Study objectives: To investigate the progression and mechanism(s) for fixed maximum expiratory airflow (V̇max) limitation in patients with chronic persistent asthma.
Methods: When optimally treated and in clinically stable condition, we studied 21 asthmatic patients and classified them into three groups based on the severity of expiratory airflow limitation: (1) group A included 5 asthmatic patients (four women; mean ± SD age, 51 ± 17 years) with mild persistent asthma (FEV1 > 80% predicted) with serial FEV1 measurements obtained prior to the present study for 16 ± 4 years; (2) group B included 11 asthmatic patients (three women; mean age, 64 ± 11 years) with moderate persistent asthma (FEV1 of 60 to 80% predicted) with serial FEV1 measurements for 12 ± 4 years; and (3) group C included 5 asthmatic patients (three women; mean age, 55 ± 16 years) with severe persistent asthma (FEV1 < 60% predicted) with serial FEV1 measurements for 11 ± 5 years.
Results: Lung CT indicated no or trivial emphysema, and diffusion was normal in all asthmatics. There was a marked loss of lung elastic recoil at total lung capacity (TLC) in all asthmatic patients in group B (16 ± 4 cm H2O) and group C (15 ± 5 cm H2O), but none or minimal in group A (22 ± 1 cm H2O) [p < 0.01], and loss of elastic recoil accounted for 34% and 50% of decreased maximal expiratory airflow (V̇max) at 80% and 70% TLC, respectively. Comparison with previous longitudinal data indicated individual asthmatics when in clinically stable condition remained predominantly in the same FEV1 percent predicted classification group as in the current study.
Conclusion: Patients with chronic moderate and severe persistent asthma, despite optimal therapy, have reduced V̇max for many years in part due to (early?) loss of lung elastic recoil from unknown mechanism(s). This challenges current concept of airway remodeling.