Lung Density Changes With Growth and Inflation

Robert, H; Wise, Robert A.; Kirk, Gregory D.; Drummond, M. Bradley; Mitzner, Wayne

doi:10.1378/chest.15-0264

Cited by 25 publications

(20 citation statements)

References 19 publications

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“…The lung density of the proposed phantom was comparable to the density of the human lung that was reported in another study . Robert et al .…”

Section: Discussionsupporting

confidence: 85%

“…The lung density of the proposed phantom was comparable to the density of the human lung that was reported in another study. 39 Robert et al reported that the mean lung densities for nonsmokers were À836 HU for males (63 people) and À811 HU for females (51 people). 39 These values are similar to the density of our phantom (mean À813.24 HU in the decompressed state for the baseline breath-hold CT scan).…”

Section: Discussionmentioning

confidence: 99%

“…39 Robert et al reported that the mean lung densities for nonsmokers were À836 HU for males (63 people) and À811 HU for females (51 people). 39 These values are similar to the density of our phantom (mean À813.24 HU in the decompressed state for the baseline breath-hold CT scan). The proposed airway phantom has two major differentiating features from those of previous 3D-printed phantoms.…”

Section: Discussionmentioning

confidence: 99%

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Development of a deformable lung phantom with 3D‐printed flexible airways

et al. 2020

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Purpose Deformable lung phantoms have been proposed to investigate four‐dimensional (4D) imaging and radiotherapy delivery techniques. However, most phantoms mimic only the lung and tumor without pulmonary airways. The purpose of this study was to develop a reproducible, deformable lung phantom with three‐dimensional (3D)‐printed airways. Methods The phantom consists of: (a) 3D‐printed flexible airways, (b) flexible polyurethane foam infused with iodinated contrast agents, and (c) a motion platform. The airways were simulated using publicly available breath‐hold computed tomography (CT) image datasets of a human lung through airway segmentation, computer‐aided design modeling, and 3D printing with a rubber‐like material. The lung was simulated by pouring liquid expanding foam into a mold with the 3D‐printed airways attached. Iodinated contrast agents were infused into the lung phantom to emulate the density of the human lung. The lung/airways phantom was integrated into our previously developed motion platform, which allows for compression and decompression of the phantom in the superior–inferior direction. We quantified the reproducibility of the density (lung), motion/deformation (lung and airways), and position (airways) using breath‐hold CT scans (with the phantom compressed and decompressed) repeated every two weeks over a 2‐month period as well as 4D CT scans (with the phantom continuously compressed and decompressed) repeated twice over four weeks. The density reproducibility was quantified with a difference image (created by subtracting the rigidly registered baseline and the repeated images) in each of the compressed and decompressed states. Reproducibility of the motion/deformation was evaluated by comparing the baseline displacement vector fields (DVFs) derived from deformable image registration (DIR) between the compressed and decompressed phantom CT images with those of repeated scans and calculating the difference in the displacement vectors. Reproducibility of the airway position was quantified based on DIR between the baseline and repeated images. Results For the breath‐hold CT scans, the mean difference in lung density between baseline and week 8 was −1.3 (standard deviation 33.5) Hounsfield unit (HU) in the compressed state and 0.4 (36.8) HU in the decompressed state, while large local differences were observed around the high‐contrast structures (caused by small misalignments). By visual inspection, the DVFs (between the compressed and decompressed states) at baseline and last time point (week 8 for the breath‐hold CT scans) demonstrated a similar pattern. The mean lengths of displacement vector differences between baseline and week 8 were 0.5 (0.4) mm for the lung and 0.3 (0.2) mm for the airways. The mean airway displacements between baseline and week 8 were 0.6 (0.5) mm in the compressed state and 0.6 (0.4) mm in the decompressed state. We also observed similar results for the 4D CT scans (week 0 vs week 4) as well as for the breath‐hold CT scans at other time points (week 0 vs weeks 2, 4, a...

