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Chronic obstructive pulmonary disease (COPD) and lung cancer are common global causes of morbidity and mortality. Because both diseases share several predisposing risks, the 2 diseases may occur concurrently in susceptible individuals. The diagnosis of COPD has important implications for the diagnostic approach and treatment options if lesions concerning for lung cancer are identified during screening. Importantly, the presence of COPD has significant implications on prognosis and management of patients with lung cancer. In this monograph, we review the mechanistic linkage between lung cancer and COPD, the impact of lung cancer screening on patients at risk, and the implications of the presence of COPD on the approach to the diagnosis and treatment of lung cancer. This manuscript succinctly reviews the epidemiology and common pathogenetic factors for the concurrence of COPD and lung cancer. Importantly for the clinician, it summarizes the indications, benefits, and complications of lung cancer screening in patients with COPD, and the assessment of risk factors for patients with COPD undergoing consideration of various treatment options for lung cancer.

Rationale: Exacerbations of chronic obstructive pulmonary disease are an important endpoint in multinational clinical treatment trials, but the observed event rate is often lower than anticipated and appears to vary between countries. Objectives: We investigated whether systematic differences in national exacerbation rates might explain this observed variation. Methods: We reviewed data from three large multicenter international randomized trials conducted over an 18-year period with different designs and clinical severities of chronic obstructive pulmonary disease, comparing bronchodilator and/or inhaled corticosteroids with bronchodilators alone and/or placebo. Exacerbations were defined by antibiotic and/or oral corticosteroid use (moderate) or need for hospitalization (severe). We calculated crude exacerbation rates in the 30 countries contributing 30 or more patients to at least two trials. We grouped data by exacerbation rate based on their first study contribution. Measurements and Main Results: For the 29,756 patients in 41 countries analyzed, the mean exacerbation rate was 2–3-fold different between the highest and lowest tertiles of the recruiting nations. These differences were not explained by demographic features, study protocol, or reported exacerbation history at enrolment. Of the 18 countries contributing to all studies, half of those in the highest and half in the lowest tertiles of exacerbation history remained in these groups across studies. Severe exacerbations showed a different rank order internationally. Conclusions: Countries contributing to chronic obstructive pulmonary disease trials differ consistently in their reporting of health care-defined exacerbations. These differences help explain why large studies have been needed to show differences between treatments that decrease exacerbation risk.

Additional file 1: Figure S1. Comorbidities prevalence bar graph comparing Young (≤ 50 years) and older (> 50 years) COPD patients. Figure S2. Kaplan–Meier survival curve comparing the three groups. In blue is the control group, red for “Young COPD” and green for the older COPD. Figure S3. Primary causes of death in the Young (< 50 years) and “Older” COPD patients (> 50 years). Table S1. Comorbidities prevalence comparison between Young COPD and controls. Table S2. Comorbidities prevalence comparing Young COPD and Old COPD.

This document summarizes the work of the COPD Technical Expert Panel working group. For patients with COPD, the most pressing current coverage barriers identified were onerous diagnostic requirements focused on oxygenation (rather than ventilation) and difficulty obtaining bilevel devices with backup rate capabilities. Because of these difficulties, many patients with COPD were instead sometimes prescribed home mechanical ventilators. Critical evidence supports changes to current policies, including randomized controlled trial evidence suggesting a mortality benefit from bilevel positive airway pressure with backup rate and updated clinical practice guidelines from the American Thoracic Society as well as the European Respiratory Society. To achieve optimal access to noninvasive ventilation for patients with COPD, we make the following key recommendations: (1) removal of the need for overnight oximetry testing; (2) the ability to initiate therapy using bilevel devices with backup rate capability; and (3) increased duration of time to meet adherence criteria (ie, a second 90-day trial period) in those patients actively engaged in their care. Clear guidelines based on medical necessity are also included for patients who require initiation of or switch to a home mechanical ventilator. Adoption of these proposed recommendations would result in the right device, for the right type of patient with COPD, at the right time. Finally, we emphasize the need for adequate clinical support during initiation and maintenance of home noninvasive ventilation in such patients.

