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      FEV 1 is a stronger mortality predictor than FVC in patients with moderate COPD and with an increased risk for cardiovascular disease

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          Abstract

          Purpose

          Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide. Impaired lung function is associated with heightened risk for death, cardiovascular events, and COPD exacerbations. However, it is unclear if forced expiratory volume in one second (FEV 1) and forced vital capacity (FVC) differ in predictive value.

          Patients and Methods

          Data from 16,485 participants in the Study to Understand Mortality and Morbidity (SUMMIT) in COPD were analyzed. Patients were grouped into quintiles for each lung function parameter (FEV 1 %predicted, FVC %predicted, FEV 1/FVC). The four highest quintiles (Q2–Q5) were compared to the lowest (Q1) to assess their relationship with all-cause mortality, cardiovascular events, and moderate-to-severe and severe exacerbations. Cox-regression was used, adjusted for age, sex, ethnicity, body-mass index, smoking status, previous exacerbations, cardiovascular disease, treatment, and modified Medical Research Council dyspnea score.

          Results

          Compared to Q1 (<53.5% FEV 1 predicted), increasing FEV 1 quintiles (Q2 53.5–457.5% predicted, Q3 57.5–461.6% predicted, Q4 61.6–465.8% predicted, and Q5 ≥65.8%) were all associated with significantly decreased all-cause mortality (20% (4–34%), 28% (13–40%), 23% (7–36%), and 30% (15–42%) risk reduction, respectively). In contrast, a significant risk reduction (21% (4–35%)) was seen only between Q1 and Q5 quintiles of FVC. Neither FEV 1 nor FVC was associated with cardiovascular risk. Increased FEV 1 and FEV 1/FVC quintiles were also associated with the reduction of moderate-to-severe and severe exacerbations while, surprisingly, the highest FVC quintile was related to the heightened exacerbation risk (28% (8–52%) risk increase).

          Conclusion

          Our results suggest that FEV 1 is a stronger predictor for all-cause mortality than FVC in moderate COPD patients with heightened cardiovascular risk and that subjects with moderate COPD have very different risks.

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          Most cited references 17

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          Chronic obstructive pulmonary disease.

          Chronic obstructive pulmonary disease (COPD) is a common disease with high global morbidity and mortality. COPD is characterized by poorly reversible airway obstruction, which is confirmed by spirometry, and includes obstruction of the small airways (chronic obstructive bronchiolitis) and emphysema, which lead to air trapping and shortness of breath in response to physical exertion. The most common risk factor for the development of COPD is cigarette smoking, but other environmental factors, such as exposure to indoor air pollutants - especially in developing countries - might influence COPD risk. Not all smokers develop COPD and the reasons for disease susceptibility in these individuals have not been fully elucidated. Although the mechanisms underlying COPD remain poorly understood, the disease is associated with chronic inflammation that is usually corticosteroid resistant. In addition, COPD involves accelerated ageing of the lungs and an abnormal repair mechanism that might be driven by oxidative stress. Acute exacerbations, which are mainly triggered by viral or bacterial infections, are important as they are linked to a poor prognosis. The mainstay of the management of stable disease is the use of inhaled long-acting bronchodilators, whereas corticosteroids are beneficial primarily in patients who have coexisting features of asthma, such as eosinophilic inflammation and more reversibility of airway obstruction. Apart from smoking cessation, no treatments reduce disease progression. More research is needed to better understand disease mechanisms and to develop new treatments that reduce disease activity and progression.
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            The impact of obesity on US mortality levels: the importance of age and cohort factors in population estimates.

