Kallianos, Kimberly

Abstract Rationale Mucus plugs occur in chronic obstructive pulmonary disease (COPD), but little is known about their size and airway location or whether these mucus plug features change as emphysema worsens. Methods Computed tomographic lung scans from 31 participants with COPD from the SubPopulations and InteRmediate Outcomes In COPD Study (SPIROMICS) cohort were analyzed to quantify mucus plug size and airway location and extent of emphysema. Radiologist annotations of mucus plugs were incorporated in an image processing pipeline to generate size and location information. Emphysema was quantified as the percentage of voxels less than -950 Hounsfield units. Measurements and Main Results The length distribution of 563 annotated mucus plugs varied from 2 to 50 mm. The distribution was multimodal, and an 11-mm length defined short (“stubby,” ≤11 mm) and long (“stringy,” >11 mm) plug phenotypes, with stubby plugs being most common (64%). Mucus plugs localized predominantly to airway generations 6 to 9, and their prevalence was highest in lower lobes. On a lobar basis, the mucus plug number decreased as emphysema percentage increased, whereas average mucus plug volume tended to increase. Conclusion COPD is characterized by mucus plugs of varying size and shape, and emphysematous lung regions may be differentially susceptible to formation of these plugs. The location of mucus plugs in segmental and subsegmental airways in COPD makes them amenable to treatment with inhaled medications or bronchoscopy.

Purpose: Studies have shown a modest association between pericardial fat volume (PFV) and coronary artery disease (CAD), potentially mediated by local inflammation. We aimed to investigate the association between a new biomarker of pericardial fat inflammation, named pericardial fat enhancement (PFE), and the severity of CAD on coronary computed tomography angiography (CCTA). Materials and Methods: We evaluated 114 patients referred for CCTA from 2007 to 2011. PFV, presence of obstructive CAD, and the burden of CAD were determined. PFE was measured in 10 mm2 regions of interest, adjusted to aortic enhancement (aPFE). The population was divided into those with greater than median (G-PFE) versus less than median pericardial fat enhancement (L-PFE). Stratified adjusted logistic regressions were performed. A P-value <0.05 was considered significant. The study was approved by our institutional review board. Results: Patients were 54.3±14.8 years of age, and 57/114 (50%) were male individuals, with body mass index of 27.3±6.3. There was an independent association between CAD severity and PFV. There was a significant independent association between PFV and obstructive CAD (odds ratio=1.26, P=0.005), and PFV and burden of CAD (odds ratio=1.25, P=0.05) in those with greater PFE. However, there was no significant association between obstructive CAD and CAD burden in either adjusted model for patients with less PFE. Conclusions: Our results suggest that PFE influences significantly the relationship between PFV and CAD, supporting the hypothesis of local pericardial fat inflammation as a mechanism for CAD development.