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PurposePrior research has shown a significant relationship between 6-minute walking distance (6MWD) and health-related quality of life (HRQOL) in patients with chronic obstructive pulmonary disease (COPD). However, few studies have examined this relationship above and below the 350-m threshold that prognosticates survival and whether serum biomarkers could provide insight into the causes of quality-of-life differences above and below this threshold.MethodsMeasures of lung function, 6MWD, and HRQOL were compared in patients with COPD. Differences in HRQOL domains and serum biomarkers were compared in patients whose 6MWD were > or < 350 m.ResultsIn patients walking < 350 m, scores in the physical domains of the SF-36 and the St. George's Respiratory Questionnaire (SGRQ) were significantly different from scores of their counterparts with greater 6MWD. However, there was no association between any biomarkers and the physical domains of the SF-36 and the SGRQ. In patients walking < 350 m, only the IL-8 levels were associated with lower scores in SF-36 domains of emotional role, pain, vitality, and mental health (average r = -0.702; P = .01). In contrast, in patients walking > 350 m, surfactant protein D levels were associated with higher SF-36 scores in general pain, vitality, and social functioning (average r = 0.42; P = .04).ConclusionsIn COPD, there is an association between 6MWD and the physical domains of the SF-36 and SGRQ in those patients walking < 350 m. The physical differences between patients walking < or > 350 m are not related to systemic inflammation. The association between interleukin 8 with nonphysical domains in patients with 6MWD < 350 m suggests that inflammation may play a larger role in the perceptive domain than previously recognized.

BackgroundWe aimed to assess whether chronic obstructive pulmonary disease (COPD) is associated with expansion of the myocardial extracellular volume (ECV) using T1 measurements.MethodsAdult COPD patients Global Initiative for Chronic Obstructive Lung Disease [GOLD] stage 2 or higher and free of known cardiovascular disease were recruited. All study patients underwent measures of pulmonary function, 6-minute walk test, serum measures of inflammation, overnight polysomnography, and a contrast cardiac magnetic resonance study.ResultsEight patients with COPD were compared with 8 healthy control subjects. The mean predicted forced expiratory volume at 1 second of COPD subjects was 68%. Compared with control subjects, patients had normal left ventricular (LV) and right ventricular size, mass, and function. However, compared with control subjects, the LV remodelling index (median, 0.87; interquartile range [IQR], 0.71-1.14; vs median, 0.62; IQR, 0.60-0.77; P ¼ 0.03) and active left atrial emptying fraction was increased (median, 46; IQR, 41-49; vs median, 38; IQR, 33-43; P ¼ 0.005), and passive left atrial emptying fraction was reduced (median, 24; IQR, 20-30; vs median, 44; IQR, 31-51; P ¼ 0.007). The ECV was increased in patients with COPD (median, 0.32; IQR, 0.05; vs median, 0.27; IQR, 0.05; P = 0.001). The ECV showed a strong positive association with LV remodelling (r = 0.72; P = 0.04) and an inverse association with the 6-minute walk duration (r = -0.79; P = 0.02) and passive left atrial emptying fraction (r = -0.68; P = 0.003).ConclusionsExpansion of the ECV, suggestive of diffuse myocardial fibrosis, is present in COPD and is associated with LV remodelling, and reduced left atrial function and exercise capacity.

Smoking and human immunodeficiency virus 1 (HIV-1) infection are risk factors for chronic obstructive pulmonary disease (COPD), which is among the most common comorbid conditions in people living with HIV-1. HIV-1 infection leads to persistent expansion of CD81 T cells, and CD81 T cell-mediated inflammation has been implicated in COPD pathogenesis. In this study, we investigated the effects of HIV-1 infection and smoking on T-cell dynamics in patients at risk of COPD. BAL fluid, endobronchial brushings, and blood from HIV-1 infected and uninfected nonsmokers and smokers were analyzed by flow cytometry, and lungs were imaged by computed tomography. Chemokines were measured in BAL fluid, and CD81 T-cell chemotaxis in the presence of cigarette smoke extract was assessed in vitro. HIV-1 infection increased CD81 T cells in the BAL fluid, but this increase was abrogated by smoking. Smokers had reduced BAL fluid concentrations of the T cell-recruiting chemokines CXCL10 and CCL5, and cigarette smoke extract inhibited CXCL10 and CCL5 production by macrophages and CD81 T-cell transmigration in vitro. In contrast to the T cells in BAL fluid, CD81 T cells in endobronchial brushings were increased in HIV-1-infected smokers, which was driven by an accumulation of effector memory T cells in the airway mucosa and an increase in tissue-resident memory T cells. Mucosal CD81 T-cell numbers inversely correlated with lung aeration, suggesting an association with inflammation and remodeling. HIV-1 infection and smoking lead to retention of CD81 T cells within the airway mucosa. [ABSTRACT FROM AUTHOR]

