Rapid lung function decline in smokers is a risk factor for COPD and is attenuated by angiotensin-converting enzyme inhibitor use.

Abstract

Cigarette smoking is the most important risk factor for COPD in the United States. Host factors that influence the rapid rate of FEV1 decline in smokers and how decline rate influences risk for developing COPD are unknown. The aim of this study was to characterize the rate of FEV1 decline in ever smokers, compare the risk of incident COPD between those with rapid decline and others, and determine the effect of selected drugs on rapid decline. A total of 1,170 eligible ever smokers from the longitudinal Lovelace Smokers Cohort with repeat spirometry tests over a minimum follow-up period of 3 years (mean follow-up, 5.9 years) were examined, including 809 ever smokers without a spirometric abnormality at baseline. Longitudinal absolute decline in postbronchodilator FEV1 from the slope of the spirometric values over all examinations was annualized and classified as rapid (≥30 mL/y), normal (0-29.9 mL/y), or no (>0 mL/y) decline. Logistic regression and Kaplan-Meier survival curves were used for the analysis. Approximately 32% of ever smokers exhibited rapid decline. Among ever smokers without a baseline spirometric abnormality, rapid decline was associated with an increased risk for incident COPD (OR, 1.88; P=.003). The use of angiotensin-converting enzyme (ACE) inhibitors at baseline examination was protective against rapid decline, particularly among those with comorbid cardiovascular disease, hypertension, or diabetes (ORs 0.48, 0.48, and 0.12, respectively; P≤.02 for all analyses). Ever smokers with a rapid decline in FEV1 are at higher risk for COPD. Use of ACE inhibitors by smokers may protect against this rapid decline and the progression to COPD.