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Individuals with Chronic Obstructive Pulmonary Disease (COPD) often develop anxiety and depression, which worsen illness management and prognosis. Physical and psychological symptoms, contextual and illness-related factors display complex reciprocal interactions, which give rise to heterogeneous presentations. Examining the patterns of association between specific physical and psychological symptoms in patients with COPD may help to focus on the precision of the patient-centred care.We used network analyses to examine the links between symptoms of COPD, depression and anxiety.Data from 1587 individuals with COPD from the COPDGene study were included. We estimated a Bayesian Gaussian Graphical Model to highlight the unique associations between symptoms of COPD (assessed with the COPD Assessment Test), depression and anxiety (assessed with the Hospital Anxiety and Depression Scale (HADS), while examining the role of sociodemographic characteristics, lung function tests, and health status.Unique Variable Analysis reduced 14 HADS items to Tension/worry (chronic anxiety), Fear/panic (acute anxiety), Restlessness, Anhedonia, Sadness and Slowing. In network analyses, chest-tightness was related to acute anxiety, while cough and weakness were connected with core depressive symptoms (sadness and lack of pleasure). Chronic anxiety was linked with acute anxiety and depressive symptoms. Findings were confirmed accounting for the role of confounders, including lung function, sex, ethnicity and lifestyle factors. A simulation based on our model yielded distinct predictions about anxiety and depression in two participants with similar COPD severity, but different symptom profiles.Network analyses highlighted specific associations between symptoms of COPD, depression and anxiety. Accounting for symptom-level interactions may help to promote personalized treatment approaches.

Several factors occurring in early life, including lower respiratory tract illnesses (LRIs), are involved in determining lung structure and function in adulthood, but the effects of these factors on lung development remain largely unknown. Hereby, we evaluated the parameters from computed tomography (CT) scans performed at the age of 26 years in 39 subjects from the birth cohort of the Tucson Children's Respiratory Study (TCRS) in order to determine the relationship between early childhood factors and lung structural changes in young adult life. We found that participants with LRIs in childhood had increased air trapping at the age of 26 suggesting an association between childhood infections and lung development.

BACKGROUND: Lower heart rate (HR) increases during exercise and slower HR recovery (HRR) after exercise are markers of worse autonomic function that may be associated with risk of acute respiratory events (ARE). METHODS: Data from 6-minute walk testing (6MWT) in COPDGene were used to calculate the chronotropic index (CI) [(HR immediately post 6MWT – resting HR) / ((220 – age) – resting HR)] and HRR at one minute after 6MWT completion. We used zero-inflated negative binomial regression to test associations of CI and HRR with rates of any ARE (requiring steroids and/or antibiotics) and severe ARE (requiring emergency department visit or hospitalization), among all participants and in spirometry subgroups (normal, chronic obstructive pulmonary disease [COPD], and preserved ratio with impaired spirometry). RESULTS: Among 4,484 participants, mean follow-up time was 4.1 years, and 1,966 had COPD. Among all participants, CI-6MWT was not associated with rate of any ARE [adjusted incidence rate ratio (aIRR) 0.98 (0.95 to 1.01)], but higher CI-6MWT was associated with lower rate of severe ARE [0.95 (0.92 to 0.99)]. Higher HRR was associated with a lower rate of both any ARE [0.97 (0.95 to 0.99)] and severe ARE [0.95 (0.92 to 0.98)]. Results were similar in the COPD spirometry subgroup. CONCLUSION: Heart rate measures derived from 6MWT tests may have utility in predicting risk of acute respiratory events and COPD exacerbations.

BACKGROUND: High N-terminal pro-brain natriuretic peptide (NT-proBNP) during COPD exacerbations is associated with worse clinical outcomes. The prognostic value of NT-proBNP measured during clinical stability has not been well characterized. METHODS: We studied SPIROMICS participants 40–80 years of age with COPD GOLD spirometric stages 1–4. The association between baseline NT-proBNP and incident COPD exacerbations within one year of follow-up was tested using zero-inflated Poisson regression models adjusted for age, gender, race, body mass index, current smoking status, smoking history, FEV(1) percent predicted, COPD Assessment Test score, exacerbation history, total lung capacity on chest CT and cardiovascular disease (any of coronary artery disease, myocardial infarction or congestive heart failure). RESULTS: Among 1,051 participants (mean age 66.1 years, 41.4% women), mean NT-proBNP was 608.9 pg/ml. Subjects in GOLD stage D had the highest mean NT-proBNP. After one year of follow-up, 268 participants experienced one or more COPD exacerbations. One standard deviation increase in baseline NT-proBNP was associated with a 13% increase in the risk of incident exacerbations (incident risk ratio 1.13; 95% CI 1.06–1.19; p

SummaryPurposeAcute exacerbations of chronic obstructive pulmonary disease (COPD) sometimes appear to occur without a precipitating cause. Heterogeneous repolarization and arrhythmias occur in COPD patients. Given the close inter-relation between heart and lung, we hypothesized that unrecognized arrhythmias might be precipitants of acute exacerbations.MethodsElectrocardiograms (ECG) of thirty patients during acute exacerbations were compared with ECG during stable phase. P wave dispersion was used to assess atrial depolarization heterogeneity, and dispersion of QT interval to assess ventricular repolarization. p

Summary Introduction Predictors of readmission for acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are not well defined. Identifying modifiable predictors may help reduce the burden of readmissions. This study was done to evaluate the role of serum magnesium in frequent readmissions. Methods One hundred patients admitted with a diagnosis of AECOPD to a tertiary care center from April 2004 to March 2006 were retrospectively followed from the time of index admission until the next admission or death. Number of admissions was calculated for the year after index admission, and frequent readmission was defined as ⩾3 per year. Patients with other respiratory diseases, renal failure, and congestive heart failure were excluded. Serum magnesium was assayed at the time of admission by the colorimetric method. Logistic regression analysis was used to find independent risk factors for readmission. Results The mean age of patients was 71.9 (±10.9 standard deviation (SD)) years. Fifty-seven were females. Ninety percent were current or ex-smokers. The median duration of time to next admission was 108 days (range 2–842). A total of 87 patients were readmitted at least once during the first year of follow-up, while 5% died; 23% had frequent readmissions; 85% had received pneumococcal vaccine within 5 years; and 29% received influenza vaccine in the current season. Frequency of readmissions was not influenced by the administration of inhaled or oral steroids, and diuretics at the time of discharge. Vaccination did not protect against frequent readmissions. The sole predictor of frequent readmissions was serum magnesium level (1.77±0.19 vs. 1.86±0.24mEq/L; adjusted odds ratio 0.003, 95% Confidence intervals p =0.03). Conclusions Lower serum magnesium level independently predicts readmission for AECOPD. This is an easily modifiable risk factor.