The present study showed that impaired RV systolic function, hypertrophy, and dilation were present even at a slight increase of mPAP, which indicates an early impact on RV function and structure in patients with COPD. RV isovolumic acceleration, performance index, and strain could detect subclinical disease and separate controls from those with no PH.

The present study aimed to explore the prevalence of pre-capillary pulmonary hypertension (PH) and characterise haemodynamic vascular responses to physical exercise in chronic obstructive pulmonary disease (COPD) outpatients, where left ventricular dysfunction and comorbidities were excluded.98 patients with COPD underwent right heart catheterisation at rest and during supine exercise. Mean pulmonary artery pressure (Ppa), pulmonary capillary wedge pressure (Ppcw) and cardiac output (CO) were measured at rest and during exercise. Exercise-induced increase in mean Ppa was interpreted relative to increase in blood flow, mean Ppa/CO, workload (W) and mean Ppa/W. Pulmonary vascular resistance (PVR) and pulmonary artery compliance (PAC) were calculated. PH at rest was defined as mean Ppa at rest o25 mmHg and Ppcw at rest ,15 mmHg.Prevalence of PH was 5%, 27% and 53% in Global Initiative for Chronic Obstructive Lung Disease stages II, III and IV, respectively. The absolute exercise-induced rise in mean Ppa did not differ between subjects with and without PH. Patients without PH showed similar abnormal haemodynamic responses to exercise as the PH group, with increased PVR, reduced PAC and steeper slopes for mean Ppa/CO and mean Ppa/W.Exercise revealed abnormal physiological haemodynamic responses in the majority of the COPD patients. The future definition of PH on exercise in COPD should rely on the slope of mean Ppa related to cardiac output and workload rather than the absolute values of mean Ppa.

BackgroundEarly identification of patients with a prolonged stay due to acute exacerbation of chronic obstructive pulmonary disease (COPD) may reduce risk of adverse event and treatment costs. This study aimed to identify predictors of prolonged stay after acute exacerbation of COPD based on variables on admission; the study also looked to establish a prediction model for length of stay (LOS).MethodsWe extracted demographic and clinical data from the medical records of 599 patients discharged after an acute exacerbation of COPD between March 2006 and December 2008 at Oslo University Hospital, Aker. We used logistic regression analyses to assess predictors of a length of stay above the 75th percentile and assessed the area under the receiving operating characteristic curve to evaluate the model’s performance.ResultsWe included 590 patients (54% women) aged 73.2±10.8 years (mean ± standard deviation) in the analyses. Median LOS was 6.0 days (interquartile range [IQR] 3.5–11.0). In multivariate analysis, admission between Thursday and Saturday (odds ratio [OR] 2.24 [95% CI 1.60–3.51], P<0.001), heart failure (OR 2.26, 95% CI 1.34–3.80), diabetes (OR 1.90, 95% CI 1.07–3.37), stroke (OR 1.83, 95% CI 1.04–3.21), high arterial PCO2 (OR 1.26 [95% CI 1.13–1.41], P<0.001), and low serum albumin level (OR 0.92 [95% CI 0.87–0.97], P=0.001) were associated with a LOS >11 days. The statistical model had an area under the receiver operating characteristic curve of 0.73.ConclusionAdmission between Thursday and Saturday, heart failure, diabetes, stroke, high arterial PCO2, and low serum albumin level were associated with a prolonged LOS. These findings may help physicians to identify patients that will need a prolonged LOS in the early stages of admission. However, the predictive model exhibited suboptimal performance and hence is not ready for clinical use.

The objectives of this study were to examine within and between individual variation detected during forced expiratory (FE) and forced inspiratory (FI) manoeuvers in a general population and to investigate the dependence of these variables on age, body size, and gender. A random sample of asymptomatic never smokers who had never been exposed occupationally to quartz or asbestos and who were living on the south-western coast of Norway were examined by spirometry; 81% of the individuals invited to attend did so. Of the 488 subjects between 18 and 73 years of age, 98% contributed three acceptable recordings for forced expiratory vital capacity (FVC) and one-second forced expiratory volume (FEV1), 94% contributed three acceptable recordings for forced inspiratory vital capacity (FIVC) and 85% contributed three acceptable recordings for one-second forced inspiratory volume (FIV(1)). The within-subject variation increased with body height and was considerably larger for FIV(1) than for FVC, FEV(1) or FIVC. A four-parameter model of pulmonary function measurement divided by height squared, including a gender term and a linear and quadratic term of age, fit the median of the observed values well. The residuals had a close-to-normal distribution, and the fifth-percentile values were estimated as the lower limit of normal. The peak value of dynamic lung volumes was observed into the middle of the fourth decade of life, and the decline thereafter did not differ greatly between the genders or among the different indices. The forced inspiratory volumes are the first reported in any reference population.

There have been few community-based randomized, controlled intervention trials for cessation in high-risk smokers. In such a trial we evaluated the effects of postal smoking cessation advice in smokers with asbestos exposure and/or reduced forced expiratory volume in one second (FEV1). All men aged 30-45 yrs (n=22,392) living in 34 municipalities in western Norway were invited to a cross-sectional community survey. Information on smoking habits and occupational asbestos exposure were obtained from self-administered questionnaires and measurements of FEV1 were performed with dry-wedge bellow spirometers. Among 16,393 participants we identified a group of 2,610 smokers with previous occupational asbestos exposure and/or adjusted FEV1 in the lowest quartile. A random half (n=1,300) received a mailed personal letter from a respiratory physician with a person-specific health advice to quit smoking and a pamphlet on smoking cessation. The remaining smokers (n=1,310) acted as controls and did not receive any information. Twelve months after the intervention, information on smoking habits was re-examined using a postal questionnaire. Among the respondents (n=2,282), smoking cessation was reported altogether by 13.7% in the intervention group versus 9.9% in the control group (p<0.01). The 1 yr sustained quit rate (no smoking at all during the last year) was 5.6 versus 35% (p<0.05), respectively. Measurements of carbon monoxide in expired air (with < or = 10 parts per million) confirmed self-reported nonsmoking in samples of the two groups. In a community this simple postal smoking cessation advice from a respiratory physician based on person-specific risk factors improved the 1 yr sustained success rate by 60% in identified high-risk smokers.