Chad A Witt1, Ajay Sheshadri1, Luke Carlstrom1, Jaime Tarsi1, James Kozlowski1, Brad Wilson2, David S Gierada3, Eric Hoffman4, Sean B Fain5, Janice Cook-Granroth4, Geneline Sajol1, Oscar Sierra1, Tusar Giri1, Michael O'Neill1, Jie Zheng2, Kenneth B Schechtman2, Leonard B Bacharier6, Nizar Jarjour7, William Busse8, Mario Castro9. 1. Division of Pulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, Campus Box 8052, 660 S. Euclid Ave, St. Louis, MO 63110-1093. 2. Division of Biostatistics, Washington University School of Medicine, St. Louis, Missouri. 3. Department of Radiology, Washington University School of Medicine, St. Louis, Missouri. 4. Department of Radiology, University of Iowa College of Medicine, Iowa City, Iowa. 5. Department of Medical Physics, University of Wisconsin, Madison, Wisconsin. 6. Division of Pediatric Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri. 7. Division of Pulmonary and Critical Care, University of Wisconsin, Madison, Wisconsin. 8. Division of Allergy and Immunology, University of Wisconsin, Madison, Wisconsin. 9. Division of Pulmonary and Critical Care Medicine, Department of Medicine, Washington University School of Medicine, Campus Box 8052, 660 S. Euclid Ave, St. Louis, MO 63110-1093. Electronic address: castrom@wustl.edu.
Abstract
RATIONALE AND OBJECTIVES: Previous cross-sectional studies have demonstrated that airway wall thickness and air trapping are greater in subjects with severe asthma than in those with mild-to-moderate asthma. However, a better understanding of how airway remodeling and lung density change over time is needed. This study aimed to evaluate predictors of airway wall remodeling and change in lung function and lung density over time in severe asthma. MATERIALS AND METHODS: Phenotypic characterization and quantitative multidetector-row computed tomography (MDCT) of the chest were performed at baseline and ∼2.6 years later in 38 participants with asthma (severe n = 24 and mild-to-moderate n = 14) and nine normal controls from the Severe Asthma Research Program. RESULTS: Subjects with severe asthma had a significant decline in postbronchodilator forced expiratory volume in 1 second percent (FEV1%) predicted over time (P < .001). Airway wall thickness measured by MDCT was increased at multiple airway generations in severe asthma compared to mild-to-moderate asthma (wall area percent [WA%]: P < .05) and normals (P < .05) at baseline and year 2. Over time, there was an increase in WA% and wall thickness percent (WT%) in all subjects (P = .030 and .009, respectively) with no change in emphysema-like lung or air trapping. Baseline prebronchodilator FEV1% inversely correlated with WA% and WT% (both P < .05). In a multivariable regression model, baseline WA%, race, and health care utilization were predictors of subsequent airway remodeling. CONCLUSIONS: Severe asthma subjects have a greater decline in lung function over time than normal subjects or those with mild-to-moderate asthma. MDCT provides a noninvasive measure of airway wall thickness that may predict subsequent airway remodeling.
RATIONALE AND OBJECTIVES: Previous cross-sectional studies have demonstrated that airway wall thickness and air trapping are greater in subjects with severe asthma than in those with mild-to-moderate asthma. However, a better understanding of how airway remodeling and lung density change over time is needed. This study aimed to evaluate predictors of airway wall remodeling and change in lung function and lung density over time in severe asthma. MATERIALS AND METHODS: Phenotypic characterization and quantitative multidetector-row computed tomography (MDCT) of the chest were performed at baseline and ∼2.6 years later in 38 participants with asthma (severe n = 24 and mild-to-moderate n = 14) and nine normal controls from the Severe Asthma Research Program. RESULTS: Subjects with severe asthma had a significant decline in postbronchodilator forced expiratory volume in 1 second percent (FEV1%) predicted over time (P < .001). Airway wall thickness measured by MDCT was increased at multiple airway generations in severe asthma compared to mild-to-moderate asthma (wall area percent [WA%]: P < .05) and normals (P < .05) at baseline and year 2. Over time, there was an increase in WA% and wall thickness percent (WT%) in all subjects (P = .030 and .009, respectively) with no change in emphysema-like lung or air trapping. Baseline prebronchodilator FEV1% inversely correlated with WA% and WT% (both P < .05). In a multivariable regression model, baseline WA%, race, and health care utilization were predictors of subsequent airway remodeling. CONCLUSIONS: Severe asthma subjects have a greater decline in lung function over time than normal subjects or those with mild-to-moderate asthma. MDCT provides a noninvasive measure of airway wall thickness that may predict subsequent airway remodeling.
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