consideration objectives: To investigate the progression and mechanism(s) for fixed maximum expiratory airflow (Vmax) 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 arranges based on the severity of expiratory airflow limitation: (1) assign places to A included 5 asthmatic patients (four women; mean [+ or -] SD age, 51 [+ or -] 17 years) with mild persistent asthma (FE[Vsub1] > 80% predicted) with serial FE[Vsub1] measurements obtained prior to the not away study for 16 [+ or -] 4 years; (2) arrange B included 11 asthmatic patients (three women; mean age, 64 [+ or -] 11 years) with moderate persistent asthma (FE[Vsub1] of 60 to 80% predicted) with serial FE[Vsub1] measurements for 12 [+ or -] 4 years; and (3) arrange C included 5 asthmatic patients (three women; mean age, 55 [+ or -] 16 years) with unadorned persistent asthma (FE[V.sub.1] < 60% predicted) with serial FE[Vsub1] measurements for 11 [+ or -] 5 years.

Results: Lung CT indicated no or trivial emphysema, and diffusion was normal in all asthmatics. There was a marked los of lung elastic recoil at total lung capacity (TLC) in all asthmatic patients in collection B (16 [+ or -] 4 cm [Hsub2]O) and arrange C (15 [+ or -] 5 cm [Hsub2]O) nevertheless none or minimal in clump A (22 [+ or -] 1 cm [Hsub2]O) [p < 001] and los of elastic recoil accounted for 34% and 50% of decreased maximal expiratory airflow (Vmax) at 80% and 70% TLC respectively. Comparison with previous longitudinal data indicated individual asthmatics when in clinically stable condition remained predominantly in the same FE[Vsub1] percent predicted classification assemblage as in the current study

Conclusion: Patients with chronic moderate and bitter persistent asthma, despite optimal therapy, have reduc Vmax for many years in part to be paid to (early?) loss of lung elastic recoil from unknown mechanism(s). This challenges general concept of airway remodeling. (CHEST 2002; 121:715-721)

fundamental note words: airflow limitation; airway remodeling; asthma; elastic recoil

Abbreviations: G = conductance of s segment determined from flow-pressure curve; TLC = total lung capacity; Vmax = maximum expiratory airflow

**********

Many symptomatic patients with chronic asthma, despite maximal medical therapy, have irreversible expiratory airflow limitation cause to grow ie, FE[V.sub.1] < 80% predicted. Based forward the reduction of FE[V.sub.1], these asthmatic patients are classified as having moderate (60 to 80% predicted) or chaste (< 60% predicted), persistent asthma. (1) They have near-daily complaints of cough wheezing, chest tightness, shortness of breath, and/or decreased exercise tolerance despite polytherapy.

Asthma is believed on most investigators to be an "inflammatory" disease of the airways. (2) It has been put in mind ofed that unchecked, persistent, acute inflammation eventually leads to chronic inflammation and ultimately airway remodeling, luminal narrowing, and fixed expiratory airflow obstruction. (2) However, available evidenee put in mind ofs that there is no correlation between progressive airway changes and longitudinal deterioration of lung function in asthmatic patients. (2)

We newly reported the unsuspected marked los of lung elastic recoil not fit to emphysema in patients with chronic, stable asthma, which accounted for 25 to 39% of fixed expiratory airflow limitation. (3) The at hand study further explores the mechanism of expiratory airflow limitation in treated patients with chronic, stable asthma. Since these asthmatics had been followed up for many years with longitudinal spirometry, it provided an opportunity to further define the progression of expiratory airflow limitation.

MATERIALS AND METHODS

We reviewed the medical records of all asthmatic patients generally receiving treatment in our outpatient clinic to preferable every patient with longitudinal lung function studies > 5 years. All asthmatics had been treated concurrently by dint of the same physician (A.F.G.), and medications included short-acting and/or long-acting aerosolized and/or oral [[Beta].sub.2]-agonists, aerosolized ipratropium bromide, oral and/or inhaled corticosteroids, cromoglycate, nedocromil, oral theophylline, and leukotriene inhibitors. At all times, in all asthmatic patients, maximal therapy was used to achieve optimal clinical status and spirometric documented bronchodilation, as judg on FE[V.sub.1].

Similar to our earlier meditation (3) all patients satisfied the criteria for at least partially reversible bronchial reactivity. (1) Chronic bronchitis was not at any time diagnosed, and only one asthmatic was a general mild cigarette smoker (< 30 pack-years); the others not at any time smoked. Eleven of the 21 asthmatic patients in the current study were previously studied. (3) Longitudinal data have in no degree been reported.

Lung Studies

After obtaining informed co-operation we measured serial spirometry, maximum expiratory airflow (Vmax)-volume crooks static lung elastic recoil, (3-6) coefficient of retraction, (7) Vmax-static lung elastic recoil urgency curves, (3,4,8,9) maximum inspiratory and expiratory jaws pressures, (10) and lung CT (11) in patients with clinically stable asthma using similar techniques and equipment to those lately published. (3-5) We estimated the contribution of los of lung elastic recoil to reduction in Vmax as lately reported. (3)

...