This document summarizes the work of the COPD Technical Expert Panel working group. For patients with COPD, the most pressing current coverage barriers identified were onerous diagnostic requirements focused on oxygenation (rather than ventilation) and difficulty obtaining bilevel devices with backup rate capabilities. Because of these difficulties, many patients with COPD were instead sometimes prescribed home mechanical ventilators. Critical evidence supports changes to current policies, including randomized controlled trial evidence suggesting a mortality benefit from bilevel positive airway pressure with backup rate and updated clinical practice guidelines from the American Thoracic Society as well as the European Respiratory Society. To achieve optimal access to noninvasive ventilation for patients with COPD, we make the following key recommendations: (1) removal of the need for overnight oximetry testing; (2) the ability to initiate therapy using bilevel devices with backup rate capability; and (3) increased duration of time to meet adherence criteria (ie, a second 90-day trial period) in those patients actively engaged in their care. Clear guidelines based on medical necessity are also included for patients who require initiation of or switch to a home mechanical ventilator. Adoption of these proposed recommendations would result in the right device, for the right type of patient with COPD, at the right time. Finally, we emphasize the need for adequate clinical support during initiation and maintenance of home noninvasive ventilation in such patients.

Andras Bikov,1,2 Peter Lange,3,4 Julie A Anderson,5 Robert D Brook,6 Peter MA Calverley,7 Bartolome R Celli,8 Nicholas J Cowans,9 Courtney Crim,10 Ian J Dixon,9 Fernando J Martinez,11 David E Newby,12 Julie C Yates,10 Jørgen Vestbo1,2 1Manchester University NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester, UK; 2Division of Infection, Immunity & Respiratory Medicine, University of Manchester, Manchester, UK; 3Medical Department, Herlev and Gentofte Hospital, Herlev, Denmark; 4Section of Epidemiology, Department of Public Health, University of Copenhagen, Copenhagen, Denmark; 5Research & Development, GlaxoSmithKline, Middlesex, UK; 6University of Michigan Health System, Ann Arbor, MI, USA; 7University of Liverpool, Department of Medicine, Clinical Sciences Centre, University Hospital Aintree, Liverpool, UK; 8Pulmonary and Critical Care Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA; 9Statistics & Programming, Veramed Ltd., Twickenham, UK; 10Research & Development, GlaxoSmithKline, Research Triangle Park, NC, USA; 11Division of Pulmonary and Critical Care Medicine, Weill Cornell Medicine, New York, NY, USA; 12British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UKCorrespondence: Andras Bikov 2nd Floor ERC Building, Wythenshawe Hospital, Southmoor Road, Manchester M23 9LT, UKTel +36203141599Fax +441612915730Email andras.bikov@gmail.comPurpose: Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide. Impaired lung function is associated with heightened risk for death, cardiovascular events, and COPD exacerbations. However, it is unclear if forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) differ in predictive value.Patients and Methods: Data from 16,485 participants in the Study to Understand Mortality and Morbidity (SUMMIT) in COPD were analyzed. Patients were grouped into quintiles for each lung function parameter (FEV1 %predicted, FVC %predicted, FEV1/FVC). The four highest quintiles (Q2–Q5) were compared to the lowest (Q1) to assess their relationship with all-cause mortality, cardiovascular events, and moderate-to-severe and severe exacerbations. Cox-regression was used, adjusted for age, sex, ethnicity, body-mass index, smoking status, previous exacerbations, cardiovascular disease, treatment, and modified Medical Research Council dyspnea score.Results: Compared to Q1 (< 53.5% FEV1 predicted), increasing FEV1 quintiles (Q2 53.5– 457.5% predicted, Q3 57.5– 461.6% predicted, Q4 61.6– 465.8% predicted, and Q5 ≥ 65.8%) were all associated with significantly decreased all-cause mortality (20% (4– 34%), 28% (13– 40%), 23% (7– 36%), and 30% (15– 42%) risk reduction, respectively). In contrast, a significant risk reduction (21% (4– 35%)) was seen only between Q1 and Q5 quintiles of FVC. Neither FEV1 nor FVC was associated with cardiovascular risk. Increased FEV1 and FEV1/FVC quintiles were also associated with the reduction of moderate-to-severe and severe exacerbations while, surprisingly, the highest FVC quintile was related to the heightened exacerbation risk (28% (8– 52%) risk increase).Conclusion: Our results suggest that FEV1 is a stronger predictor for all-cause mortality than FVC in moderate COPD patients with heightened cardiovascular risk and that subjects with moderate COPD have very different risks.Keywords: airflow limitation, cardiovascular risk, exacerbation, lung function, lung volumes, death rate

