Airway Wall Thickness in Asthma Assessed by Computed Tomography

Abstract

Postmortem studies have shown that airway wall thickening is present in asthmatic patients and may play a pathophysiologic role. We investigated the presence and characteristics of airway wall thickening in patients with asthma, using helical computed tomography. Eighty-one asthmatic patients and 28 healthy control subjects were studied cross-sectionally. Airway wall thickness was assessed by a validated method on the basis of wall area (WA), WA corrected by body surface area (WA/BSA), and WA%, defined as (WA/total area) x 100 at the apical bronchus of the right upper lobe. Airway luminal area (Ai) and Ai/BSA were also examined. Asthma duration and severity, pulmonary function, and serum eosinophil cationic protein levels were evaluated. Intraobserver and interobserver reproducibility of WA, WA%, and Ai measurements were good. As compared with control, WA, WA/BSA, and WA% were significantly increased in patients with mild (n = 13), moderate (39), and severe persistent (22) asthma but not in patients with intermittent asthma (7). Comparison of the four asthmatic subgroups demonstrated thicker airways in more severe disease, but no difference in Ai or Ai/BSA. When all asthmatic patients were analyzed together, WA and WA/BSA correlated with the duration, although weakly, and severity of asthma. WA and WA/BSA negatively correlated with FEV(1) (percentage of predicted), FEV(1)/FVC (%), and FEF(25-75%) (percentage of predicted), whereas WA% negatively correlated with only FEV(1). We conclude that airway wall thickening occurs in patients with asthma and is not limited to those with severe disease. The degree of airway wall thickening may relate to the duration and severity of disease and the degree of airflow obstruction.

Ventilation Heterogeneity in Ex-smokers without Airflow Limitation

“…Eighteen subjects (18 of 60 = 30%) reported normal VDP and 42 (42 of 60 = 70%) subjects reported abnormally elevated VDP. As shown in Figure 1 for three representative subjects, volunteers with normal VDP showed small or no ventilation defects along the periphery of the lung, whereas (16) 27 (14) 28 (17) .86 (1.0) Years quit smoking 19 (15) 13 (12) 21 (15) .06 (1.0) BMI, kg/m 2 29 (4) 29 (5) 30 (4) .5 (1.0) FVC, % pred 97 (13) 100 (10) 95 (14) .18 (1.0) FEV 1 , % pred 104 (13) 106 (12) 102 (14) .28 (1.0) FEV 1 /FVC 80 (6) 80 (6) 80 (6) .78 (1.0) RV/TLC, % pred 103 (15) 104 (12) 103 (16 ADC, apparent diffusion coefficient; BMI, body mass index; BSA, body surface area; DL CO , diffusing capacity for carbon monoxide; FEV 1 , forced expiratory volume in 1 second; FVC, forced vital capacity; LA, mean fifth generation airway lumen area; 6MWD, six-minute walk distance; RA 950 , relative area of the lung parenchyma with attenuation #À950 HU; RV, residual volume; SD, standard deviation; SGRQ, St. Georges Respiratory Questionnaire; TLC, total lung capacity; VDP, ventilation defect percent; WA%, mean fifth generation airway wall area percent.…”

“…It was previously shown that airway LA is related to body surface area (BSA) (17,18), and therefore, LA was normalized to BSA (LA/BSA). CT WA %, LA, and LA/BSA were measured for subsegmental bronchi including RB1, RB5, RB8, LB1, and LB8 airways because each of these feed individual lobes (RB1-RUL, RB5-RML, RB8-RLL, LB1-LUL, and LB8-LLL), and they were measurable for each subject.…”

Computed tomographic imaging of the airways: relationship to structure and function

“…In addition, the airway lumen diameter to arterial diameter ratio has been reported to be lower in asthmatic patients with a forced expiratory volume in one second (FEV1) ,60% (mean¡SD 0.48¡0.11) compared with control subjects (0.65¡0.16) and asthmatics who had normal or slightly decreased FEV1 values (0.60¡0.16 and 0.60¡0.18, respectively) [71]. Conversely, NIIMI et al [72] found no decrease in lumen area in the right apical upper lobe bronchus in asthmatics, irrespective of disease severity, compared with a normal group.…”

“…All relevant studies of adults and children [14,34,66,72,[77][78][79] show that airway wall thickness is increased in asthmatic subjects, even when the asthma is mild. The degree of wall thickening is related to the duration and severity of asthma, and to the level of airway obstruction [66,72,77,79].…”

Local genetic and environmental factors in asthma disease pathogenesis: chronicity and persistence mechanisms

“…This is characterised by epithelial mucus metaplasia, thickening of the subepithelial lamina reticularis, deposition of interstitial (repair) collagens, proteoglycans and other matrix proteins throughout the airway wall (including smooth muscle) and alterations in the mass and orientation of the smooth muscle. These events lead to airway wall thickening, as observed by high-resolution computed tomography [25,33,34], an increase in peripheral lung resistance even in the presence of normal spirometry [35] and an increase in airway wall stiffness [36]. A second fundamental outcome of chronic asthma is BHR, which, as the disease becomes more severe and chronic, becomes refractory to corticosteroids [29].…”