Effect Of Emphysema Research Articles

Effect of emphysema on AI software and human reader performance in lung nodule detection from low-dose chest CT

BackgroundEmphysema influences the appearance of lung tissue in computed tomography (CT). We evaluated whether this affects lung nodule detection by artificial intelligence (AI) and human readers (HR).MethodsIndividuals were selected from the “Lifelines” cohort who had undergone low-dose chest CT. Nodules in individuals without emphysema were matched to similar-sized nodules in individuals with at least moderate emphysema. AI results for nodular findings of 30–100 mm3 and 101–300 mm3 were compared to those of HR; two expert radiologists blindly reviewed discrepancies. Sensitivity and false positives (FPs)/scan were compared for emphysema and non-emphysema groups.ResultsThirty-nine participants with and 82 without emphysema were included (n = 121, aged 61 ± 8 years (mean ± standard deviation), 58/121 males (47.9%)). AI and HR detected 196 and 206 nodular findings, respectively, yielding 109 concordant nodules and 184 discrepancies, including 118 true nodules. For AI, sensitivity was 0.68 (95% confidence interval 0.57–0.77) in emphysema versus 0.71 (0.62–0.78) in non-emphysema, with FPs/scan 0.51 and 0.22, respectively (p = 0.028). For HR, sensitivity was 0.76 (0.65–0.84) and 0.80 (0.72–0.86), with FPs/scan of 0.15 and 0.27 (p = 0.230). Overall sensitivity was slightly higher for HR than for AI, but this difference disappeared after the exclusion of benign lymph nodes. FPs/scan were higher for AI in emphysema than in non-emphysema (p = 0.028), while FPs/scan for HR were higher than AI for 30–100 mm3 nodules in non-emphysema (p = 0.009).ConclusionsAI resulted in more FPs/scan in emphysema compared to non-emphysema, a difference not observed for HR.Relevance statementIn the creation of a benchmark dataset to validate AI software for lung nodule detection, the inclusion of emphysema cases is important due to the additional number of FPs.Key points• The sensitivity of nodule detection by AI was similar in emphysema and non-emphysema.• AI had more FPs/scan in emphysema compared to non-emphysema.• Sensitivity and FPs/scan by the human reader were comparable for emphysema and non-emphysema.• Emphysema and non-emphysema representation in benchmark dataset is important for validating AI.Graphical

Impact of emphysema on sputum culture conversion in male patients with pulmonary tuberculosis: a retrospective analysis

BackgroundAlthough cigarette smoking may have a negative impact on the clinical outcome of pulmonary tuberculosis (PTB), few studies have investigated the impact of smoking-associated lung diseases. Emphysema is a major pathological finding of smoking-related lung damage. We aimed to clarify the effect of emphysema on sputum culture conversion rate for Mycobacterium tuberculosis (MTB).MethodsWe retrospectively studied 79 male patients with PTB confirmed by acid-fast bacillus smear and culture at Jikei University Daisan Hospital between January 2015 and December 2018. We investigated the sputum culture conversion rates for MTB after starting standard anti-TB treatment in patients with or without emphysema. Emphysema was defined as Goddard score ≥ 1 based on low attenuation area < − 950 Hounsfield Unit (HU) using computed tomography (CT). We also evaluated the effect on PTB-related CT findings prior to anti-TB treatment.ResultsMycobacterial median time to culture conversion (TCC) in 38 PTB patients with emphysema was 52.0 days [interquartile range (IQR) 29.0–66.0 days], which was significantly delayed compared with that in 41 patients without emphysema (28.0 days, IQR 14.0–42.0 days) (p < 0.001, log-rank test). Multivariate Cox proportional hazards analysis showed that the following were associated with delayed TCC: emphysema [hazard ratio (HR): 2.43; 95% confidence interval (CI): 1.18–4.97; p = 0.015), cavities (HR: 2.15; 95% CI: 1.83–3.89; p = 0.012) and baseline time to TB detection within 2 weeks (HR: 2.95; 95% CI: 1.64–5.31; p < 0.0001). Cavities and consolidation were more often identified by CT in PTB patients with than without emphysema (71.05% vs 43.90%; p = 0.015, and 84.21% vs 60.98%; p = 0.021, respectively).ConclusionsThis study suggests that emphysema poses an increased risk of delayed TCC in PTB. Emphysema detection by CT might be a useful method for prediction of the duration of PTB treatment required for sputum negative conversion.

