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Background: Pulmonary endothelial damage has been shown to precede the development of emphysema in animals, and vascular changes in humans have been observed in COPD and emphysema., Research Question: Is intraparenchymal vascular pruning associated with longitudinal progression of emphysema on CT imaging or decline in lung function over 5 years?, Study Design and Methods: The Genetic Epidemiology of COPD Study enrolled ever smokers with and without COPD from 2008 through 2011. The percentage of emphysema-like lung, or "percent emphysema," was assessed at baseline and after 5 years on noncontrast CT imaging as the percentage of lung voxels < -950 Hounsfield units. An automated CT imaging-based tool assessed and classified intrapulmonary arteries and veins. Spirometry measures are postbronchodilator. Pulmonary arterial pruning was defined as a lower ratio of small artery volume (< 5 mm 2 cross-sectional area) to total lung artery volume. Mixed linear models included demographics, anthropomorphics, smoking, and COPD, with emphysema models also adjusting for CT imaging scanner and lung function models adjusting for clinical center and baseline percent emphysema., Results: At baseline, the 4,227 participants were 60 ± 9 years of age, 50% were women, 28% were Black, 47% were current smokers, and 41% had COPD. Median percent emphysema was 2.1 (interquartile range, 0.6-6.3) and progressed 0.24 percentage points/y (95% CI, 0.22-0.26 percentage points/y) over 5.6 years. Mean FEV 1 to FVC ratio was 68.5 ± 14.2% and declined 0.26%/y (95% CI, -0.30 to -0.23%/y). Greater pulmonary arterial pruning was associated with more rapid progression of percent emphysema (0.11 percentage points/y per 1-SD increase in arterial pruning; 95% CI, 0.09-0.16 percentage points/y), including after adjusting for baseline percent emphysema and FEV 1 . Arterial pruning also was associated with a faster decline in FEV 1 to FVC ratio (-0.04%/y per 1-SD increase in arterial pruning; 95% CI, -0.008 to -0.001%/y)., Interpretation: Pulmonary arterial pruning was associated with faster progression of percent emphysema and more rapid decline in FEV 1 to FVC ratio over 5 years in ever smokers, suggesting that pulmonary vascular differences may be relevant in disease progression., Trial Registry: ClinicalTrials.gov; No.: NCT00608764; URL: www.clinicaltrials.gov., (Copyright © 2021 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Rationale and Objectives: Bronchiectasis (BE) is associated with chronic obstructive pulmonary disease (COPD), but emphysema and small airways disease, main pathologic features of COPD, have been sparsely studied in BE. We aimed to objectively assess those features in smokers with and without radiographic BE and examine its relationships to airflow obstruction and exercise capacity., Material and Methods: We measured emphysema and small airways disease on paired inspiratory-expiratory computed tomography (CT) scans with the parametric response map (PRM EMPH and PRM SAD ) method in 1184 smokers with and without radiographic BE. PRM SAD and PRM EMPH are expressed as the percentage of lung area. Clinical, spirometry, and exercise capacity data were measured with standardized methods. The differences in PRM SAD and PRM EMPH between subjects with and without radiographic BE were assessed using multivariable linear regression analysis, and their associations with FEV 1 and six-minute walk test (6MWT) were assessed with generalized linear models., Results: Out of 1184 subjects, 383 (32%) had radiographic BE. PRM EMPH but not PRM SAD was higher in subjects with radiographic BE than those without radiographic BE in adjusted models. Subjects with radiographic BE and PRM EMPH (defined as ≥5% on paired CTs) had lower FEV 1 (least square mean, 1479 mL vs. 2350 mL p < 0.0001) and 6MWT (372 m vs. 426 m p = 0.0007) than those with radiographic BE alone in adjusted models., Conclusion: Smokers with radiographic BE have an increased burden of emphysema on paired CTs, and those with radiographic BE and emphysema have lower airflow and exercise capacity., (Copyright © 2020 The Association of University Radiologists. Published by Elsevier Inc. All rights reserved.)

Alpha-1 Antitrypsin Deficiency (AATD) is a progressive pulmonary disease under-recognized or misdiagnosed by clinicians. Patients with AATD can develop a variety of organ-specific complications and as a result, often require hospitalization and treatment within critical care and ICU settings. Due to the complexity of AATD there are minimal guidelines in place to address the specific and highly variable needs of these patients in the critical care setting. This review presents clinical considerations with respect to the management of patients with AATD and provides treatment recommendations for these patients in the critical care setting. In addition, we have outlined certain aspects of the care of this patient population that may be of interest to critical care practitioners. With greater disease awareness and earlier diagnosis the onset of symptoms can be delayed, which will ultimately reduce the frequency of deleterious health consequences., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Alpha-1 antitrypsin deficiency (AATD) is under-recognized by clinicians, with long diagnostic delays between patients' first symptom and initial diagnosis. Recent recommendations by official societies encourage testing for AATD in all symptomatic adults with spirometric evidence of COPD, though compliance with this recommendation has been variable. For 6 months, the following physician alert was added to PFT reports of patients with airflow obstruction of GOLD Stage II or higher: "The American Thoracic Society recommends testing for AATD in all patients with FEV1 < 80% predicted and FEV1/FVC less than 0.70, if clinically indicated. Appropriate counseling suggested." During the "Pre-alert Period," 821 spirometry tests were performed; 178 of these 821 unique patients (22%) satisfied spirometric criteria of > GOLD Stage II and 11 (6%) were tested for AATD. In contrast, during the "Physician Alert" intervention period, 689 spirometry tests were performed on 689 unique patients, of whom 140 (20%) satisfied criteria for > GOLD II airflow obstruction; AAT testing was done more frequently (18 [13%], p = 0.04). The overall rate of misclassifying patients' reports for testing by the respiratory therapists was very low (3.3%). An analysis of "number needed to test" suggests that 98-290 patients must be tested to have 95% certainty to identify a single patient with severe AATD. In conclusion, implementing a physician alert on PFT reports of patients with COPD can increase physicians' testing for AATD. The incomplete rate of testing suggests the need for additional strategies to enhance clinicians' detection of individuals with AATD.