Alejandro A Diaz1, Matthew Strand2, Harvey O Coxson3, James C Ross4, Raul San Jose Estepar4, David Lynch5, Eva M van Rikxoort6, Ivan O Rosas1, Gary M Hunninghake1, Rachel K Putman1, Hiroto Hatabu4, Andrew Yen7, Gregory L Kinney8, John E Hokanson8, Edwin K Silverman9, James Crapo10, George R Washko1. 1. Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. 2. Division of Biostatistics and Bioinformatics, National Jewish Health, Denver, CO. 3. Department of Radiology, Vancouver General Hospital, Vancouver, British Columbia, Canada. 4. Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. 5. Department of Radiology, National Jewish Health, Denver, CO. 6. Diagnostic Image Analysis Group, Radboud University Medical Center, Nijmegen, the Netherlands. 7. Department of Radiology, University of California, San Diego, San Diego, CA. 8. Colorado School of Public Health, University of Colorado-Denver, Aurora, CO. 9. Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. 10. Department of Medicine, Division of Pulmonary and Critical Care Medicine, National Jewish Health, Denver, CO.
Abstract
BACKGROUND: In smokers, the lung parenchyma is characterized by inflammation and emphysema, processes that can result in local gain and loss of lung tissue. CT measures of lung density might reflect lung tissue changes; however, longitudinal data regarding the effects of CT lung tissue on FEV1 in smokers with and without COPD are scarce. METHODS: The 15th percentile of CT lung density was obtained from the scans of 3,390 smokers who completed baseline and 5-year follow-up of the Genetic Epidemiology of COPD (COPDGene) study visits. The longitudinal relationship between total lung capacity-adjusted lung density (TLC-PD15) and FEV1 was assessed by using multivariable mixed models. Separate models were performed in smokers at risk, smokers with preserved ratio and impaired spirometry (PRISm), and smokers with COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) staging system. RESULTS: The direction of the relationship between lung density and lung function was GOLD stage dependent. In smokers with PRISm, a 1-g/L decrease in TLC-PD15 was associated with an increase of 2.8 mL FEV1 (P = .02). In contrast, among smokers with GOLD III to IV COPD, a 1-g/L decrease in TLC-PD15 was associated with a decrease of 4.1 mL FEV1 (P = .002). CONCLUSIONS: A decline in TLC-PD15 was associated with an increase or decrease in FEV1 depending on disease severity. The associations are GOLD stage specific, and their presence might influence the interpretation of future studies that use CT lung density as an intermediate study end point for a decline in lung function. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT00608764; URL: www.clinicaltrials.gov.
BACKGROUND: In smokers, the lung parenchyma is characterized by inflammation and emphysema, processes that can result in local gain and loss of lung tissue. CT measures of lung density might reflect lung tissue changes; however, longitudinal data regarding the effects of CT lung tissue on FEV1 in smokers with and without COPD are scarce. METHODS: The 15th percentile of CT lung density was obtained from the scans of 3,390 smokers who completed baseline and 5-year follow-up of the Genetic Epidemiology of COPD (COPDGene) study visits. The longitudinal relationship between total lung capacity-adjusted lung density (TLC-PD15) and FEV1 was assessed by using multivariable mixed models. Separate models were performed in smokers at risk, smokers with preserved ratio and impaired spirometry (PRISm), and smokers with COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) staging system. RESULTS: The direction of the relationship between lung density and lung function was GOLD stage dependent. In smokers with PRISm, a 1-g/L decrease in TLC-PD15 was associated with an increase of 2.8 mL FEV1 (P = .02). In contrast, among smokers with GOLD III to IV COPD, a 1-g/L decrease in TLC-PD15 was associated with a decrease of 4.1 mL FEV1 (P = .002). CONCLUSIONS: A decline in TLC-PD15 was associated with an increase or decrease in FEV1 depending on disease severity. The associations are GOLD stage specific, and their presence might influence the interpretation of future studies that use CT lung density as an intermediate study end point for a decline in lung function. TRIAL REGISTRY: ClinicalTrials.gov; No.: NCT00608764; URL: www.clinicaltrials.gov.
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