- Article
Effect of Medical Comorbidities on Procedural Success in Bronchoscopic Lung Volume Reduction
- Christopher N. Nemeh,
- William F. Parker and
- Ajay A. Wagh
- + 1 author
Background: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity, mortality, and healthcare utilization. Lung volume reduction surgery improves outcomes in a select cohort but portends high morbidity. Bronchoscopic lung volume reduction (BLVR) is a less invasive, reversible manner of lung volume reduction, using one-way valves to improve lung function, quality of life, and exercise capacity. Nevertheless, knowledge gaps persist regarding factors that predict procedural success. Methods: We retrospectively reviewed 142 patients who underwent BLVR at the University of Chicago between December 2018 and July 2024 to assess the relationship between comorbidities and procedural outcomes. Using logistic and multinomial regression, we determined odds ratios (ORs) for a binary outcome of success and failure and relative risk ratios (RRRs) for failure sub-categories relative to procedural success. Results: We observed a procedural success rate of 48.1% and pneumothorax prevalence of 21.8%. After adjusting for age, sex, race, and body mass index (BMI), comorbidities associated with procedural failure included chronic kidney disease (CKD), congestive heart failure (CHF), anemia, and a BMI, Obstruction, Dyspnea and Exercise (BODE) Index of 5 or greater. Obstructive sleep apnea (OSA) was associated with procedural success. Conclusions: Comorbidities associated with dyspnea appear to have a significant effect on procedural success in BLVR.
14 January 2026





![Immune dysregulation in Cystic Fibrosis. A. The periciliary layer of the Cystic Fibrosis airway is dehydrated leading to poor mucociliary clearance as a result of dysfunctional CFTR protein that is normally expressed in airway epithelial cells [47,48]. B. Mucus plugging and biofilm buildup becomes a nidus for inhaled pathogens or allergens such as Aspergillus spp. C. Macrophages with impaired CFTR kill pathogens less efficiently and increase secretion of pro-inflammatory cytokines such as IL-6, IL-4, IL-13, and TNF-α [44,49]. D. CFTR deficient airway epithelial cells lead to increased IL-33 when exposed to allergens, resulting in higher expression of Th2 cell with increased release of IL-5, increased eosinophils, and IL-4 and IL-13, stimulating IgE expression by B cells [50,51]. E. Neutrophils, the predominant type of cell in CF airways, have reduced phagocytosis and can release toxic granule contents (e.g., serine and metalloproteases, oxidants) that can cause tissue damage over time. Neutrophils are known to release neutrophil extracellular traps (NETs), which are DNA fibers that immobilize and kill bacterial and fungal pathogens such as Pseudomonas aeruginosa and Aspergillus fumigatus, respectively. Abundant NET formations may attribute to common colonization of such pathogens in people with CF and reduced lung function; recombinant DNase (e.g., inhaled dornase alfa) improves mucociliary clearance by clearing the NET-DNA meshwork [49,51,52].](https://mdpi-res.com/jor/jor-05-00019/article_deploy/html/images/jor-05-00019-g001-550.jpg)