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      Improved spirometric detection of small airway narrowing: concavity in the expiratory flow–volume curve in people aged over 40 years

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          Abstract

          Background and objective

          We have explored whether assessing the degree of concavity in the descending limb of the maximum expiratory flow–volume curve enhanced spirometric detection of early small airway disease.

          Methods

          We used spirometry records from 890 individuals aged ≥40 years (mean 59 years), recruited for the Burden of Obstructive Lung Disease Australia study. Central and peripheral concavity indices were developed from forced expired flows at 50% and 75% of the forced vital capacity, respectively, using an ideal line joining peak flow to zero flow.

          Results

          From the 268 subjects classified as normal never smokers, mean values for post-bronchodilator central concavity were 18.6% in males and 9.1% in females and those for peripheral concavity were 50.5% in males and 52.4% in females. There were moderately strong correlations between concavity and forced expired ratio (forced expiratory volume in 1 second/forced vital capacity) and mid-flow rate (forced expiratory flow between 25% and 75% of the FVC [FEF 25%–75%]; r=−0.70 to −0.79). The additional number of individuals detected as abnormal using the concavity indices was substantial, especially compared with FEF 25%–75%, where it was approximately doubled. Concavity was more specific for symptoms.

          Conclusion

          The inclusion of these concavity measures in the routine reports of spirometry would add information on small airway obstruction at no extra cost, time, or effort.

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          Most cited references 28

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          Site and nature of airway obstruction in chronic obstructive lung disease.

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            The relations between structural changes in small airways and pulmonary-function tests.

            To examine the relation between small-airways abnormalities and specific lung functions, we performed pulmonary-function tests in 36 patients, of whom two were nonsmokers, one to three days before open-lung biopsy for localized pulmonary lesions. The primary lesion in the small airways was a progressive inflammatory reaction leading to fibrosis with connective-tissue deposition in the airway walls. Increase in disease in small airways correlated with deterioration in lung function. Lesions could be reliably detected (P less than 0.05) by tests for closing capacity, the volume at which air and helium flow ere equal (a test of airway caliber and elastic recoil), and the slope of phase III of the single-breath washout curve (which tests evenness of ventilation). These tests showed abnormalities at a time when the pathologic changes were still potentially reversible and when other tests were not appreciably changed.
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              Noninvasive assessment of airway alterations in smokers: the small airways revisited.

              It has been shown that structural changes in small airways of smokers with average smoking histories greater than 35 pack-years could be reflected in the single-breath washout test. The more sophisticated multiple breath washout test (MBW) has the potential to anatomically locate the affected small airways in acinar and conductive lung zones through increased phase III slope indices S(acin) and S(cond), respectively. Pulmonary function, S(acin), and S(cond) were obtained in 63 normal never-smokers and in 169 smokers classified according to smoking history ( 30 pack-years). Compared with never-smokers, significant changes in S(acin) (p = 0.02), S(cond) (p < 0.001), and diffusing capacity (DL(CO); p < 0.001) were detected from greater than 10 pack-years onwards. Spirometric abnormality was significant only from greater than 20 pack-years onwards. In smokers with greater than 30 pack-years and DL(CO) less than 60% predicted, the presence of emphysema resulted in disproportionally larger S(acin) than S(cond) increases. We conclude that S(cond) and S(acin) can noninvasively detect airway changes from as early as 10 pack-years onwards, locating the earliest manifestations of smoking-induced small airways alterations around the acinar entrance. In these early stages, the associated DL(CO) decrease may be a reflection of ventilation heterogeneity rather than true parenchymal destruction. In more advanced stages of smoking-induced lung disease, differential patterns of S(acin) and S(cond) are characteristic of the presence of parenchymal destruction in addition to peripheral airways alterations.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2017
                13 December 2017
                : 12
                : 3567-3577
                Affiliations
                [1 ]Faculty of Health, NHMRC Centre of Research Excellence for Chronic Respiratory Disease, School of Medicine, University of Tasmania, Hobart, Tasmania
                [2 ]Woolcock Emphysema Centre, Woolcock Institute of Medical Research, University of Sydney
                [3 ]Sydney Local Health District, Sydney, New South Wales
                [4 ]Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Victoria
                [5 ]South Western Sydney Clinical School, University of New South Wales, Sydney, New South Wales
                [6 ]Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, School of Population and Global Health, University of Melbourne, Melbourne, Victoria, Australia
                Author notes
                Correspondence: David P Johns, School of Medicine, University of Tasmania, MSP 17 Liverpool Street, Private Bag 34, MS1 UTAS, Hobart, Tasmania 7001, Australia, Tel +61 75 435 2485, Email david.johns@ 123456utas.edu.au
                Article
                copd-12-3567
                10.2147/COPD.S150280
                5732561
                © 2017 Johns 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.

                Categories
                Original Research

                Respiratory medicine

                copd, early airway disease, airflow obstruction

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