학술논문

Lobar Emphysema Distribution Is Associated With 5-Year Radiological Disease Progression
Document Type
article
Author
Boueiz, AdelChang, YaleCho, Michael HWashko, George RSan José Estépar, RaulBowler, Russell PCrapo, James DDeMeo, Dawn LDy, Jennifer GSilverman, Edwin KCastaldi, Peter JCrapo, JamesSilverman, EdwinMake, BarryRegan, ElizabethBeaty, TerriLaird, NanLange, ChristophSantorico, StephanieHokanson, JohnDeMeo, DawnHansel, NadiaHersh, CraigCastaldi, PeterMcDonald, Merry-LynnWan, EmilyHardin, MeganHetmanski, JacquelineParker, MargaretForeman, MarilynHobbs, BrianBusch, RobertQiao, DandiHalper-Stromberg, EitanBegum, FerdouseWon, SunghoLutz, SharonLynch, David ACoxson, Harvey OHan, MeiLan KHoffman, Eric AHumphries, StephenJacobson, Francine LJudy, Philip FKazerooni, Ella ANewell, John DRoss, James CEstépar, Raul JoséStoel, Berend CTschirren, Juergvan Rikxoort, Evavan Ginneken, BramWilson, Carla GQaisi, Mustafa AlGray, TeresaKluiber, AlexMann, TanyaSieren, JeredStinson, DouglasSchroeder, JoyceVan Beek, EdwinJensen, RobertEverett, DouglasFaino, AnnaStrand, MattWilson, CarlaHokanson, John EKinney, GregoryYoung, KendraPratte, KatherineDuca, LindseyCurtis, Jeffrey LMartinez, Carlos HPernicano, Perry GHanania, NicolaAlapat, PhilipBandi, VenkataAtik, MustafaBoriek, AladinGuntupalli, KalpathaGuy, ElizabethParulekar, AmitNachiappan, ArunJacobson, FrancineBarr, R GrahamThomashow, ByronAustin, JohnD’Souza, BelindaPearson, Gregory DN
Source
CHEST Journal. 153(1)
Subject
Clinical Research
Chronic Obstructive Pulmonary Disease
Lung
Emphysema
Prevention
2.1 Biological and endogenous factors
Aetiology
Respiratory
Aged
Comorbidity
Disease Progression
Female
Forced Expiratory Volume
Humans
Male
Middle Aged
Pulmonary Emphysema
Severity of Illness Index
Tomography
X-Ray Computed
clustering
COPD
COPD disease progression
emphysema distribution
machine learning
COPDGene Investigators
Clinical Sciences
Respiratory System
Language
Abstract
BackgroundEmphysema has considerable variability in its regional distribution. Craniocaudal emphysema distribution is an important predictor of the response to lung volume reduction. However, there is little consensus regarding how to define upper lobe-predominant and lower lobe-predominant emphysema subtypes. Consequently, the clinical and genetic associations with these subtypes are poorly characterized.MethodsWe sought to identify subgroups characterized by upper-lobe or lower-lobe emphysema predominance and comparable amounts of total emphysema by analyzing data from 9,210 smokers without alpha-1-antitrypsin deficiency in the Genetic Epidemiology of COPD (COPDGene) cohort. CT densitometric emphysema was measured in each lung lobe. Random forest clustering was applied to lobar emphysema variables after regressing out the effects of total emphysema. Clusters were tested for association with clinical and imaging outcomes at baseline and at 5-year follow-up. Their associations with genetic variants were also compared.ResultsThree clusters were identified: minimal emphysema (n = 1,312), upper lobe-predominant emphysema (n = 905), and lower lobe-predominant emphysema (n = 796). Despite a similar amount of total emphysema, the lower-lobe group had more severe airflow obstruction at baseline and higher rates of metabolic syndrome compared with subjects with upper-lobe predominance. The group with upper-lobe predominance had greater 5-year progression of emphysema, gas trapping, and dyspnea. Differential associations with known COPD genetic risk variants were noted.ConclusionsSubgroups of smokers defined by upper-lobe or lower-lobe emphysema predominance exhibit different functional and radiological disease progression rates, and the upper-lobe predominant subtype shows evidence of association with known COPD genetic risk variants. These subgroups may be useful in the development of personalized treatments for COPD.