Altres ajuts: A. Schötzau performed data management of PROMISE for which he received financial compensation.Thermo Scientific Biomarkers (Hennigsdorf, Germany) provided all the reagents for copeptin measurements. Several composite markers have been proposed for risk assessment in chronic obstructive pulmonary disease (COPD). However, choice of parameters and score complexity restrict clinical applicability. Our aim was to provide and validate a simplified COPD risk index independent of lung function. The PROMISE study (n=530) was used to develop a novel prognostic index. Index performance was assessed regarding 2-year COPD-related mortality and all-cause mortality. External validity was tested in stable and exacerbated COPD patients in the ProCOLD, COCOMICS and COMIC cohorts (total n=2988). Using a mixed clinical and statistical approach, body mass index (B), severe acute exacerbations of COPD frequency (AE), modified Medical Research Council dyspnoea severity (D) and copeptin (C) were identified as the most suitable simplified marker combination. 0, 1 or 2 points were assigned to each parameter and totalled to B-AE-D or B-AE-D-C. It was observed that B-AE-D and B-AE-D-C were at least as good as BODE (body mass index, airflow obstruction, dyspnoea, exercise capacity), ADO (age, dyspnoea, airflow obstruction) and DOSE (dyspnoea, obstruction, smoking, exacerbation) indices for predicting 2-year all-cause mortality (c-statistic: 0.74, 0.77, 0.69, 0.72 and 0.63, respectively; Hosmer-Lemeshow test all p>0.05). Both indices were COPD specific (c-statistic for predicting COPD-related 2-year mortality: 0.87 and 0.89, respectively). External validation of B-AE-D was performed in COCOMICS and COMIC (c-statistic for 1-year all-cause mortality: 0.68 and 0.74; c-statistic for 2-year all-cause mortality: 0.65 and 0.67; Hosmer-Lemeshow test all p>0.05). The B-AE-D index, plus copeptin if available, allows a simple and accurate assessment of COPD-related risk. The B-AE-D indices allow a simple and accurate assessment of COPD-related risk in the absence of lung function

RATIONALE: Acute exacerbations of chronic obstructive pulmonary disease (AECOPD) are common, associated with acute inflammation, and may increase subsequent cardiovascular disease (CVD) risk.OBJECTIVE: Determine if AECOPD events are associated with increased risk of subsequent CVD.METHODS: A secondary cohort analysis of the Study to Understand Mortality and MorbidITy (SUMMIT) trial, a convenience sample of current/former smokers with moderate COPD from 1,368 centers in 43 countries. All had CVD or increased CVD risk. AECOPD was defined as an increase in respiratory symptoms requiring treatment with antibiotics, systemic corticosteroids and/or hospitalization. CVD events were a composite outcome of cardiovascular death, myocardial infarction, stroke, unstable angina, and transient ischemic attack. All CVD events were adjudicated. Cox proportional hazards models compared the hazard for a CVD event prior to AECOPD versus following AECOPD.MEASUREMENTS AND MAIN RESULTS: Among 16,485 participants in SUMMIT, 4,704 participants had at least one AECOPD and 688 had at least one CVD event. The hazard ratio (HR) for CVD events following AECOPD was increased, particularly in the first 30 days following AECOPD (HR 3.8; 95%CI: 2.7 to 5.5) and was elevated up to one year post-AECOPD. The 30-day HR following hospitalized AECOPD was more than two-fold greater (HR 9.9; 95%CI: 6.6 to 14.9).CONCLUSIONS: In COPD patients with CVD or risk factors for CVD, exacerbations confer an increased risk of subsequent CVD events, especially in hospitalized patients and within the first 30 days post-exacerbation. Patients and clinicians should have heightened vigilance for early CVD events following AECOPD. Clinical trial registration available at www.clinicaltrials.gov, ID NCT01313676.