The effect of emphysema on survival in patients with idiopathic pulmonary fibrosis: A retrospective study in Taiwan.

Idiopathic pulmonary fibrosis (IPF) is a rare and chronic fibrosing interstitial lung disease. However, the clinical features and outcomes of IPF in Taiwan have not been well studied. In addition, the survival difference between patients with IPF alone and combined pulmonary fibrosis and emphysema (CPFE) remains controversial. Patients diagnosed with IPF between 2006 and 2016 were retrospectively enrolled in this study. IPF was defined according to the 2011 American Thoracic Society/European Respiratory Society guideline. The clinical features, comorbidities, and outcomes of CPFE group and IPF-alone group were compared. The extents of emphysema and fibrosis were evaluated. In total, 114 patients with IPF were enrolled, and 86.8% of them were men with a mean age of 77.8 years. The median survival was 3.33 years in all patients with IPF. Moreover, 30 patients (26.3%) met the CPFE criteria. The CPFE group had a higher percentage of smokers (90% vs 50%, p < 0.001), higher forced vital capacity (82% vs 59%, p < 0.001), and lower fibrosis scores (8.5 ± 2.9 vs 10 ± 3.2, p = 0.022) than did the IPF-alone group. The baseline room air saturation and percentage of pulmonary hypertension were similar between the two groups. The survival time was not significantly different between the CPFE and IPF-alone groups (median survival, 3.58 vs 2.39 years, p = 0.163). In the multivariate analysis, higher fibrosis score, room air saturation < 90%, and lung cancer were significant factors associated with mortality. Our study showed that emphysema had no significant effect on the survival of patients with IPF. The outcome of IPF was mainly determined by the baseline disease severity and other comorbidities.

Emphysema affects the number and characteristics of solitary pulmonary nodules identified by chest low-dose computed tomography. A study on screenees with high-risk lung cancer recruited in Upper Silesia.

Chest low-dose computed tomography (LDCT) has recently been proved effective in lung cancer screening. We aimed to assess the association between the occurrence of emphysema and solitary pulmonary nodules (SPNs) in first‑round screening with LDCT. A total of 601 asymptomatic volunteers with a smoking history underwent LDCT; 523 patients were assigned to one of the following groups: E, emphysema without nodules (n = 103); E + N, emphysema with coexisting nodules (n = 96); N, nodules without emphysema (n = 142); and NENN, no nodules and no emphysema (n = 182). The effect of emphysema and demographic factors on the profile of SPNs was assessed. Patients in the E + N group were older than those in the N group (median age, 65 vs 63 years; P = 0.001) and they smoked more (median pack‑years, 37.8 vs 32; P = 0.01). Emphysema was detected in 199 of the 523 patients (38%), while nodules, in 238 (45.5%). The number of nodules in the E + N group was 390 (4.1 nodules per patient), and in the N group, 540 (3.8 nodules per patient). Multiple SPNs, of different size and morphology, constituted 93.3% of the nodules in the E + N group. Seven cases of cancer were detected among 238 patients with nodules, and their distribution was similar in the groups with and without emphysema (4.2 per 100 patients in the E + N group and 2.1 per 100 in the N group; P = 0.44). Emphysema was more frequently associated with multiple SPNs of different morphology among elderly patients with a higher number of smoking pack‑years.

The effect of emphysema induced by tobacco smoke exposure and different rearing ways on the atherosclerosis formation

