Eosinophilia (≥300 cells/µL) in COPD patients was not independently associated with coronary artery disease or heart failure with reduced ejection fraction (OR 1.51; 95% CI 0.55-4.15; p=0.419).
Cohort (n=90)
No
Is eosinophilia associated with chest CT inflammation and cardiovascular comorbidities (CAD/HFrEF) in patients with COPD?
In patients with COPD, eosinophilia ≥300 cells/µL was not significantly associated with inflammatory findings on chest CT or the presence of CAD/HFrEF, though point estimates suggest a possible signal warranting further study.
Effect estimate: OR 1.51 (95% CI 0.55-4.15)
p-value: p=0.419
Abstract The structural correlates of type 2-high COPD (T2-high) on chest computed tomography, such as inflammatory bronchopathy and mucus impaction, and their relationship with major cardiovascular comorbidities are underreported in routine clinical practice. It is independently associated with inflammatory findings on chest computed tomography, coronary artery disease, and/or heart failure with reduced ejection fraction. Methods Retrospective, single-center cohort study (June 2022 to June 2025) using electronic medical record data. Peripheral blood eosinophils were serially extracted (immediately after each dated record). CT scan reports were performed searching for “inflammatory bronchopathy” and/or “mucus plug,” and all CT scans were reviewed by the authors; interobserver agreement was substantial (κ ≈ 0.75). Only consensus findings were classified as present/absent for inflammatory bronchopathy or mucous tamponade. Comorbidities were extracted from medical records: coronary artery disease was defined by documented angioplasty or known coronary artery disease; heart failure with reduced ejection fraction less than a recorded diagnosis corroborated by an echocardiogram performed between 2022 and 2025 showing reduced left ventricular ejection fraction. Multivariate logistic regression of complete cases estimated adjusted odds ratios (OR) for (a) worsening on CT scan and (b) CAD/HFrEF, controlling for age, predicted FEV1%, inhaled corticosteroid (ICS) use, and LAMA/LABA use. Eosinophilia was assessed ≥300 vs 300 cells/µL; sub-analyses of persistence or fluctuation were not performed due to limited incremental value. Results Ninety new patients were included in the adjusted models. Inflammation on CT: eosinophilia OR 1.37 (95% CI 0.54-3.47; p = 0.504). CAD/HFrEF: eosinophilia OR 1.51 (95% CI 0.55-4.15; p = 0.419). The models took into account spirometric severity and inhaled therapy; the effects of inhaled corticosteroids were not interpreted due to confounding by indication. Binary eosinophilia (≥300 cells/µL) was not independently associated with symptomatic findings on chest CT or coronary artery disease/heart failure with reduced ejection fraction. Point estimates 1 suggest a possible structural and cardiovascular signal that justifies prospective studies with blinded review of images, standardized CT criteria, and broader control of covariates e.g., smoking, sex, systemic corticosteroid exposure. These data support serial eosinophil assessment to refine risk stratification in COPD with high T2 levels. This abstract is funded by: None
Franco et al. (2026) conducted a cohort in COPD (n=90). Eosinophilia (≥300 cells/µL) vs. Eosinophils <300 cells/µL was evaluated on Coronary artery disease or heart failure with reduced ejection fraction (CAD/HFrEF) (OR 1.51, 95% CI 0.55-4.15, p=0.419). Eosinophilia (≥300 cells/µL) in COPD patients was not independently associated with coronary artery disease or heart failure with reduced ejection fraction (OR 1.51; 95% CI 0.55-4.15; p=0.419).
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