Chronic Obstructive Pulmonary Disease Morbidity Research Articles

Osteoporosis in chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a lifestyle-related chronic inflammatory pulmonary disease associated with significant morbidity and mortality worldwide. COPD is associated with various comorbidities found in all stages of COPD. The comorbidities have significant impact in terms of morbidity, mortality, and economic burden in COPD. Management of comorbidities should be incorporated into the comprehensive management of COPD as this will also have an effect on the outcome in COPD patients. Various comorbidities reported in COPD include cardiovascular disease, skeletal muscle dysfunction, anemia, metabolic syndrome, and osteoporosis. Osteoporosis is a significant comorbidity in COPD patients. Various risk factors, such as tobacco smoking, systemic inflammation, vitamin D deficiency, and the use of oral or inhaled corticosteroids (ICSs) are responsible for its occurrence in patients with COPD. This review will focus on the prevalence, pathogenesis, risk factors, diagnosis, and treatment of osteoporosis in COPD patients.

Subclinical atherosclerotic vascular disease in chronic obstructive pulmonary disease: Prospective hospital-based case control study.

Introduction:Chronic obstructive pulmonary disease (COPD) is an important non-communicable disease worldwide with a rising global incidence. COPD is associated with multiple co-morbidities. Patients with COPD are at increased risk of atherosclerosis and other cardiovascular events. Cardiovascular diseases are an important cause of morbidity and mortality in COPD. The present case-control study was designed to assess the relationship between sub-clinical atherosclerotic vascular diseases with COPD.Methods:It was a prospective case-control blinded observational study. There were 142 COPD patients and 124 age-and sex-matched controls without COPD and cardiovascular diseases. Frequency of sub-clinical atherosclerosis was assessed by the carotid B-mode duplex ultrasonography assessment of carotid wall intima medial thickness (IMT). Plaque was defined as IMT of more than 1.2 mm.Results:Prevalence of carotid plaqing was significantly higher amongst patients of COPD (38.7%) compared to controls (13.7%, odds ratio 3.9, P < 0.0001). Multinomial logistic regression analysis revealed COPD as an independent predictor of carotid plaqing (r = 0.85, P < 0.023).Conclusion:The frequency of carotid plaqing is high in COPD patients. Carotid plaqing may be due to shared risk factors or the presence of low-grade systemic inflammation. Presence of increased CIMT and carotid plaqing in COPD patients identifies early atherosclerotic changes and future cardiovascular risk. Hence screening of CIMT should be a part of cardiovascular assessment in patients with COPD.

Cardiac Sympathetic Dominance and Systemic Inflammation in COPD

Cardiac autonomic dysfunction is an independent determinant of adverse outcomes in many diseases. The available literature on the relative changes in sympathetic and parasympathetic components in chronic obstructive pulmonary disease (COPD) is equivocal, the clinical and physiological correlates are poorly defined and association with markers of systemic inflammation has not been explored. As both autonomic dysfunction and systemic inflammation may contribute to cardiovascular morbidity in COPD, we hypothesized that these may be associated. Sixty three stable patients of COPD and 36 controls underwent spirometry, estimation of diffusion capacity, six-minute walk test and measurements of serum interleukin-6 (IL-6) and high-sensitivity C-Reactive protein. Cardiac autonomic activity was evaluated by standard five-minute heart rate variability (HRV) recordings to obtain time- and frequency-domain indices and the averaged heart rate. We observed that HRV indices of overall autonomic modulation, the standard deviation of time intervals between consecutive normal beats (SDNN) and total power, were greater in patients with higher levels of indices of both parasympathetic and sympathetic activity. The heart rate was significantly higher in patients indicating an overall sympathetic dominance and was inversely correlated with diffusion capacity. Serum IL-6 was inversely correlated with pNN50, an index of parasympathetic activity, and positively with LF/HF ratio, a measure of sympathetic: parasympathetic balance. None of the HRV indices was significantly correlated with physiological measures of severity. It was concluded that patients with COPD have increased cardiac autonomic modulation with sympathetic dominance. This is associated with decreased lung diffusion capacity and systemic inflammation.

Influence of sex on chronic obstructive pulmonary disease risk and treatment outcomes.

Chronic obstructive pulmonary disease (COPD), one of the most common chronic diseases and a leading cause of death, has historically been considered a disease of men. However, there has been a rapid increase in the prevalence, morbidity, and mortality of COPD in women over the last two decades. This has largely been attributed to historical increases in tobacco consumption among women. But the influence of sex on COPD is complex and involves several other factors, including differential susceptibility to the effects of tobacco, anatomic, hormonal, and behavioral differences, and differential response to therapy. Interestingly, nonsmokers with COPD are more likely to be women. In addition, women with COPD are more likely to have a chronic bronchitis phenotype, suffer from less cardiovascular comorbidity, have more concomitant depression and osteoporosis, and have a better outcome with acute exacerbations. Women historically have had lower mortality with COPD, but this is changing as well. There are also differences in how men and women respond to different therapies. Despite the changing face of COPD, care providers continue to harbor a sex bias, leading to underdiagnosis and delayed diagnosis of COPD in women. In this review, we present the current knowledge on the influence of sex on COPD risk factors, epidemiology, diagnosis, comorbidities, treatment, and outcomes, and how this knowledge may be applied to improve clinical practices and advance research.