Objective To explore the relationship and its mechanism of emphysema induced by different ways of rearing and tobacco smoke exposure with the atherosclerosis formation. Methods Forty-eight SD rats were randomly divided into 6 groups (n=8, each): a normal diet + tobacco smoke exposure (TSE) group, a fat-rich diet + TSE group, a limit intake + TSE group, a normal diet group, a fat-rich diet group, and a limit intake group for 24 weeks.Lee's index, serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), adiponectin (APN) levels, mean linear intercept (MLI), mean alveoli number (MAN), the aortic pathology change, vascular endothelial growth factor (VEGF) of aorta, and bone morphogenetic protein-2 (BMP-2) level were collected. Results Tobacco smoke exposure, fat-rich diet, and limit intake increased the severity of emphysema.The microscopic features of aorta showed an early atherosclerosis in the tobacco smoke exposure groups, but no atherosclerosis in the non-smoking groups.Interactions between tobacco smoke exposure and different ways of rearing on serum APN level (F=10.68, P<0.05) were found.In the tobacco smoke exposure groups, Pearson correlation analysis showed positive correlations of aortic VEGF and BMP-2 levels with MLI, serum TNF-α and IL-6 levels (r=0.431, 0.471, 0, 448, 0.449, 0.428, 0.447, all P<0.05), and an negative correlation with MAN (r=-0.411, -0.442, P<0.05). Conclusions Both tobacco smoke exposure and different ways of rearing can influence the formation of emphysema.There is a positive correlation between the severities of emphysema and atherosclerosis, and systemic inflammation may be involved. Key words: Tobacco smoke pollution; Pulmonary emphysema; Atherosclerosis; Feeding methods

The effect of emphysema on readmission and survival among smokers with heart failure.

Heart Failure (HF) and chronic obstructive pulmonary disease (COPD) are morbid diseases that often coexist. In patients with coexisting disease, COPD is an independent risk factor for readmission and mortality. However, spirometry is often inaccurate in those with active heart failure. Therefore, we investigated the association between the presence of emphysema on computed tomography (CT) and readmission rates in smokers admitted with heart failure (HF). The cohort included a consecutive group of smokers discharged with HF from a tertiary center between January 1, 2014 and April 1, 2014 who also had a CT of the chest for dyspnea. The primary endpoint was any readmission for HF before April 1, 2016; secondary endpoints were 30-day readmission for HF, length of stay and all-cause mortality. Over the study period, there were 225 inpatient smokers with HF who had a concurrent chest CT (155 [69%] males, age 69±11 years, ejection fraction [EF] 46±18%, 107 [48%] LVEF of < 50%). Emphysema on CT was present in 103 (46%) and these were older, had a lower BMI, more pack-years, less diabetes and an increased afterload. During a follow-up of 2.1 years, there were 110 (49%) HF readmissions and 55 (24%) deaths. When separated by emphysema on CT, any readmission, 30-day readmission, length of stay and mortality were higher among HF patients with emphysema. In multivariable regression, emphysema by CT was associated with a two-fold higher (adjusted HR 2.11, 95% CI 1.41–3.15, p < 0.001) risk of readmission and a trend toward increased mortality (adjusted HR 1.70 95% CI 0.86–3.34, p = 0.12). In conclusion, emphysema by CT is a frequent finding in smokers hospitalized with HF and is associated with adverse outcomes in HF. This under recognized group of patients with both emphysema and heart failure may benefit from improved recognition and characterization of their co-morbid disease processes and optimization of therapies for their lung disease.

The effects of emphysema on airway disease: Correlations between multi-detector CT and pulmonary function tests in smokers

BackgroundChronic obstructive pulmonary disease (COPD) is characterized by airflow limitation caused by emphysema and small airway narrowing. Quantitative evaluation of airway dimensions by multi-detector computed tomography (MDCT) has revealed a correlation between airway dimension and airflow limitation. However, the effect of emphysema on this correlation is unclear. ObjectiveThe goal of this study was to determine whether emphysematous changes alter the relationships between airflow limitation and airway dimensions as measured by inspiratory and expiratory MDCT. MethodsNinety-one subjects underwent inspiratory and expiratory MDCT. Images were evaluated for mean airway luminal area (Ai), wall area percentage (WA%) from the third to the fifth generation of three bronchi (B1, B5, B8) in the right lung, and low attenuation volume percent (LAV%). Correlations between each airway index and airflow limitation were determined for each patient and compared between patients with and without evidence of emphysema. ResultsIn patients without emphysema, Ai and WA% from both the inspiratory and expiratory scans were significantly correlated with FEV1. No correlation was detected in patients with emphysema. In addition, emphysematous COPD patients with GOLD stage 1 or 2 disease had significantly lower changes in B8 Ai than non-emphysematous patients. ConclusionsA significant correlation exists between airway parameters and FEV1 in patients without emphysema. Emphysema may influence airway dimensions even in patients with mild to moderate COPD.

