Almirall, Astra Zeneca, Boehringer Ingelheim, GSK, Merck, Novartis for investigator initiated projects. All remaining author(s) declare that they have no competing interests. This does not alter the authors’ adherence to PLOS ONE policies on sharing data and materials.

                Conceived and designed the experiments: LL SSD JB CB. Performed the experiments: LL MZ PC KG. Analyzed the data: LL MZ PC KG. Contributed reagents/materials/analysis tools: SSD CB. Wrote the paper: LL SSD JB CB.

                Article
                PONE-D-15-49706
                10.1371/journal.pone.0149974
                4767820
                26914709
                38eeb5c2-3089-4796-a429-fa634b5f9545
                © 2016 Labonté et al

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 13 November 2015
                : 8 February 2016
                Page count
                Figures: 3, Tables: 2, Pages: 13
                Funding
                This study was funded as an investigator-initiated grant by GlaxoSmithKline Canada Ltd. LL was funded by a Canadian Institute of Health Research Doctoral Award. Infrastructure for this project was supported by the Canada Foundation for Innovation (CFI) -Leaders Opportunities Fund (CJB). CJB was supported by a salary award from the Fonds de Recherche du Quebec- Sante (FRQ-S).The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Medicine and Health Sciences
                Pulmonology
                Chronic Obstructive Pulmonary Disease
                Biology and Life Sciences
                Immunology
                Immune Response
                Inflammation
                Medicine and Health Sciences
                Immunology
                Immune Response
                Inflammation
                Medicine and Health Sciences
                Pathology and Laboratory Medicine
                Signs and Symptoms
                Inflammation
                Physical Sciences
                Materials Science
                Material Properties
                Mechanical Properties
                Stiffness
                Biology and Life Sciences
                Biochemistry
                Biomarkers
                Medicine and Health Sciences
                Health Care
                Health Care Facilities
                Hospitals
                Medicine and Health Sciences
                Inflammatory Diseases
                Physical Sciences
                Materials Science
                Materials by Attribute
                Surfactants
                Medicine and Health Sciences
                Vascular Medicine
                Blood Pressure
                Custom metadata
                All relevant data are within the paper and its Supporting Information files.

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                Uncategorized

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