Approximately half of cases of COPD in older adults appear to stem from low forced expiratory volume in 1 second in early adulthood that declines at a normal rate, rather than the accelerated decline in normal FEV1 that has been considered “an obligate feature” of the disease, according to a report published online July 9 in the New England Journal of Medicine.
“Even though we cannot precisely estimate the contribution of the trajectory of low maximally attained lung function to COPD using our study design, our results suggest that this contribution may be substantial and that populations of patients with COPD comprise persons with different rates of decline in FEV1,” said Dr. Peter Lange of the Institute of Public Health, Copenhagen University, and his associates.
“This observation is in accord with previous studies and suggests that a substantial proportion of patients with COPD may not have had a rapid decline in FEV1, which for decades has been regarded as the hallmark of COPD,” the researchers added.
Previous authors have questioned the prevailing paradigm of COPD pathogenesis, but the possibility that low lung function in early adulthood can lead to later COPD has never been examined in a long-term, prospective study.
Dr. Lange and his colleagues explored that question using data from three large, independent longitudinal cohort studies: the Framingham Offspring Cohort, the Copenhagen City Heart Study, and the Lovelace Smokers Cohort. A total of 2,864 participants in the studies underwent serial spirometry beginning in early adulthood and continuing through approximately 22 years of follow-up. That allowed Dr. Lange and his associates to track their decline in lung function over time.
Overall, 332 participants (12% of the entire study population) had grade 2 or higher COPD at final follow-up when they were age 55 years or older, according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) grading system.
A total of 48% of the COPD patients followed the typical trajectory of a normal FEV1 at baseline that declined an average of 53 mL per year. However, 52% followed a different trajectory, with a low FEV1 at baseline that declined only 27 mL per year, the investigators said (N. Engl. J. Med. 2015;373:111-22).
Compared with participants who had normal FEV1 at baseline, those with initially low FEV1 were significantly more likely to be hospitalized with respiratory disease (25% vs. 18%), to be admitted for COPD (9% vs. 4%), and to die (32% vs. 25%) during follow-up.
People with a low FEV1 at baseline “had a risk of COPD at midlife that was more than three times as high as the risk among those with a higher baseline FEV1 (26% vs 7%),” Dr. Lange and his associates added.
The three cohort studies that contributed data to this analysis were funded by the National Heart, Lung, and Blood Institute, GlaxoSmithKline, the Capital Region of Copenhagen, the Danish Heart Foundation, the Danish Lung Foundation, the Velux Foundation, the state of New Mexico, and the National Institutes of Health. Dr. Lange reported receiving grants and personal fees from Almirall, AstraZeneca, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, Norpharma, Novartis, Pfizer, Takeda, and TEVA. His associates reported ties to numerous industry sources.