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      Novel Respiratory Disability Score Predicts COPD Exacerbations and Mortality in the SPIROMICS Cohort

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          Abstract

          Rationale

          Some COPD patients develop extreme breathlessness, decreased exercise capacity and poor health status yet respiratory disability is poorly characterized as a distinct phenotype.

          Objective

          To define respiratory disability in COPD based on available functional measures and to determine associations with risk for exacerbations and death.

          Methods

          We analyzed baseline data from a multi-center observational study (SPIROMICS). This analysis includes 2332 participants (472 with severe COPD, 991 with mild/moderate COPD, 726 smokers without airflow obstruction and 143 non-smoking controls).

          Measurements

          We defined respiratory disability by ≥4 of 7 criteria: mMRC dyspnea scale ≥3; Veterans Specific Activity Questionnaire <5; 6-minute walking distance <250 m; St George’s Respiratory Questionnaire activity domain >60; COPD Assessment Test >20; fatigue (FACIT-F Trial Outcome Index) <50; SF-12 <20.

          Results

          Using these criteria, respiratory disability was identified in 315 (13.5%) participants (52.1% female). Frequencies were severe COPD 34.5%; mild-moderate COPD 11.2%; smokers without obstruction 5.2% and never-smokers 2.1%. Compared with others, participants with disability had more emphysema (13.2 vs. 6.6%) and air-trapping (37.0 vs. 21.6%) on HRCT (P<0.0001). Using principal components analysis to derive a disability score, two factors explained 71% of variance, and a cut point −1.0 reliably identified disability. This disability score independently predicted future exacerbations (ß=0.34; CI 0.12, 0.64; P=0.003) and death (HR 2.97; CI 1.54, 5.75; P=0.001). Thus, participants with disability by this criterion had almost three times greater mortality compared to those without disability.

          Conclusion

          Our novel SPIROMICS respiratory disability score in COPD was associated with worse airflow obstruction as well as airway wall thickening, lung parenchymal destruction and certain inflammatory biomarkers. The disability score also proved to be an independent predictor of future exacerbations and death. These findings validate disability as an important phenotype in the spectrum of COPD.

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          Most cited references 17

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          The natural history of chronic airflow obstruction.

          A prospective epidemiological study of the early stages of the development of chronic obstructive pulmonary disease was performed on London working men. The findings showed that forced expiratory volume in one second (FEV1) falls gradually over a lifetime, but in most non-smokers and many smokers clinically significant airflow obstruction never develops. In susceptible people, however, smoking causes irreversible obstructive changes. If a susceptible smoker stops smoking he will not recover his lung function, but the average further rates of loss of FEV1 will revert to normal. Therefore, severe or fatal obstructive lung disease could be prevented by screening smokers' lung function in early middle age if those with reduced function could be induced to stop smoking. Infective processes and chronic mucus hypersecretion do not cause chronic airflow obstruction to progress more rapidly. There are thus two largely unrelated disease processes, chronic airflow obstruction and the hypersecretory disorder (including infective processes).
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            Clinical Significance of Symptoms in Smokers with Preserved Pulmonary Function.

            Currently, the diagnosis of chronic obstructive pulmonary disease (COPD) requires a ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) of less than 0.70 as assessed by spirometry after bronchodilator use. However, many smokers who do not meet this definition have respiratory symptoms.
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              Comparison of computed density and microscopic morphometry in pulmonary emphysema.

              The purpose of this prospective study was to verify whether the percentage area of lung occupied by lowest attenuation values on high-resolution computed tomography (HRCT) scans reflects microscopic emphysema and to compare this quantification with the information yielded by the most widely used pulmonary function tests (PFT). Preoperative HRCT scans were obtained with 1-cm intervals in 38 subjects. With a semiautomatic evaluation procedure, the percentage areas occupied by attenuation values inferior to thresholds ranging from -900 Hounsfield units (HU) to -970 HU were calculated for the lobe or lung to be resected. Emphysema was microscopically quantified by using a computer-based method, measuring the perimeters and interwall distances of alveoli and alveolar ducts. The strongest correlation was found for -950 HU. As a second step, we evaluated possible correlations between PFT and microscopic measurements. Finally, considering the microscopic measurements as a standard, we tried to investigate their relationships with each of the PFT and with the relative area occupied by attenuation values lower than -950 HU for both lungs. This revealed that the diffusing capacity for carbon monoxide associated with HRCT quantification is sufficient to predict microscopic measurements. We concluded that the percentage area of lung occupied by attenuation values lower than -950 HU is a valid index of pulmonary emphysema.
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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
                04 August 2020
                2020
                : 15
                : 1887-1898
                Affiliations
                [1 ]Departments of Medicine and Physiology, David Geffen School of Medicine, University of California Los Angeles , Los Angeles, CA, USA
                [2 ]Section of Pulmonary and Critical Care Medicine, Department of Veterans Affairs Medical Center, University of Utah , Salt Lake City, UT, USA
                [3 ]Pulmonary and Critical Care Medicine Division, Department of Internal Medicine, University of Michigan Health System , Ann Arbor, MI, USA
                [4 ]Veterans Affairs Ann Arbor Healthcare System , Ann Arbor, MI, USA
                [5 ]National Jewish Health, University of Colorado School of Medicine , Denver, CO, USA
                [6 ]University of North Carolina Marisco Lung Institute , Chapel Hill, NC, USA
                [7 ]Department of Radiology, University of Iowa , Iowa City, IA, USA
                [8 ]Department of Pulmonary and Critical Care Medicine, Temple University , Philadelphia, PA, USA
                [9 ]Department of Medicine, University of Alabama at Birmingham , Birmingham, AL, USA
                [10 ]Johns Hopkins University School of Medicine , Baltimore, MD, USA
                [11 ]Department of Medicine, University of Illinois at Chicago , Chicago, IL, USA
                [12 ]Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California San Francisco , San Francisco, CA, USA
                [13 ]Wake Forest School of Medicine , Winston-Salem, NC, USA
                [14 ]Department of Medicine, Columbia University Medical Center , New York, NY, USA
                [15 ]Joan and Sanford I Weill Department of Medicine, Division of Pulmonary and Critical Care Medicine, Weill Cornell Medicine , New York, NY, USA
                Author notes
                Correspondence: Christopher B Cooper Departments of Medicine and Physiology,David Geffen School of Medicine,University of California Los Angeles ,10833 Le Conte Avenue, 37-131 CHS, Los Angeles, CA90095, USA Email ccooper@mednet.ucla.edu
                Article
                250191
                10.2147/COPD.S250191
                7417644
                © 2020 Cooper 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: 2, Tables: 3, References: 24, Pages: 12
                Funding
                SPIROMICS was supported by contracts from the NIH/NHLBI (HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C), grants from the NIH/NHLBI (U01 HL137880 and U24 HL141762), and supplemented by contributions made through the Foundation for the NIH and the COPD Foundation from AstraZeneca/MedImmune; Bayer; Bellerophon Therapeutics; Boehringer-Ingelheim Pharmaceuticals, Inc.; Chiesi Farmaceutici S.p.A.; Forest Research Institute, Inc.; GlaxoSmithKline; Grifols Therapeutics, Inc.; Ikaria, Inc.; Novartis Pharmaceuticals Corporation; Nycomed GmbH; ProterixBio; Regeneron Pharmaceuticals, Inc.; Sanofi; Sunovion; Takeda Pharmaceutical Company; and Theravance Biopharma and Mylan.
                Categories
                Original Research

                Respiratory medicine

                mortality, exacerbation rate, frailty, disability, spiromics

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