Clinical Epidemiology of COPD: Insights From 10 Years of the COPDGene Study

Diego J Maselli, Surya P Bhatt, Antonio Anzueto, Russell P Bowler, Dawn L DeMeo, Alejandro A Diaz, Mark T Dransfield, Ashraf Fawzy, Marilyn G Foreman, Nicola A Hanania, Craig P Hersh, Victor Kim, Gregory L Kinney, Nirupama Putcha, Emily S Wan, J Michael Wells, Gloria E Westney, Kendra A Young, Edwin K Silverman, MeiLan K Han, Barry J Make, Diego J Maselli, Surya P Bhatt, Antonio Anzueto, Russell P Bowler, Dawn L DeMeo, Alejandro A Diaz, Mark T Dransfield, Ashraf Fawzy, Marilyn G Foreman, Nicola A Hanania, Craig P Hersh, Victor Kim, Gregory L Kinney, Nirupama Putcha, Emily S Wan, J Michael Wells, Gloria E Westney, Kendra A Young, Edwin K Silverman, MeiLan K Han, Barry J Make

Abstract

The Genetic Epidemiology of COPD (COPDGene) study is a noninterventional, multicenter, longitudinal analysis of > 10,000 subjects, including smokers with a ≥ 10 pack-year history with and without COPD and healthy never smokers. The goal was to characterize disease-related phenotypes and explore associations with susceptibility genes. The subjects were extensively phenotyped with the use of comprehensive symptom and comorbidity questionnaires, spirometry, CT scans of the chest, and genetic and biomarker profiling. The objective of this review was to summarize the major advances in the clinical epidemiology of COPD from the first 10 years of the COPDGene study. We highlight the influence of age, sex, and race on the natural history of COPD, and the impact of comorbid conditions, chronic bronchitis, exacerbations, and asthma/COPD overlap.

Trial registration: ClinicalTrials.gov NCT00608764.

Keywords: COPD; COPDGene; chronic bronchitis; comorbidities; epidemiology; sex.

Copyright © 2019. Published by Elsevier Inc.

Figures

Figure 1
Figure 1
Sex distribution according to age groups of subjects with an FEV1 < 50% predicted (n = 532). A female predominance is noted at both ends of the spectrum: ages 45 to 54 years and 75 to 80 years. (Adapted with permission from Foreman et al.16)
Figure 2
Figure 2
Three-dimensional surface plots showing the relations between emphysema percentage, wall thickness, and COPD exacerbation frequency (vertical axis). A, Surface view of entire relation shows the largely independent effects of emphysema percentage and segmental wall thickness. B, Horizontal view emphasizes the increased exacerbation frequency at greater levels of emphysema. The very strong effect of the bronchial wall thickness at low levels of emphysema is also noted. (Adapted with permission from Han et al.29)
Figure 3
Figure 3
Relation between the PA:A ratio and the occurrence of severe exacerbations at baseline and during follow-up in the Genetic Epidemiology of COPD (COPDGene) study. The rates of exacerbations are shown by increments of 0.1 unit. The risk increased for exacerbations at the threshold of PA:A ratio of 1. PA:A = pulmonary artery:aorta. (Adapted with permission from Wells et al.30)
Figure 4
Figure 4
ORs with 95% CIs (in parentheses) for the risk of specific comorbidities based on COPD case status. Adjusted for age at enrollment, sex, race, pack-years smoked, and education level. For all conditions shown, COPD case status was significantly associated with increased risk for the condition with the exception of high cholesterol and obesity. CAD = coronary artery disease; CHF = congestive heart failure; GERD = gastroesophageal reflux disease; PVD = peripheral vascular disease. (Adapted with permission from Putcha et al.25)
Figure 5
Figure 5
Epidemiologic associations and findings of COPDGene. CVA = cerebrovascular accident; HTN = hypertension. See Figure 3 and 4 legends for expansion of other abbreviations.
Figure 6
Figure 6
Complex and multifactorial influence of demographic characteristics, comorbidities, emphysema, chronic bronchitis, and genetics on the disease progression of COPD. ACO = asthma/COPD overlap.

Source: PubMed

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