Effect of Emphysema on CT Scan Measures of Airway Dimensions in Smokers

In CT scans of smokers with COPD, the subsegmental airway wall area percent (WA%) is greater and more strongly correlated with FEV1 % predicted than WA% obtained in the segmental airways. Because emphysema is linked to loss of airway tethering and may limit airway expansion, increases in WA% may be related to emphysema and not solely to remodeling. We aimed to first determine whether the stronger association of subsegmental vs segmental WA% with FEV1 % predicted is mitigated by emphysema and, second, to assess the relationships among emphysema, WA%, and total bronchial area (TBA). We analyzed CT scan segmental and subsegmental WA% (WA% = 100 × wall area/TBA) of six bronchial paths and corresponding lobar emphysema, lung function, and clinical data in 983 smokers with COPD. Compared with segmental WA%, the subsegmental WA% had a greater effect on FEV1% predicted (-0.8% to -1.7% vs -1.9% to -2.6% per 1-unit increase in WA%, respectively; P < .05 for most bronchial paths). After adjusting for emphysema, the association between subsegmental WA% and FEV1 % predicted was weakened in two bronchial paths. Increases in WA% between bronchial segments correlated directly with emphysema in all bronchial paths (P < .05). In multivariate regression models, emphysema was directly related to subsegmental WA% in most bronchial paths and inversely related to subsegmental TBA in all bronchial paths. The greater effect of subsegmental WA% on airflow obstruction is mitigated by emphysema. Part of the emphysema effect might be due to loss of airway tethering, leading to a reduction in TBA and an increase in WA%.

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Effect of Emphysema on Lung Cancer Risk in Smokers: A Computed Tomography–Based Assessment

The contribution of emphysema to lung cancer risk has been recognized, but the effect size needs to be further defined. In this study, 565 primary lung cancer cases were enrolled though a prospective lung cancer cohort at Mayo Clinic, and 450 controls were smokers participating in a lung cancer screening study in the same institution using spiral computed tomography (CT). Cases and controls were frequency matched on age, gender, race, smoking status, and residential region. CT imaging using standard protocol at the time of lung cancer diagnosis (case) or during the study (control) was assessed for emphysema by visual scoring CT analysis as a percentage of lung tissue destroyed. The clinical definition of emphysema was the diagnosis recorded in the medical documentation. Using multiple logistic regression models, emphysema (≥ 5% on CT) was found to be associated with a 3.8-fold increased lung cancer risk in Caucasians, with higher risk in subgroups of younger (<65 years old, OR = 4.64), heavy smokers (≥ 40 pack-years, OR = 4.46), and small-cell lung cancer (OR = 5.62). When using >0% or ≥ 10% emphysema on CT, lung cancer risk was 2.79-fold or 3.33-fold higher than controls. Compared with CT evaluation (using criterion ≥ 5%), the sensitivity, specificity, positive and negative predictive values, and the accuracy of the clinical diagnosis for emphysema in controls were 19%, 98%, 73%, 84%, and 83%, respectively. These results imply that an accurate evaluation of emphysema could help reliably identify individuals at greater risk of lung cancer among smokers.

The effect of emphysema on lung function and survival in patients with idiopathic pulmonary fibrosis

In this study the prevalence, lung function and prognosis of IPF combined with emphysema were evaluated. Consecutive patients with usual interstitial pneumonia (UIP) on high-resolution computed tomography (HRCT), with or without emphysema, were assessed retrospectively. The area of fibrosis in the base of the lungs was assessed by HRCT as minimal (<2 cm from the subpleura), moderate (>or=2 cm from the subpleura, <1/3 of the area of the base of the lungs) or severe (>or=1/3 of the area of the base of the lungs). Among 660 patients with UIP on HRCT, 221 showed upper-lobe emphysema. Pulmonary function results for patients with UIP and UIP/emphysema, respectively, were: FVC, 71.8% and 87.1%; FEV1%, 86.7% and 87.9%; and DL(CO), 74.3% and 65.2% of predicted. The relationship between FVC, the extent of fibrosis and survival was investigated in 362 patients with records of pulmonary function tests and no lung cancer at the time of entry into the study. Although the extent of fibrosis was similar between the groups, 71.3% of UIP patients met the lung volume criteria for IPF (FVC <80% of predicted), whereas only 26.5% of UIP/emphysema patients met the lung volume criteria for IPF. Median survival was 7.5 years in the UIP group and 8.5 years in the UIP/emphysema group. Emphysema was a common finding in patients with UIP. Patients with UIP and emphysema had greater lung volumes and better survival compared with those with UIP alone.