Rationale: Cardiovascular disease is a common comorbidity in patients with chronic obstructive pulmonary disease (COPD). Although beta-blockers can be used safely in COPD, concerns remain regarding safety and efficacy interactions in patients using concomitant inhaled long-acting beta-agonists. Objectives: To compare the differential effects of long-acting beta agonist or inhaled corticosteroid use on clinical outcomes in patients with heightened cardiovascular risk treated and not treated with beta-blockers. Methods: We examined data from 16,485 participants in the Study to Understand Mortality and MorbidITy in COPD (SUMMIT) who were randomized to once daily inhaled fluticasone furoate (FF), vilanterol (VI), their combination (FF/VI), or placebo and examined the associations between treatment allocation and lung function, COPD exacerbations, cardiovascular events, and all-cause mortality stratified by baseline beta-blocker therapy. Results: Baseline beta-blocker therapy was used by 31% (n=5,159) of SUMMIT participants. There was no evidence of an interaction between baseline beta-blocker therapy and the association between inhaled treatments and FEV1 at 3 months (p=0.27), 6 months (p=0.14), or 12 months (p=0.33). The placebo-adjusted mean difference in post-bronchodilator FEV1 at 3 months in the VI alone group was 58 mL [95% confidence interval (CI) 38, 78] in those taking baseline beta-blocker therapy, and 51 mL [95%CI 38, 65], in those not taking baseline beta-blocker therapy. The placebo-adjusted mean difference in post-bronchodilator FEV1 at 3 months in the FF/VI group was 85 mL [95%CI 65, 105] in those taking baseline beta-blocker therapy, and 68 mL [95%CI 54, 82] in those not taking baseline beta-blocker therapy. Overall, there was no evidence of interactions by randomized treatment, including VI alone or in combination with FF, for COPD exacerbations (p=0.18), cardiovascular composite events (p=0.33), and all-cause mortality (p=0.41). Conclusions: There is no evidence to suggest that baseline beta-blocker therapy reduces the respiratory benefits or increases the cardiovascular risk of inhaled long-acting beta-agonists in patients with COPD and heightened cardiovascular risk. Clinical trial registered with ClinicalTrials.gov (NCT01313676)