            To estimate the percentage of excess death for US Black and White men and women associated with high body mass, we examined the combined effects of age variation in the obesity-mortality relationship and cohort variation in age-specific obesity prevalence. We examined 19 National Health Interview Survey waves linked to individual National Death Index mortality records, 1986-2006, for age and cohort patterns in the population-level association between obesity and US adult mortality. The estimated percentage of adult deaths between 1986 and 2006 associated with overweight and obesity was 5.0% and 15.6% for Black and White men, and 26.8% and 21.7% for Black and White women, respectively. We found a substantially stronger association than previous research between obesity and mortality risk at older ages, and an increasing percentage of mortality attributable to obesity across birth cohorts. Previous research has likely underestimated obesity's impact on US mortality. Methods attentive to cohort variation in obesity prevalence and age variation in obesity's effect on mortality risk suggest that obesity significantly shapes US mortality levels, placing it at the forefront of concern for public health action.
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              Chronic obstructive pulmonary disease mortality and prevalence: the associations with smoking and poverty—a BOLD analysis

              Background Chronic obstructive pulmonary disease (COPD) is a commonly reported cause of death and associated with smoking. However, COPD mortality is high in poor countries with low smoking rates. Spirometric restriction predicts mortality better than airflow obstruction, suggesting that the prevalence of restriction could explain mortality rates attributed to COPD. We have studied associations between mortality from COPD and low lung function, and between both lung function and death rates and cigarette consumption and gross national income per capita (GNI). Methods National COPD mortality rates were regressed against the prevalence of airflow obstruction and spirometric restriction in 22 Burden of Obstructive Lung Disease (BOLD) study sites and against GNI, and national smoking prevalence. The prevalence of airflow obstruction and spirometric restriction in the BOLD sites were regressed against GNI and mean pack years smoked. Results National COPD mortality rates were more strongly associated with spirometric restriction in the BOLD sites (<60 years: men rs=0.73, p=0.0001; women rs=0.90, p<0.0001; 60+ years: men rs=0.63, p=0.0022; women rs=0.37, p=0.1) than obstruction (<60 years: men rs=0.28, p=0.20; women rs=0.17, p<0.46; 60+ years: men rs=0.28, p=0.23; women rs=0.22, p=0.33). Obstruction increased with mean pack years smoked, but COPD mortality fell with increased cigarette consumption and rose rapidly as GNI fell below US$15 000. Prevalence of restriction was not associated with smoking but also increased rapidly as GNI fell below US$15 000. Conclusions Smoking remains the single most important cause of obstruction but a high prevalence of restriction associated with poverty could explain the high ‘COPD’ mortality in poor countries.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                COPD
                copd
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove
                1176-9106
                1178-2005
                20 May 2020
                2020
                : 15
                : 1135-1142
                Affiliations
                [1 ]Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre , Manchester, UK
                [2 ]Division of Infection, Immunity & Respiratory Medicine, University of Manchester , Manchester, UK
                [3 ]Medical Department, Herlev and Gentofte Hospital , Herlev, Denmark
                [4 ]Section of Epidemiology, Department of Public Health, University of Copenhagen , Copenhagen, Denmark
                [5 ]Research & Development, GlaxoSmithKline , Middlesex, UK
                [6 ]University of Michigan Health System , Ann Arbor, MI, USA
                [7 ]University of Liverpool, Department of Medicine, Clinical Sciences Centre, University Hospital Aintree , Liverpool, UK
                [8 ]Pulmonary and Critical Care Division, Brigham and Women’s Hospital, Harvard Medical School , Boston, MA, USA
                [9 ]Statistics & Programming, Veramed Ltd ., Twickenham, UK
                [10 ]Research & Development, GlaxoSmithKline , Research Triangle Park, NC, USA
                [11 ]Division of Pulmonary and Critical Care Medicine, Weill Cornell Medicine , New York, NY, USA
                [12 ]British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh , Edinburgh, UK
                Author notes
                Correspondence: Andras Bikov 2nd Floor ERC Building, Wythenshawe Hospital, Southmoor Road, ManchesterM23 9LT, UKTel +36203141599Fax +441612915730 Email andras.bikov@gmail.com
                Article
                242809
                10.2147/COPD.S242809
                7247606
                32547001
                © 2020 Bikov et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 1, Tables: 2, References: 29, Pages: 8
                Funding
                This study was funded by GlaxoSmithKline plc (HZC113782/NCT01313676).
                Categories
                Original Research

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