Lung-function trajectories leading to chronic obstructive pulmonary disease

Peter Lange, Bartolome Celli, Alvar Agustí, Gorm Boje Jensen, Miguel Divo, Rosa Faner, Stefano Guerra, Jacob Louis Marott, Fernando Martinez, Pablo Martinez-Camblor, Paula Meek, Caroline A. Owen, Hans Petersen, Victor Pinto-Plata, Peter Schnohr, Akshay Sood, Joan B. Soriano, Yohannes Tesfaigzi, Jørgen Vestbo

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Abstract

BACKGROUND Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms. METHODS We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end. RESULTS Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure. CONCLUSIONS Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD.

Original languageEnglish (US)
Pages (from-to)111-122
Number of pages12
JournalNew England Journal of Medicine
Volume373
Issue number2
DOIs
StatePublished - Jul 9 2015

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Forced Expiratory Volume
Chronic Obstructive Pulmonary Disease
Lung
Observation

ASJC Scopus subject areas

  • Medicine(all)

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Lange, P., Celli, B., Agustí, A., Jensen, G. B., Divo, M., Faner, R., ... Vestbo, J. (2015). Lung-function trajectories leading to chronic obstructive pulmonary disease. New England Journal of Medicine, 373(2), 111-122. https://doi.org/10.1056/NEJMoa1411532

Lung-function trajectories leading to chronic obstructive pulmonary disease. / Lange, Peter; Celli, Bartolome; Agustí, Alvar; Jensen, Gorm Boje; Divo, Miguel; Faner, Rosa; Guerra, Stefano; Marott, Jacob Louis; Martinez, Fernando; Martinez-Camblor, Pablo; Meek, Paula; Owen, Caroline A.; Petersen, Hans; Pinto-Plata, Victor; Schnohr, Peter; Sood, Akshay; Soriano, Joan B.; Tesfaigzi, Yohannes; Vestbo, Jørgen.

In: New England Journal of Medicine, Vol. 373, No. 2, 09.07.2015, p. 111-122.

Research output: Contribution to journalArticle

Lange, P, Celli, B, Agustí, A, Jensen, GB, Divo, M, Faner, R, Guerra, S, Marott, JL, Martinez, F, Martinez-Camblor, P, Meek, P, Owen, CA, Petersen, H, Pinto-Plata, V, Schnohr, P, Sood, A, Soriano, JB, Tesfaigzi, Y & Vestbo, J 2015, 'Lung-function trajectories leading to chronic obstructive pulmonary disease', New England Journal of Medicine, vol. 373, no. 2, pp. 111-122. https://doi.org/10.1056/NEJMoa1411532
Lange, Peter ; Celli, Bartolome ; Agustí, Alvar ; Jensen, Gorm Boje ; Divo, Miguel ; Faner, Rosa ; Guerra, Stefano ; Marott, Jacob Louis ; Martinez, Fernando ; Martinez-Camblor, Pablo ; Meek, Paula ; Owen, Caroline A. ; Petersen, Hans ; Pinto-Plata, Victor ; Schnohr, Peter ; Sood, Akshay ; Soriano, Joan B. ; Tesfaigzi, Yohannes ; Vestbo, Jørgen. / Lung-function trajectories leading to chronic obstructive pulmonary disease. In: New England Journal of Medicine. 2015 ; Vol. 373, No. 2. pp. 111-122.
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abstract = "BACKGROUND Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms. METHODS We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80{\%} or <80{\%} of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end. RESULTS Among 657 persons who had an FEV1 of less than 80{\%} of the predicted value before 40 years of age, 174 (26{\%}) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80{\%} of the predicted value before 40 years of age, 158 (7{\%}) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure. CONCLUSIONS Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD.",
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T1 - Lung-function trajectories leading to chronic obstructive pulmonary disease

AU - Lange, Peter

AU - Celli, Bartolome

AU - Agustí, Alvar

AU - Jensen, Gorm Boje

AU - Divo, Miguel

AU - Faner, Rosa

AU - Guerra, Stefano

AU - Marott, Jacob Louis

AU - Martinez, Fernando

AU - Martinez-Camblor, Pablo

AU - Meek, Paula

AU - Owen, Caroline A.

AU - Petersen, Hans

AU - Pinto-Plata, Victor

AU - Schnohr, Peter

AU - Sood, Akshay

AU - Soriano, Joan B.

AU - Tesfaigzi, Yohannes

AU - Vestbo, Jørgen

PY - 2015/7/9

Y1 - 2015/7/9

N2 - BACKGROUND Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms. METHODS We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end. RESULTS Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure. CONCLUSIONS Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD.

AB - BACKGROUND Chronic obstructive pulmonary disease (COPD) is thought to result from an accelerated decline in forced expiratory volume in 1 second (FEV1) over time. Yet it is possible that a normal decline in FEV1 could also lead to COPD in persons whose maximally attained FEV1 is less than population norms. METHODS We stratified participants in three independent cohorts (the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort) according to lung function (FEV1 ≥80% or <80% of the predicted value) at cohort inception (mean age of patients, approximately 40 years) and the presence or absence of COPD at the last study visit. We then determined the rate of decline in FEV1 over time among the participants according to their FEV1 at cohort inception and COPD status at study end. RESULTS Among 657 persons who had an FEV1 of less than 80% of the predicted value before 40 years of age, 174 (26%) had COPD after 22 years of observation, whereas among 2207 persons who had a baseline FEV1 of at least 80% of the predicted value before 40 years of age, 158 (7%) had COPD after 22 years of observation (P<0.001). Approximately half the 332 persons with COPD at the end of the observation period had had a normal FEV1 before 40 years of age and had a rapid decline in FEV1 thereafter, with a mean (±SD) decline of 53±21 ml per year. The remaining half had had a low FEV1 in early adulthood and a subsequent mean decline in FEV1 of 27±18 ml per year (P<0.001), despite similar smoking exposure. CONCLUSIONS Our study suggests that low FEV1 in early adulthood is important in the genesis of COPD and that accelerated decline in FEV1 is not an obligate feature of COPD.

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