Is ct a new research tool for copd

Recommendations for epidemiological studies on COPD. European Respiratory Journal. Quantitative computed tomography measures of emphysema and airway wall thickness are related to respiratory symptoms.

American journal of respiratory and critical care medicine. Clinical and paraclinical guidelines for management of sulfur mustard induced bronchiolitis obliterans; from bench to bedside. Inhalation toxicology. View 2 excerpts, cites background. Quantitative computed tomography: emphysema and airway wall thickness by sex, age and smoking. Selenoprotein N deficiency in mice is associated with abnormal lung development.

View 1 excerpt. Radiology of chronic obstructive pulmonary disease. Radiologic clinics of North America. Computed tomography in pulmonary emphysema. Hatt, who has worked with the COPDGene study for the past six years, said the goal of his research is to better understand the genetic factors around the disease with the aim of improving quality of life for patients. In the Radiology: Cardiothoracic Imaging study, Dr. The low-dose CT scan used about a quarter of the amount of radiation as a standard full-dose CT scan — the same low-dose scan used in the National Lung Cancer Screening Trial that enrolled more than 50, current or former heavy smokers.

Hatt and colleagues also sought to determine if radiologists could detect emphysema and measure change in disease progression from the low-dose CT scans. Researchers wanted to determine the overestimation level and whether anything can be done to correct for that difference. Hatt and colleagues analyzed the low-dose CT scans of participants using iterative reconstruction such as applying median filtering to reduce noise on the images.

So, anyone who has the right software can take a low-dose scan, run it through the median filter, and get similar results. Based on those findings and the predictive capacity of the low-dose scans, Dr.

Hatt is confident that low-dose CT imaging can be used to provide a wealth of information beyond information obtained in lung cancer screening. Hatt cited a study that demonstrated the effectiveness of low-dose CT in identifying emphysema in patients with and without a prior COPD diagnosis. In the Clinical Imaging study, David Steiger, MD, and colleagues reviewed a prospective cohort of 52, patients who underwent baseline low-dose CT screening for lung cancer from to in the International Early Lung Cancer Action Program.

Emphysema was identified in Perpendicular planes across the targeted bronchi can be acquired, and WA indices are automatically extracted. These softwares allow a fast and accurate postprocessing quantification, and this is relevant knowing the heterogeneity of alterations in asthma. However, the bronchial human tree displays a mean of 24 divisions including the trachea, and only 10 divisions are reasonably achievable using either manual or semiautomatic methods.

Bronchial tree volume automatically segmented using homemade dedicated software, extracted from a whole set of lung CT images.

The skeleton of the bronchial tree is computed to obtain a simplified three-dimensional geometry of the bronchial tree. Another quantitative parameter has recently been assessed in both asthma and COPD: the bronchial wall attenuation [ 17 — 19 ].

Lederlin et al. The manual method described in their study consisted in a manual segmentation of the peribronchial area, arbitrarily equal to the radius of the target bronchi lumen. The mean PWA was calculated by taking the mean peak attenuation along one-dimensional mural rays, radiating outward from the centroid of the airway lumen, using a circumferential measure.

Small conductive and distal airways are beyond the spatial resolution of CT. Intralobular structures are not clearly visible, such as alveolar membranes, capillaries, or interstitial tissue. However, lung parenchyma density is a consequence of the X-ray attenuation by these lung structures, and any change in either of them may modify it. Therefore, lung attenuation provides an indirect tool to assess structural changes in distal airways, though it is nonspecific [ 20 ].

Lung alterations can be seen on CT images such as centrilobular micronodules, ground-glass opacities, mosaic pattern, air trapping, and emphysema and have been described in both pathologies [ 21 , 22 ]. Quantification of these abnormalities has been studied through visual grading, but this method is potentially exposed to variability [ 23 ].

In asthma, Mikos et al. The number of squares containing low lung attenuation was counted manually in every lung section. Two semiautomatic methods have been further developed [ 25 , 26 ]. The rationale is the lower lung attenuation measured in emphysema and air trapping areas compared with normal areas. Theoric models of voxel attenuation frequencies in a normal subject green curve and emphysematous patient red curve.

The percentile method is based on predefined percentages at which voxels have lower attenuation values. Blue arrows indicate the crossing points of green and red curves with the 15th percentile. Some drawbacks of these methods have been reported. Since lung attenuation values are not the same between different levels of radiation doses, CT manufacturers [ 27 ], or postprocessing softwares [ 28 ], Bakker et al.

Age and lung volume involve variation of the voxel attenuation values, but not sex gender [ 29 ]. Densities are not the same on inspiration or expiration CT scans [ 30 , 31 ]. The 15th percentile method has been reported to be more independent from lung volume changes than the density mask. Stoel et al. Attenuation values are modified when CT is performed with or without contrast injection.

Heussel et al. Therefore, the amount of emphysema may be underestimated, and they concluded that nonenhanced CT scans should be the reference [ 33 ].

Asthma involves both proximal and distal airways [ 1 , 2 ]. Several studies have shown that airway wall thickness WA indices are increased in asthmatic patients compared with healthy volunteers [ 34 — 37 ].

According to histological data coming from autopsy studies of fatal cases, this may result from inflammatory changes such as oedema and infiltration of inflammatory cells, and structural changes such as an increased basal membranous thickness, smooth muscle cell layer and peribronchial fibrosis. From bronchial biopsies, Aysola et al. Montaudon et al. They showed that the bronchial geometric parameters correlated with smooth muscle area and with infiltration of the smooth muscle by mast cells.