The article focuses on a student's perspective concerning the significance of the faculty to help facilitate successful mentoring with the medical students in the U.S. Accordingly, career mentoring of the students by the faculty has been found to be one of the areas in the curriculum that has been overlooked. The Society of General Internal Medicine will be focusing on mentorship during their 2008 meeting in order to address such issue.

Smoking and human immunodeficiency virus 1 (HIV-1) infection are risk factors for chronic obstructive pulmonary disease (COPD), which is among the most common comorbid conditions in people living with HIV-1. HIV-1 infection leads to persistent expansion of CD8 + T cells, and CD8 + T cell-mediated inflammation has been implicated in COPD pathogenesis. In this study, we investigated the effects of HIV-1 infection and smoking on T-cell dynamics in patients at risk of COPD. BAL fluid, endobronchial brushings, and blood from HIV-1 infected and uninfected nonsmokers and smokers were analyzed by flow cytometry, and lungs were imaged by computed tomography. Chemokines were measured in BAL fluid, and CD8 + T-cell chemotaxis in the presence of cigarette smoke extract was assessed in vitro . HIV-1 infection increased CD8 + T cells in the BAL fluid, but this increase was abrogated by smoking. Smokers had reduced BAL fluid concentrations of the T cell-recruiting chemokines CXCL10 and CCL5, and cigarette smoke extract inhibited CXCL10 and CCL5 production by macrophages and CD8 + T-cell transmigration in vitro . In contrast to the T cells in BAL fluid, CD8 + T cells in endobronchial brushings were increased in HIV-1-infected smokers, which was driven by an accumulation of effector memory T cells in the airway mucosa and an increase in tissue-resident memory T cells. Mucosal CD8 + T-cell numbers inversely correlated with lung aeration, suggesting an association with inflammation and remodeling. HIV-1 infection and smoking lead to retention of CD8 + T cells within the airway mucosa.

Chronic obstructive pulmonary disease (COPD) is the most common noninfectious pulmonary disease among people living with HIV, independent of smoking. However, the cause for this enhanced susceptibility remains unclear, and the effects of HIV on pulmonary perfusion and ventilation are unknown. Methods: We used PET/CT in 46 smokers and nonsmokers, 23 of whom had documented HIV infection. Emphysema was assessed by CT and perfusion by 13 N ( 13 NN) PET scans. After removal of image noise, vertical and axial gradients in perfusion were calculated. We tested for differences in the total spatial heterogeneity of perfusion (CV 2 Qtotal ) and its components (CV 2 Qtotal = CV 2 Qvgrad [vertical gradient] + CV 2 Qzgrad [axial gradient] + CV 2 Qr [residual heterogeneity]) among groups. Results: There were no significant differences in demographic parameters among groups, and all subjects had minimal radiographic evidence of emphysema. Compared with controls, nonsmokers living with HIV had a significantly greater CV 2 Qr /CV 2 Qtotal (0.48 vs. 0.36, P = 0.05) and reduced CV 2 Qvgrad /CV 2 Qtotal (0.46 vs. 0.65, P = 0.038). Smokers also had a reduced CV 2 Qvgrad /CV 2 Qtotal , however, there was no significant difference in CV 2 Qvgrad /CV 2 Qtotal between smokers living with and without HIV (0.39 vs. 0.34, P = 0.58), despite a decreased vertical perfusion gradient (Qv grad ) in smokers living with HIV. Conclusion: In nonsmokers living with well-controlled HIV and minimal radiographic emphysema, HIV infection contributes to pulmonary perfusion abnormalities similar to smokers. These data indicate the onset of subclinical pulmonary perfusion abnormalities that could herald the development of significant lung disease in these susceptible individuals., (© 2021 by the Society of Nuclear Medicine and Molecular Imaging.)