RATIONALE: Cardiovascular disease is a common comorbidity in patients with chronic obstructive pulmonary disease (COPD). Although beta-blockers can be used safely in COPD, concerns remain regarding safety and efficacy interactions in patients using concomitant inhaled long-acting beta-agonists.OBJECTIVES: To compare the differential effects of long-acting beta agonist or inhaled corticosteroid use on clinical outcomes in patients with heightened cardiovascular risk treated and not treated with beta-blockers.METHODS: We examined data from 16,485 participants in the Study to Understand Mortality and MorbidITy in COPD (SUMMIT) who were randomized to once daily inhaled fluticasone furoate (FF), vilanterol (VI), their combination (FF/VI), or placebo and examined the associations between treatment allocation and lung function, COPD exacerbations, cardiovascular events, and all-cause mortality stratified by baseline beta-blocker therapy.RESULTS: Baseline beta-blocker therapy was used by 31% (n=5,159) of SUMMIT participants. There was no evidence of an interaction between baseline beta-blocker therapy and the association between inhaled treatments and FEV1 at 3 months (p=0.27), 6 months (p=0.14), or 12 months (p=0.33). The placebo-adjusted mean difference in post-bronchodilator FEV1 at 3 months in the VI alone group was 58 mL [95% confidence interval (CI) 38, 78] in those taking baseline beta-blocker therapy, and 51 mL [95%CI 38, 65], in those not taking baseline beta-blocker therapy. The placebo-adjusted mean difference in post-bronchodilator FEV1 at 3 months in the FF/VI group was 85 mL [95%CI 65, 105] in those taking baseline beta-blocker therapy, and 68 mL [95%CI 54, 82] in those not taking baseline beta-blocker therapy. Overall, there was no evidence of interactions by randomized treatment, including VI alone or in combination with FF, for COPD exacerbations (p=0.18), cardiovascular composite events (p=0.33), and all-cause mortality (p=0.41).CONCLUSIONS: There is no evidence to suggest that baseline beta-blocker therapy reduces the respiratory benefits or increases the cardiovascular risk of inhaled long-acting beta-agonists in patients with COPD and heightened cardiovascular risk. Clinical trial registered with ClinicalTrials.gov (NCT01313676).

BackgroundCardiovascular disease is a common comorbidity in patients with chronic obstructive pulmonary disease (COPD). Concerns remain regarding safety and efficacy interactions in patients using both beta-blockers and inhaled long-acting beta-agonists. MethodsIn 16,485 patients with COPD and heightened cardiovascular risk who were randomized to once daily inhaled fluticasone furoate (FF), vilanterol (VI), their combination (FF/VI) or placebo, we assessed the effects of beta-blocker therapy usage on lung function, COPD exacerbations, cardiovascular events and all-cause mortality.ResultsThe presence or absence of beta-blocker therapy resulted in no difference in the effect of VI alone versus placebo on post-bronchodilator FEV1 at 3 months (increases of 58 mL [95% confidence interval (CI) 38, 78] and 51 mL [95%CI 38, 65], respectively) or in the effect of FF/VI vs placebo with increases of 85 mL [95%CI 65, 105] and 68 mL [95%CI 54, 82] respectively). Overall, there were no interactions by randomized treatment, including VI alone or in combination with FF, for COPD exacerbations, cardiovascular composite events and all-cause mortality.ConclusionsPatients with COPD and heightened cardiovascular risk continue to receive respiratory benefit without an excess of cardiovascular risk from inhaled long-acting beta-agonist therapy regardless of beta-blocker therapy.

BACKGROUND: Inhaled corticosteroids have been shown to decrease exacerbations in COPD patients with moderate to severe COPD. Their effect in patients with milder airflow obstruction remains unclear.OBJECTIVE: This was an analysis of exacerbations in the Study to Understand Mortality and MorbidITy (SUMMIT) study.DESIGN: In a double-blind randomized controlled trial, once daily inhaled placebo, fluticasone furoate (FF, 100 μg), vilanterol (VI, 25 μg) or the combination (FF/VI) was administered. The primary outcome was all-cause mortality. Exacerbations of COPD were an additional pre-defined endpoint.SETTING: 1,368 centers in 43 countries.PARTICIPANTS: 16,485 patients with moderate COPD and heightened cardiovascular risk.RESULTS: Compared with placebo, FF/VI reduced the rate of moderate/severe exacerbations by 29% (95% CI 22, 35; pCONCLUSIONS: Patients with moderate chronic airflow obstruction experienced a reduction in exacerbations with FF/VI, compared with placebo, irrespective of a prior history of exacerbations or baseline FEV1. Clinical trial registration available at www.clinicaltrials.gov, ID NCT01313676.

