Rapid lung function decline raises risk of death and hospitalization

May 01, 2006

Rapid lung function decline significantly increases the risk of death and hospitalization for individuals with chronic obstructive pulmonary disease (COPD).

These findings appear in the May 1 issue of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

David Mannino, M.D., of the University of Kentucky Medical Center, and two associates found that patients with advanced COPD and rapid lung function decline are 10 times more likely to die than individuals with normal lung function.

COPD, an important cause of hospitalization and death, results from persistent obstruction of the airways associated with either severe emphysema or chronic bronchitis. In emphysema, the tiny air sacs of the lung (alveoli) become enlarged and their walls are destroyed. In chronic bronchitis, the bronchial glands enlarge, causing chronic cough and excess mucus. Ten to 15 percent of all smokers develop COPD as a result of irritants in tobacco that causes inflammation of the alveoli.

Over the course of three years, the investigators analyzed 13,756 middle-aged adults, all of whom participated in the 1986 Atherosclerosis Risk in the Communities Study and provided baseline information on respiratory symptoms and diseases. The researchers tested the participants' lung function twice--once at the start of the study and during a follow-up three years later.

The authors classified patients with the worst lung function as "rapid decliners." Twenty-five percent of the entire study population (3,437 individuals) fell into this high-mortality category. Of the 720 subjects who died during the study, 273 (38 percent) were considered "rapid decliners."

In addition, patients in advanced stages of COPD who were also "rapid decliners" were hospitalized at rate 40 times higher than those with normal lung function at baseline who had no rapid lung decline over the three-year period.

"Mean annual loss of lung function in the overall cohort was 62 ml," said Dr. Mannino. "The mean loss of lung function (FEV1) as a percentage of the baseline value was 1.5 percent annually. Participants in the most rapidly declining quartile of FEV1 had a mean annual loss of 171 ml, which was 4.7 percent of the baseline level per year."

The authors noted that the average annual loss of 62 ml in lung function was higher than that shown in other similar studies, including the Honolulu Heart Cohort at 26 ml, the Busselton Health Study at 30 to 40 ml, the Nottingham Study at 38 ml, and the Copenhagen City Heart Study at 22 to 38 ml.

The authors acknowledged the limitations of their analysis. For example, they only measured lung function twice during the three-year investigation. "It is possible that people may have had a really good day or really bad day at either the baseline or follow-up examination, influencing our results," said Dr. Mannino.

He noted that the group in which rapid decline in FEV1 showed the greatest predictive value for death and hospitalization was also the one least like to be affected by any source of error. Although 461 "rapid decliners" were classified as having respiratory symptoms, none had either a lung abnormality or lung disease.

"The impact of rapid decline in FEV1 was stronger in adults with normal or near-normal lung function at baseline and suggests that this group of people may need more frequent screening and interventions beyond what is recommended," said Dr. Mannino.
Contact: David M. Mannino, M.D. Division of Pulmonary and Critical Care Medicine, University of Kentucky Medical Center, 800 Rose Street, MN 614, Lexington, KY 40536
Phone: (859) 323-6608
E-mail: dmannino@uky.edu

American Thoracic Society

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