George R Washko1, Gregory L Kinney2, James C Ross3, Raúl San José Estépar3, MeiLan K Han4, Mark T Dransfield5, Victor Kim6, Hiroto Hatabu7, Carolyn E Come1, Russell P Bowler8, Edwin K Silverman9, James Crapo8, David A Lynch10, John Hokanson2, Alejandro A Diaz11. 1. Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115. 2. Department of Epidemiology, Colorado School of Public Health, University of Colorado, Denver, Colorado. 3. Surgical Planning Laboratory, Laboratory of Mathematics in Imaging, Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts. 4. Department of Medicine, Division of Pulmonary and Critical Care, University of Michigan, Ann Arbor, Michigan. 5. Division of Pulmonary and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama. 6. Department of Medicine, Division of Pulmonary and Critical Care Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania. 7. Department of Radiology, Brigham and Women's Hospital, Boston, Massachusetts. 8. Department of Medicine, Division of Pulmonary and Critical Care Medicine, National Jewish Health, Denver, Colorado. 9. Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts. 10. Department of Radiology, National Jewish Health, Denver, Colorado. 11. Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, MA 02115. Electronic address: ADiaz6@Partners.org.
Abstract
RATIONALE AND OBJECTIVE: Emphysema is characterized by airspace dilation, inflammation, and irregular deposition of elastin and collagen in the interstitium. Computed tomographic studies have reported that lung mass (LM) may be increased in smokers, a finding attributed to inflammatory and parenchymal remodeling processes observed on histopathology. We sought to examine the epidemiologic and clinical associations of LM in smokers. MATERIALS AND METHODS: Baseline epidemiologic, clinical, and computed tomography (CT) data (n = 8156) from smokers enrolled into the COPDGene Study were analyzed. LM was calculated from the CT scan. Changes in lung function at 5 years' follow-up were available from 1623 subjects. Regression analysis was performed to assess for associations of LM with forced expiratory volume in 1 second (FEV1) and FEV1 decline. RESULTS: Subjects with Global Initiative for Chronic Obstructive Lung Disease (GOLD) 1 chronic obstructive pulmonary disease had greater LM than either smokers with normal lung function or those with GOLD 2-4 chronic obstructive pulmonary disease (P < 0.001 for both comparisons). LM was predictive of the rate of the decline in FEV1 (decline per 100 g, -4.7 ± 1.7 mL/y, P = 0.006). CONCLUSIONS: Our cross-sectional data suggest the presence of a biphasic radiological remodeling process in smokers: the presence of such nonlinearity must be accounted for in longitudinal computed tomographic studies. Baseline LM predicts the decline in lung function.
RATIONALE AND OBJECTIVE:Emphysema is characterized by airspace dilation, inflammation, and irregular deposition of elastin and collagen in the interstitium. Computed tomographic studies have reported that lung mass (LM) may be increased in smokers, a finding attributed to inflammatory and parenchymal remodeling processes observed on histopathology. We sought to examine the epidemiologic and clinical associations of LM in smokers. MATERIALS AND METHODS: Baseline epidemiologic, clinical, and computed tomography (CT) data (n = 8156) from smokers enrolled into the COPDGene Study were analyzed. LM was calculated from the CT scan. Changes in lung function at 5 years' follow-up were available from 1623 subjects. Regression analysis was performed to assess for associations of LM with forced expiratory volume in 1 second (FEV1) and FEV1 decline. RESULTS: Subjects with Global Initiative for Chronic Obstructive Lung Disease (GOLD) 1 chronic obstructive pulmonary disease had greater LM than either smokers with normal lung function or those with GOLD 2-4 chronic obstructive pulmonary disease (P < 0.001 for both comparisons). LM was predictive of the rate of the decline in FEV1 (decline per 100 g, -4.7 ± 1.7 mL/y, P = 0.006). CONCLUSIONS: Our cross-sectional data suggest the presence of a biphasic radiological remodeling process in smokers: the presence of such nonlinearity must be accounted for in longitudinal computed tomographic studies. Baseline LM predicts the decline in lung function.
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