Rationale: Many patients with chronic obstructive pulmonary disease (COPD) have an accelerated loss of lung function. It is unclear whether drug treatment can modify this in moderately severe disease. Objectives: In a pre-specified analysis of the key secondary outcome in the Study to Understand Mortality and MorbidITy (SUMMIT), we investigated whether the inhaled corticosteroid fluticasone furoate 100 μg (FF), the long-acting beta-agonist vilanterol 25 µg (VI) or the combination (FF/VI) modified the rate of decline in FEV1 compared with placebo. We also investigated how baseline co-variates affected this decline. Methods: Spirometry was measured every 12 weeks in this event-driven randomized, placebo controlled trial of 16,485 patients with moderate COPD and heightened cardiovascular risk. An average of 7 spirometry assessments per subject in the 15,457 patients with at least one on-treatment measurement were used in the rate of FEV1 decline analysis. All statistical comparisons are considered nominal. Main results: The adjusted rate of FEV1 decline was -46 mL/year (-3.0% of baseline) with placebo, -47 mL/year (-3.1%) with VI, -38 mL/year (-2.5%) with FF and -38 mL/year (-2.3 %) with FF/VI. FF-containing regimes had lower rates of decline than placebo (p

ImportanceInterstitial lung abnormalities have been associated with lower 6-minute walk distance, diffusion capacity for carbon monoxide, and total lung capacity. However, to our knowledge, an association with mortality has not been previously investigated.ObjectiveTo investigate whether interstitial lung abnormalities are associated with increased mortality.Design, setting, and populationProspective cohort studies of 2633 participants from the FHS (Framingham Heart Study; computed tomographic [CT] scans obtained September 2008-March 2011), 5320 from the AGES-Reykjavik Study (Age Gene/Environment Susceptibility; recruited January 2002-February 2006), 2068 from the COPDGene Study (Chronic Obstructive Pulmonary Disease; recruited November 2007-April 2010), and 1670 from ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints; between December 2005-December 2006).ExposuresInterstitial lung abnormality status as determined by chest CT evaluation.Main outcomes and measuresAll-cause mortality over an approximate 3- to 9-year median follow-up time. Cause-of-death information was also examined in the AGES-Reykjavik cohort.ResultsInterstitial lung abnormalities were present in 177 (7%) of the 2633 participants from FHS, 378 (7%) of 5320 from AGES-Reykjavik, 156 (8%) of 2068 from COPDGene, and in 157 (9%) of 1670 from ECLIPSE. Over median follow-up times of approximately 3 to 9 years, there were more deaths (and a greater absolute rate of mortality) among participants with interstitial lung abnormalities when compared with those who did not have interstitial lung abnormalities in the following cohorts: 7% vs 1% in FHS (6% difference [95% CI, 2% to 10%]), 56% vs 33% in AGES-Reykjavik (23% difference [95% CI, 18% to 28%]), and 11% vs 5% in ECLIPSE (6% difference [95% CI, 1% to 11%]). After adjustment for covariates, interstitial lung abnormalities were associated with a higher risk of death in the FHS (hazard ratio [HR], 2.7 [95% CI, 1.1 to 6.5]; P = .03), AGES-Reykjavik (HR, 1.3 [95% CI, 1.2 to 1.4]; P

Boehringer Ingelheim Pharma GmbH Co KG Pfizer, Inc. Background: Disease progression in COPD is associated with a decline in exercise performance over time. We assessed whether tiotropium might mitigate this by determining its effect on treadmill endurance time (ET) over 2 years.Methods: This was a randomized, double-blind, placebo-controlled trial of tiotropium, 18 mu g daily, in patients with COPD (FEV1/FVC