The link between airway thickness measured on CT scans and bronchial reactivity AHR is controversial. The most common accepted theory is that part of the airway wall thickness is due to an increased smooth muscle cell layer, which is leading to AHR.

Boulet et al. However, Niimi et al. They also showed a negative correlation between airway thickness and bronchial reactivity, unrelated to eosinophil count. They concluded that airway walls are stiff when thickened, indicating that remodelled asthmatic airways are less distensible and may explain chronic airway obstruction [ 35 ].

In other studies, the same authors showed that WA indices are increased in severe as in mild-to-moderate patients with asthma compared with control subjects. In addition, they showed that WA indices correlate with the duration of disease, the severity, and the degree of airflow obstruction [ 36 ].

Data around intraluminal area LA are controversial too. Niimi et al. Lynch et al. Conversely, Montaudon et al. These different features may be explained by heterogeneity of bronchial diameters in asthma. For instance, Niimi et al. Peribronchial density has been recently assessed by Lederlin et al.

They did not quantified WA or LA, but micro-CT peribronchial density PBA , and showed that the attenuation around the bronchial tree in asthmatic mice was increased compared with controls. This increase correlated with both inflammation and remodelling features.

CT bronchial dimensions have been studied to assess medication effects. Kurashima et al. Asthma is a predominant airway diseases and does not involve lung parenchyma destruction during stable stages [ 1 , 2 ]. However, CT lung parenchyma changes have been reported. Using a visual grading, Laurent et al. This result was addressed to either hypoxic vasoconstriction or small airway obstruction.

They also found that air trapping was increased in asthmatic and healthy smokers, but not in controls. Mikos et al. In a multivariate analysis of risk factors, Busacker et al. Air trapping was considered significant whether more than 9. They analysed that patients with the air trapping phenotype are more likely to have a history of asthma-related hospitalizations and mechanical ventilation.

Several risk factors of this phenotype where noted such as a history of pneumonia, neutrophilic inflammation, and atopy [ 43 ]. Images a and b were acquired with spirometrically gated CT scans in a non-severe asthmatic subject, in inspiration a and in expiration b. Same images were acquired at same levels of inspiration c and expiration d from a severe asthmatic subject. Mitsunobu et al. They concluded that D was a biomarker of emphysematous changes, which can help to characterize areas of low attenuation.

Lung density has been used to evaluate CT changes after therapy. Small airways are the main site of obstruction in COPD [ 1 , 2 ]. However, large airways are not free of abnormalities. Lee et al. They showed significant correlation between TI and severity of emphysema [ 46 ].

Sverzelatti et al. Grade 2 was defined as the presence of more than three diverticulas in large airways.

This feature correlated with a more frequent history of cough, a greater extent of emphysema, a more severe bronchial wall thickening, and a heavier level of smoking. Nakano et al. Several studies have shown that airway wall thickness correlates with pulmonary function tests PFTs [ 49 — 53 ].

In a study conducted in smokers, Nakano et al. Grydeland et al. Berger et al. Achenbach et al. Using another three-dimensional approach taking into account the PSF, they assessed a median of orthogonal airway locations per patient. This correlation was higher from large to small airways, which is in agreement with FWHM principle [ 54 ]. Shimizu et al. They concluded that remodelling is more prominent in asthma than in COPD under stable clinical conditions [ 55 ].

Bronchial wall attenuation has been recently assessed in COPD. Washko et al. They showed strong correlations between this new biomarker of airway wall structural changes and airway obstructions assessed by PFT. Correlations were stronger in small airways. Ex vivo studies in isolated lungs and in vivo invasive measurements of airway resistance revealed that distal airways are the main site of airflow obstruction in COPD [ 5 , 6 ].

Pathological studies highlighted that the small conductive airways are infiltrated by phagocytes macrophages and neutrophils , dendritic cells, and T and B lymphocytes. Structural changes include airway wall thickness and obstruction by muco-inflammatory exudates and emphysema.

Lung density provides an indirect tool to assess them in vivo, though non specific. Centrilobular nodules and branching lines are areas of high attenuation and reflect pathological changes in small conductive airways, either inflammation or fibrosis. Destruction of alveolar walls is the hallmark of emphysema, and this pathological feature induces decreased areas of lung attenuation.

Using the density mask and the percentile methods, Madani et al. Gevenois et al. However, areas of decreased attenuation can be visible on inspiratory images as a mosaic pattern, and air trapping on expiratory images. Both obstruction of the small conductive airways and loss of alveolar attachments are associated with destabilisation and premature airway closure during expiration.

Therefore, differentiating emphysema from air trapping is not reliably achievable on CT images when assessed visually. Nevertheless, Matsuoka et al. Another paradoxical fall in lung density has been reported by Shaker et al. This was ascribed to an anti-inflammatory effect of smoking cessation and is not to be misinterpreted [ 62 ].

Persistent airway inflammation and emphysema progression have been showed in exsmokers after 4-year smoking cessation [ 63 ]. Correlations between the extent of emphysema and pulmonary function tests have been long reported [ 64 — 69 ].

COPD is characterized by expiratory airflow limitation that results in delayed emptying of the lung, poorly reversible. Gurney et al. CT quantification has been assessed as a predictor of lung function decline in smokers with normal PFTs.