World Congress Thoracic Imaging June 18-21, 2017, Hynes Convention Center, Boston, Massachusetts June 18-21, 2017, Hynes Convention Center, Boston, Massachusetts

Sponsoring Societies:

Fleischner Society Society of Thoracic Radiology European Society of Thoracic Imaging Japanese Society of Thoracic Radiology Korean Society of Thoracic Radiology
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Assessment of small airway disease contribution to pulmonary dysfunction in COPD
Mariaelena Occhipinti, Matteo Paoletti, Francesca Bigazzi, Marco Palazzi, Viola Bonti, Gianna Camiciottoli, Massimo Pistolesi
University of Florence, Firenze, Italy

Purpose: COPD is a complex disorder in which airflow limitation results from different pathogenetic mechanisms including parenchymal destruction (emphysema) and small airway disease (SAD). These pathogenetic mechanisms interact differently in each patient contributing to the heterogeneity of COPD clinical presentation. This study was aimed to ascertain whether for a given value of emphysema it could be possible to quantify by CT the contribution of SAD to pulmonary dysfunction in each patient.
Materials and Methods: We measured dynamic lung volumes (FEV1, FVC, VC), static lung volumes (TLC, FRC, RV), and diffusing lung capacity (DLCO) in 150 COPD patients (GOLD 1-4). By post-processing image analysis of CT scans we measured the percent lung area with density <-950HU at full inspiration and <-856 at full expiration (Apollo 2.1,VIDA Diagnostics, Coralville, IA) and the percent of co-registered persistent and functional low density areas (Imbio LDA, Minneapolis, MN). We plotted the percent area <-950HU (x axis) vs the percent area <-856HU (y axis). The resulting graphical distribution was fitted by a curvilinear function expressing the percent level of emphysema on the x-axis. For each patient plotted in the x/y graph we computed on the y axis the positive or negative linear distance from the curvilinear fitting (CTindex, CTi) as expression of percent SAD contribution to emphysema. CTi was compared with lung function and validated by correlation with percent functional low density area (fSAD) assessed by co-registration.
Results: Patients with positive CTi had more severe functional impairment than those with negative CTi in terms of airway obstruction (significantly lower FEV1 and FEV1/VC) and hyperinflation (significantly higher RV, FRC, and RV/TLC). As expected, there was no significant difference in DLCO as CTi is, by definition, not influenced by parenchymal destruction. CTi was highly correlated with fSAD (r=0.95).
Conclusions: CTi is an accurate measure of SAD and of its contribution to pulmonary dysfunction in COPD. Identification of presence and intensity of SAD could be of interest to characterize COPD phenotype and to tailor the therapeutic intervention to the underlying predominant pathogenetic mechanism.

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