Beer and the respiratory muscles: the adverse effects of ascites

the acquisition of a beer belly is the fate of many a physiologist. Fortunately, far fewer of us pursue beer drinking to the point of liver failure and the development of ascites. Ascites is defined as the presence of excess protein-containing fluid in the peritoneal cavity, which can range in

Emphysema-Induced Reductions in Diaphragm Mass

Profound diaphragm adaptations occur secondary to chronic lung hyperinflation in emphysema (EMP). Specifically, in EMP diaphragm oxidative capacity and fiber cross sectional area are elevated whereas fiber length is reduced via sarcomere loss. However, the consequence of EMP-induced hyperinflation on diaphragm mass remains poorly understood. PURPOSE: To investigate the effect of EMP on diaphragm mass. METHODS: Male Syrian golden hamsters were either sacrificed at 4 or 8 months following intratracheal instillation of either saline (CON=10) or elastase (25 units/100 g body weight, EMP=15). RESULTS: The presence of EMP (P<0.01) was verified visually and by measurement of excised lung volume (4-month: CON=1.6±0.3 g; EMP=4.0±1.2 and 8-month: CON=1.84±0.5 g; EMP=4.8±1.3). There were no differences in costal diaphragm mass after 4-months (CON=144±22 EMP=140±32, mg) of EMP. However, there was a significant decrease (P<0.01) in costal diaphragm mass after 8-months of EMP (CON=275±54 EMP=221±33, mg) which was correlated with disease severity (r=−.65, P<0.01, Figure). CONCLUSION: These findings support the notion that EMP per se can induce decrements in diaphragm mass which might contribute to respiratory limitations in this patient population. Therapeutic interventions that maintain diaphragm mass may therefore prove beneficial in EMP.FigureSupported by Proctor and Gamble Pharmaceuticals.

Effects of Nitrendipine and Hypoxia on Pulmonary Vascular Resistance in Experimental Emphysema

We evaluated the hemodynamic effects of nitrendipine, a dihydropyridine Ca2+ channel blocker, and hypoxia in intact dogs with emphysema produced by treatments with aerosolized papain. We also determined the effects of emphysema, chronic Ca2+ channel blocker treatment, and acute hypoxia on the distribution of vascular resistance in isolated left lower lobes. Pulmonary vascular resistance was increased (4 +/- 1 mm Hg/L/min) in the animals studied 6 months after receiving 4 weekly treatments with papain compared with control animals (2.6 +/- 0.6 mm Hg/L/min, p less than 0.05), and this effect of emphysema was blunted with chronic nitrendipine, 3 mg/kg twice a day (3.1 +/- 0.9 mm Hg/L/min). Both at baseline and at 6 months, hypoxia-induced increases in pulmonary vascular resistance were abolished by nitrendipine. The total pulmonary pressure gradient (delta Pt) was partitioned into pressure gradients across arterial (delta Pa), middle (delta Pm), and venous (delta Pv) vessels by occlusions performed during normoxia (PIO2 = 200 mm Hg) and hypoxia (PIO2 = 30 mm Hg). Papain-treated animals had elevated delta Pt compared with that in control animals because of an increased delta Pv (9.7 +/- 1.1 mm Hg versus 5.2 +/- 0.4 mm Hg in control animals, p less than 0.05). In contrast, only delta Pm was increased with papain + nitrendipine (2.6 +/- 1.0 mm Hg versus 0.2 +/- 0.3 mm Hg in control animals, p less than 0.05). An increase in the downstream pressure gradient was also observed when lobes from animals with emphysema were studied under conditions of reverse perfusion. Hypoxic responses were similar in the control and papain groups, with increases in delta Pa and delta Pm.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of Preexisting Pulmonary Emphysema on Susceptibility of Rats to Chronic Inhalation Exposure to Nitrogen Dioxide