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“…The lung density of the proposed phantom was comparable to the density of the human lung that was reported in another study . Robert et al .…”

Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Development of a deformable lung phantom with 3D‐printed flexible airways

et al. 2020

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“…When lung tissue is destroyed, CT density decreases and the extent of emphysema can be quantified across the whole lung. Although people with larger lungs have bigger alveoli as assessed by CT density (Brown, et al, 2015), the magnitude of density changes in emphysema are far greater than the differences that would be seen between healthy large and small lungs. While decreased CT density has been shown in animal models of emphysema, this is not widely utilized.…”

Section: B Mouse Models Of Emphysemamentioning

confidence: 99%

“…The method normally used in preclinical models is to quantify changes in the postmortem histology, an approach clearly not appropriate for humans. The common metric is based on the mean distances between septal walls, but like alveolar size assessed by CT density (Brown, Wise, Kirk, Drummond and Mitzner, 2015), this metric also increases with lung volume (Hsia, et al, 2010). Thus in both human and animal models, it is essential to measure the lung volume changes with emphysema.…”

Section: B Mouse Models Of Emphysemamentioning

confidence: 99%

Immune-mediated inflammation in the pathogenesis of emphysema: insights from mouse models

2017

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The cellular mechanisms that result in the initiation and progression of emphysema are clearly complex. A growing body of human data combined with discoveries from mouse models utilizing cigarette smoke exposure or protease administration have improved our understanding of emphysema development by implicating specific cell types that may be important for the pathophysiology of COPD. The most important aspects of emphysematous damage appear to be oxidative or protease stress and sustained macrophage activation and infiltration of other immune cells leading to epithelial damage and cell death. Despite the identification of these associated processes and cell types in many experimental studies, the reasons why cigarette smoke and other pollutants result in unremitting damage instead of injury resolution are still uncertain. We propose an important role for macrophages in the sequence of events that lead and maintain this chronic tissue pathologic process in emphysema. This model involves chronic activation of macrophage subtypes that precludes proper healing of the lung. Further elucidation of the cross-talk between epithelial cells that release damage-associated signals and the cellular immune effectors that respond to these cues is a critical step in the development of novel therapeutics that can restore proper lung structure and function to those afflicted with emphysema.

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Loss of pulmonary capillaries in idiopathic pulmonary arterial hypertension with low diffusion capacity is accompanied by early diffuse emphysema detected by 129Xe MRI

Kern,

Park,

Fuge

et al. 2024

Eur Radiol

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Objectives Recent studies suggest the existence of an idiopathic pulmonary arterial hypertension (IPAH) phenotype affecting mostly patients with a smoking history, characterised by low diffusion capacity for carbon monoxide (DLCO) without clinically significant emphysema. This study’s objective was to test the hypothesis of a loss of pulmonary capillaries as an underlying mechanism by comparison to other patient groups with and without pulmonary hypertension (PH). Materials and methods Between March 2019 and June 2023, patients of four groups were recruited for this observational study: IPAH with preserved (1) and low DLCO (2), combined pulmonary fibrosis and emphysema with PH (3), and emphysema without PH (4). Patients underwent clinical CT and 129Xe MRI including dissolved-phase imaging yielding the ratio of 129Xe in red blood cells and membrane tissues (RBC-M), chemical shift saturation recovery for determining RBC fraction η and diffusion-weighted imaging yielding surface-volume ratio. Kruskal–Wallis tests were used for statistical analysis. Results Twenty-nine participants were recruited, of which 22 (age 64 ± 10, 11 male, 5/5/7/5 for the individual groups) could be included in the analysis. RBC-M and η were reduced in IPAH with low versus preserved DLCO and emphysema groups (p ≤ 0.01). CT low-attenuation area percentage was not increased in IPAH with low DLCO compared to any group. 129Xe MRI-derived surface-volume ratio was reduced in IPAH with low versus preserved DLCO (p = 0.04). Conclusion Results are consistent with a loss of pulmonary capillaries in patients with IPAH and low DLCO along with destruction of alveolar tissue, likely due to early diffuse emphysema. Key Points QuestionA loss of pulmonary capillaries has been suggested in patients with IPAH and low diffusion capacity without clinically significant emphysema on CT. Findings129Xe uptake in red blood cells and lung surface-volume ratio were reduced in IPAH patients with low compared to preserved diffusion capacity. Clinical relevanceThis study furthers the understanding of the underlying pathological mechanisms in IPAH with low diffusion capacity, providing evidence that loss of pulmonary capillaries is accompanied by alveolar tissue destruction despite near-normal CT.

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Lung Density Changes With Growth and Inflation

Cited by 25 publications

References 19 publications

Development of a deformable lung phantom with 3D‐printed flexible airways

Development of a deformable lung phantom with 3D‐printed flexible airways

Immune-mediated inflammation in the pathogenesis of emphysema: insights from mouse models

Loss of pulmonary capillaries in idiopathic pulmonary arterial hypertension with low diffusion capacity is accompanied by early diffuse emphysema detected by 129Xe MRI

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