TY - JOUR
T1 - Diffusing Capacity of Carbon Monoxide in Assessment of COPD
AU - Balasubramanian, Aparna
AU - MacIntyre, Neil R.
AU - Henderson, Robert J.
AU - Jensen, Robert L.
AU - Kinney, Gregory
AU - Stringer, William W.
AU - Hersh, Craig P.
AU - Bowler, Russell P.
AU - Casaburi, Richard
AU - Han, Mei Lan K.
AU - Porszasz, Janos
AU - Barr, R. Graham
AU - Make, Barry J.
AU - Wise, Robert A.
AU - McCormack, Meredith C.
N1 - Funding Information:
FUNDING/SUPPORT: This work was supported by the National Heart, Lung, and Blood Institute [T32 HL007534-36, U01 HL089897, and U01 HL089856]. The Genetic Epidemiology of COPD (COPDGene) study (NCT00608764) is also supported by the COPD Foundation through contributions made to an Industry Advisory Committee comprising AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Novartis, and Sunovion.Author contributions: M. C. M. contributed to the conception, design of the study, data analysis, interpretation, and preparation of the manuscript, and is the guarantor of the paper. A. B. contributed to data analysis, interpretation, and manuscript writing. R. J. H. contributed statistical support and performed all statistical analyses on the data. N. R. M. R. L. J. G. K. W. W. S, C. P. H. R. P. B. R. C. M. K. H. J. P. R. G. B. B. J. M. and R. A. W. contributed to data interpretation and revision of the manuscript. All authors reviewed and approved the manuscript prior to submission for publication. Financial/nonfinancial disclosures: The authors have reported to CHEST the following: N. R. M. reports site Principal Investigator for the National Institutes of Health-funded COPDGene study and consultant to Breathe Technologies, Ventec, and InspiRx Pharma, and that none of these have conflicting interests with the manuscript. C. P. H. reports research grants from Novartis and Boehringer Ingelheim; and consulting fees from AstraZeneca, Novartis, and 23andMe. R. P. B. served on the advisory boards (GlaxoSmithKline, Boehringer Ingelheim, and Mylan) and received research grants (GlaxoSmithKline and Boehringer Ingelheim) not related to the manuscript, and these activities have not influenced his work on the manuscript. R. C. reports institutional grant funding from GlaxoSmithKline, Boehringer Ingelheim, Astellas, and AstraZeneca; consulting for Astellas and Regeneron; advisory boards for Boehringer Ingelheim, AstraZeneca, GlaxoSmithKline, and MedImmune; speakers bureau for GlaxoSmithKline, AstraZeneca, and Boehringer Ingelheim; and stock ownership in Inogen. M. K. H. reports consulting for GlaxoSmithKline, Boehringer Ingelheim, and AstraZeneca; and research support from Novartis and Sunovion. R. G. B. reports grant funding from the COPD Foundation relating to and outside of this study. B. J. M. reports funding from the National Heart, Lung, and Blood Institute for the COPDGene study; grants and medical advisory boards from Boehringer Ingelheim, GlaxoSmithKline, AstraZeneca, and Sunovion; Data and Safety Monitoring Board fees from Spiration and Shire/Baxalta; CME personal fees from WebMD, National Jewish Health, American College of Chest Physicians, Projects in Knowledge, Hybrid Communications, SPIRE Learning, Ultimate Medical Academy, Catamount Medical, Eastern Pulmonary Society, Catamount Medical Communications, Medscape, Eastern VA Medical Center, Academy Continued Healthcare Learning, and Mt. Sinai Medical Center; royalties from UpToDate; medical advisory boards from Novartis, Phillips, Third Pole, Science 24/7, and Vernoa; and grants from Pearl, outside the submitted work. M. C. M. reports royalties from UpToDate for authorship and has no conflicts of interest related to the manuscript. None declared (A. B. R. J. H. R. L. J. G. K. W. W. S. J. P. R. A. W.). Role of sponsors: The sponsor had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript. Additional information: The e-Tables and e-Figures can be found in the Supplemental Materials section of the online article.
Funding Information:
FUNDING/SUPPORT: This work was supported by the National Heart, Lung, and Blood Institute [ T32 HL007534-36 , U01 HL089897 , and U01 HL089856 ]. The Genetic Epidemiology of COPD (COPDGene) study ( NCT00608764 ) is also supported by the COPD Foundation through contributions made to an Industry Advisory Committee comprising AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Novartis, and Sunovion.