Chronic obstructive pulmonary disease (COPD) is a complex, multicomponent disease at the clinical, cellular, and molecular levels. Over the past few years there has been a growing interest in the field of biomarkers in COPD and a large number of studies have evaluated potential candidate molecules in different patient settings. Data on systemic biomarkers from large cohorts, including the well-characterized population of the ECLIPSE study, are now available and provide exciting information on the association of biomarkers with clinically important outcomes, including exacerbations, hospitalizations and mortality. Moreover, recent research has provided proof for the existence of distinct “systemic inflammatory” phenotypes. This review summarizes the currently available evidence on systemic biomarkers in COPD, providing clinically relevant information on the possible role of systemic biomarkers in the evaluation of disease activity and severity, phenotypes, outcomes, COPD exacerbations and treatment response and guidance. Despite the fact that no single biomarker is currently ready to characterize sufficiently the status of COPD patients, guide treatment options, and predict future events, recent studies have rendered our current knowledge definitely more advanced than a few years ago and the possible use of biomarkers in the diagnosis and management of COPD patients looks even more promising.

Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States but is often undertreated. COPD often overlaps with other conditions such as hypertension and osteoporosis, which are less morbid but may be treated more aggressively. We evaluated the prevalence of these comorbid conditions and compared testing, patient knowledge, and management in a national sample of patients with COPD.A survey was administered by telephone in 2006 to 1003 patients with COPD to evaluate the prevalence of comorbid conditions, diagnostic testing, knowledge, and management using standardized instruments. The completion rate was 87%.Among 1003 patients with COPD, 61% reported moderate or severe dyspnea and 41% reported a prior hospitalization for COPD. The most prevalent comorbid diagnoses were hypertension (55%), hypercholesterolemia (52%), depression (37%), cataracts (31%), and osteoporosis (28%). Only 10% of respondents knew their forced expiratory volume in 1 second (95% confidence interval [CI], 8-12) compared with 79% who knew their blood pressure (95% CI, 76-83). Seventy-two percent (95% CI, 69-75) reported taking any medication for COPD, usually a short-acting bronchodilator, whereas 87% (95% CI, 84-90) of patients with COPD and hypertension were taking an antihypertensive medication and 72% (95% CI, 68-75) of patients with COPD and hypercholesterolemia were taking a statin.Although most patients with COPD in this national sample were symptomatic and many had been hospitalized for COPD, COPD self-knowledge was low and COPD was undertreated compared with generally asymptomatic, less morbid conditions such as hypertension.

The impact of blood eosinophilia in chronic obstructive pulmonary disease (COPD) remains controversial.To evaluate the prevalence and stability of a high level of blood eosinophils (>= 300 cells.mu L-1) and its relationship to outcomes, we determined blood eosinophils at baseline and over 2 years in 424 COPD patients (forced expiratory volume in 1 s (FEV1) 60% predicted) and 67 smokers without COPD from the CHAIN cohort, and in 308 COPD patients (FEV1 60% predicted) in the BODE cohort. We related eosinophil levels to exacerbations and survival using Cox hazard analysis.In COPD patients, 15.8% in the CHAIN cohort and 12.3% in the BODE cohort had persistently elevated blood eosinophils at all three visits. A significant proportion (43.8%) of patients had counts that oscillated above and below the cut-off points, while the rest had persistent eosinophil levels = 300 cells.mu L-1) and its relationship to outcomes, we determined blood eosinophils at baseline and over 2 years in 424 COPD patients (forced expiratory volume in 1 s (FEV1) 60% predicted) and 67 smokers without COPD from the CHAIN cohort, and in 308 COPD patients (FEV1 60% predicted) in the BODE cohort. We related eosinophil levels to exacerbations and survival using Cox hazard analysis.In COPD patients, 15.8% in the CHAIN cohort and 12.3% in the BODE cohort had persistently elevated blood eosinophils at all three visits. A significant proportion (43.8%) of patients had counts that oscillated above and below the cut-off points, while the rest had persistent eosinophil levels = 300 cells.mu L-1 persisting over 2 years was not a risk factor for COPD exacerbations. High eosinophil count was associated with better survival.