The effect of preexisting pulmonary emphysema on the susceptibility of rats to the effects of chronic inhalation exposure to nitrogen dioxide (NO2) was examined. Rats were exposed 7 h/day, 5 daydweek for 24 months to 9.5 ppm NO2 or sham-exposed to clean air. Emphysema was induced in one-half of the rats by intratracheal instillation of elastase 6 weeks before exposure began. Measurements included respiratory function, bronchoalveolar lavage, lung tissue collagen, clearance of radiolabeled tracer particles, excised lung weight and volume, histopathology, and mean linear intercept of terminal airspaces. Analysis of variance was used to detect significant interactions between the effects of emphysema and NO2 Increased susceptibility was defined as a significant emphysema-NO2 interaction that was greater than additive. Only one measured parameter met the criteria for increased susceptibility: a greater than additive effect was observed for the forced expiratory flow rate at 10% of forced vital capacity This finding was not supported by similar effects on closely related parameters, and could have occurred by chance among the 60 measured parameters at the p < .05 criterion used for statistical significance. The results of this study do not suggest that rats with elastase-induced pulmonary emphysema are more susceptible than normal rats to chronic exposure to high concentrations of NO2

Length-tension relationship of abdominal expiratory muscles: effect of emphysema.

The present study examined the active and passive length-tension relationship of the abdominal expiratory muscles in vitro during electrically stimulated contractions. Studies were performed on isolated strips of transverse abdominis and external oblique muscle from nine adult hamsters with normal lung function. The effect of chronic hyperinflation on the two muscles was assessed in eight hamsters with elastase-induced emphysema. In normal animals the maximal active tension per cross-sectional area (Po) was equal in the two muscles. The absolute muscle fiber length at which Po occurred (Lo) was less for the external oblique than the transverse abdominis and the length-tension curve operated at shorter fiber lengths. However, the change in tension produced by an increase or decrease in muscle length expressed in relative terms (i.e., as %Lo) was greater for the transverse abdominis than the external oblique. Mean total lung capacity of emphysematous animals was 198% of control. Po of the transverse abdominis and external oblique were the same in emphysematous and control animals. However, Lo and the length-tension curve of the transverse abdominis occurred at shorter fiber lengths in emphysematous animals because of a reduction in the number of sarcomeres in series along the fiber. The length-tension curve and the number of sarcomeres in the external oblique was the same in emphysematous and control animals. These results in normal animals indicate that the magnitude of the change in active and passive tension produced by a change in muscle length differs in the transverse abdominis and external oblique. Moreover, chronic hyperinflation of the thorax produced by elastase injection alters the length-tension relationships of some but not all the expiratory muscles.

Effect of Elastase-induced Emphysema on the Force-generating Ability of the Diaphragm

The effect of emphysema on the ability of the diaphragm to generate force was examined in costal diaphragm muscle strips from 10 Golden hamsters killed 18 mo after intratracheal injection of pancreatic elastase in a dose producing hyperinflation (mean total lung capacity [TLC] = 163% of control) and generalized panacinar emphysema. 13 saline-injected normal animals served as controls. The time course of isometric tension and the effect of alterations in muscle fiber and sarcomere length on the isometric tension (T) generated in response to tetanizing electrical stimuli (length-tension [L-T] relationship) were examined. Elastase administration caused an increase in diaphragm muscle thickness and reduction in the length of costal diaphragm muscle fibers measured in situ. Emphysema significantly increased the maximum tetanic tension as a result of hypertrophy. Maximal tension corrected for increases in muscle cross-sectional area (T/cm(2)), however, was the same in emphysematous (E) and control (C) animals. Emphysema also shifted the muscle fiber L-T curve of the diaphragm but not of a control muscle, the soleus, toward shorter lengths. In contrast to the effects of E on the diaphragm muscle fiber L-T curve, the sarcomere L-T curve was the same in E and C. Since the length at which tension was maximal correlated closely with sarcomere number (r = 0.94; P < 0.001) reduction in the number of sarcomeres in series in muscles from emphysematous animals appeared to explain the shift in the muscle fiber L-T curve. We conclude that in elastase-induced emphysema adaptive changes both in diaphragm cross-sectional area and sarcomere number augment the force-generating ability of the diaphragm. We speculate that changes in sarcomere number compensate for alterations in muscle fiber length resulting from chronic hyperinflation of the thorax, while diaphragmatic muscle hypertrophy represents a response to changes in respiratory load and/or diaphragm configuration (LaPlace relationship).