Publisher Copyright:
© 2019
PY - 2019/12
Y1 - 2019/12
N2 - Background: Diffusing capacity of the lung for carbon monoxide (DLCO) is inconsistently obtained in patients with COPD, and the added benefit of DLCO testing beyond that of more common tools is unknown. Objective: The goal of this study was to determine whether lower DLCO is associated with increased COPD morbidity independent of emphysema assessed via spirometry and CT imaging. Methods: Data for 1,806 participants with COPD from the Genetic Epidemiology of COPD (COPDGene) study 5-year visit were analyzed, including pulmonary function testing, quality of life, symptoms, exercise performance, and exacerbation rates. DLCO percent predicted was primarily analyzed as a continuous variable and additionally categorized into four groups: (1) DLCO and FEV1 > 50% (reference); (2) only DLCO ≤ 50%; (3) only FEV1 ≤ 50%; and (4) both ≤ 50% predicted. Outcomes were modeled by using multivariable linear and negative binomial regression, including emphysema and FEV1 percent predicted among other confounders. Results: In multivariable analyses, every 10% predicted decrease in DLCO was associated with symptoms and quality of life (COPD Assessment Test, 0.53 [P < .001]; St. George's Respiratory Questionnaire, 1.67 [P < .001]; Medical Outcomes Study Short Form 36 Physical Function, –0.89 [P < .001]), exercise performance (6-min walk distance, –45.35 feet; P < .001), and severe exacerbation rate (rate ratio, 1.14; P < .001). When categorized, severe impairment in DLCO alone, FEV1 alone, or both DLCO and FEV1 were associated with significantly worse morbidity compared with the reference group (P < .05 for all outcomes). Conclusions: Impairment in DLCO was associated with increased COPD symptoms, reduced exercise performance, and severe exacerbation risk even after accounting for spirometry and CT evidence of emphysema. These findings suggest that DLCO should be considered for inclusion in future multidimensional tools assessing COPD.
AB - Background: Diffusing capacity of the lung for carbon monoxide (DLCO) is inconsistently obtained in patients with COPD, and the added benefit of DLCO testing beyond that of more common tools is unknown. Objective: The goal of this study was to determine whether lower DLCO is associated with increased COPD morbidity independent of emphysema assessed via spirometry and CT imaging. Methods: Data for 1,806 participants with COPD from the Genetic Epidemiology of COPD (COPDGene) study 5-year visit were analyzed, including pulmonary function testing, quality of life, symptoms, exercise performance, and exacerbation rates. DLCO percent predicted was primarily analyzed as a continuous variable and additionally categorized into four groups: (1) DLCO and FEV1 > 50% (reference); (2) only DLCO ≤ 50%; (3) only FEV1 ≤ 50%; and (4) both ≤ 50% predicted. Outcomes were modeled by using multivariable linear and negative binomial regression, including emphysema and FEV1 percent predicted among other confounders. Results: In multivariable analyses, every 10% predicted decrease in DLCO was associated with symptoms and quality of life (COPD Assessment Test, 0.53 [P < .001]; St. George's Respiratory Questionnaire, 1.67 [P < .001]; Medical Outcomes Study Short Form 36 Physical Function, –0.89 [P < .001]), exercise performance (6-min walk distance, –45.35 feet; P < .001), and severe exacerbation rate (rate ratio, 1.14; P < .001). When categorized, severe impairment in DLCO alone, FEV1 alone, or both DLCO and FEV1 were associated with significantly worse morbidity compared with the reference group (P < .05 for all outcomes). Conclusions: Impairment in DLCO was associated with increased COPD symptoms, reduced exercise performance, and severe exacerbation risk even after accounting for spirometry and CT evidence of emphysema. These findings suggest that DLCO should be considered for inclusion in future multidimensional tools assessing COPD.
KW - COPD
KW - pulmonary diffusing capacity
KW - pulmonary gas exchange
UR - http://www.scopus.com/inward/record.url?scp=85072770597&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85072770597&partnerID=8YFLogxK
U2 - 10.1016/j.chest.2019.06.035
DO - 10.1016/j.chest.2019.06.035
M3 - Article
C2 - 31352035
AN - SCOPUS:85072770597
SN - 0012-3692
VL - 156
SP - 1111
EP - 1119
JO - CHEST
JF - CHEST
IS - 6
ER -