Study of the level of sputum matrix metalloproteinase-9 (MMP-9) and tissue inhibitor metalloproteinase-1 (TIMP-1) in COPD patients

BackgroundChronic obstructive pulmonary disease (COPD) is a major cause of respiratory morbidity and mortality worldwide. One of the main hypotheses concerning the pathogenesis of emphysema, a key cause of morbidity and mortality in COPD, is the protease antiprotease imbalance. Irreversible airflow obstruction in Chronic Obstructive Pulmonary Disease (COPD) is thought to result from airway remodeling associated with aberrant inflammation.This study examined changes in sputum as regards MMP-9, TIMP-1 and levels of inflammatory cells in COPD patients compared with sputum of healthy smokers and non smokers. MethodsForty patients were included in this study. FEV1 before and after salbutamol inhalation, MMP-9, TIMP-1 and inflammatory cell count in the sputum of COPD patients, healthy smokers and non- smokers were investigated. ResultsMMP-9 was significantly increased in both COPD patients (194.4±100.6), and healthy smokers (104.5±42.1) compared with healthy non smokers (34.5±36.1). TIMP-1 was increased more in healthy non-smokers (192.7±37.7) than COPD patients (115±55.5) and healthy smokers (145.3±35.1). MMP-9/TIMP-1 was high in COPD patients (1.7±0.9) and healthy smokers (0.7±0.3) compared with healthy non smokers (0.2±0.2). Mean sputum total leucocytic count (TLC) was highly statistically significantly different between the three groups. COPD group showed the highest means value while non smokers group showed the lowest one. ConclusionsCOPD is characterized by an imbalance between MMP-9 and TIMP-1 which may play an important role in the pathogenesis of tissue remodeling and airway obstruction.

Real‑life cost and cost‑effectiveness for tiotropium 18 μg od monotherapy in moderate and severe COPD patients: a 48‑month survey

BACKGROUND: Tiotropium monotherapy enables a significant minimization of morbidity in COPD. OBJECTIVE: to evaluate and compare cost and cost‑effectiveness of tiotropium monotherapy administrated for 24 months (18 μg od) in mild‑to‑moderate and severe chronic obstructive pulmonary disease (COPD). METHODS: Clinical outcomes (days in hospital; visits in general ward; cycles of systemic steroids; cycles of antibiotics and maintenance therapy drugs) were evaluated in two groups of patients corresponding to predicted FEV1 baseline values ≤ 50% (A) and &gt; 50% (B) from the Italian NHS perspective. In order to perform cost‑effectiveness analysis, FEV1 value, available for each patient, was converted in SGRQ score using a published multivariate linear model. Utilities were then obtained through the Ståhl equation. RESULTS: The comparison between 24 months of standard therapy and subsequent 24‑month period of tiotropium monotherapy showed that hospitalization cost, which represents the driving treatment cost, drops from 77% to 69% (A) and from 67% to 33% (B) of the total cost. Differently, maintenance therapy cost increased but the amount was more than offset by the savings accruing from the shortening of hospitalization. Furthermore, cost‑effectiveness results revealed a mean savings of about 216 € (A) and 961 € (B) other than a mean gain of 0.07 QALY (A) and 0.02 QALY (B). Dominance of tiotropium (calculated only within patients completing treatment course) revealed that in almost 29% (A) and 36% (B) of subjects tiotropium strategy is dominant while only in 2% (A) and 7% (B) of cases is associated to costs increment and worsening on quality of life. The dominance was systematic in severe COPD. Statistical analyses confirm such trend. CONCLUSIONS: Results of the present study suggest that tiotropium used as unique treatment in COPD systematically consents significant costs savings together with positive effects on evaluated quality. These effects prove proportional to COPD severity.

Relationship between COPD and lower socioeconomic status in farmers from south-eastern Poland (Lublin region)

Lower socioeconomic status is considered to be an independent risk factor of chronic conditions, such as chronic obstructive pulmonary disease (COPD). COPD, one of the major public health problems worldwide, is a chronic inflammatory lung disease of a multifactorial background. COPD morbidity in rural areas has been higher than in urban settings, as apart from the major causative factor, tobacco smoking, the burden of this disease in rural environments is also connected to additional occupational factors (organic dusts). The management of chronic diseases seems to be particularly difficult in rural areas. The aim of the study was to analyze the socioeconomic status of farmers suffering from COPD in comparison to healthy farmers. Thirty farmers with COPD and 34 healthy farmers from the Lublin region (Poland) were investigated based on the area of land they possessed (an indicator used in the health insurance system in Poland to classify farmers). The farmers from five rural communes were selected by general practitioners. Statistical analysis was performed by non-parametric Mann-Whitney U-test for the differences between area of farms. The p < 0.05 level was considered as significant. Area of land (median: 1.5 ha, 25th-75th percentile: 1.0-4.0) owned by farmers with COPD was significantly lower than area of farms belonging to healthy farmers (median: 7.0 ha, 25th-75th percentile: 3.0-10.0) (p < 0001, Mann-Whitney U-test). In rural areas individuals with COPD are characterized by significantly lower socioeconomic status than healthy persons. COPD is a major health problem, especially in rural areas, which may indicate that policy-makers should consider addressing equity in COPD management in rural areas.

Quantitative computed tomography measures of pectoralis muscle area and disease severity in chronic obstructive pulmonary disease. A cross-sectional study.

Muscle wasting in chronic obstructive pulmonary disease (COPD) is associated with a poor prognosis and is not readily assessed by measures of body mass index (BMI). BMI does not discriminate between relative proportions of adipose tissue and lean muscle and may be insensitive to early pathologic changes in body composition. Computed tomography (CT)-based assessments of the pectoralis muscles may provide insight into the clinical significance of skeletal muscles in smokers. We hypothesized that objective assessment of the pectoralis muscle area on chest CT scans provides information that is clinically relevant and independent of BMI. Data from the ECLIPSE (Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints) Study (n = 73) were used to assess the relationship between pectoralis muscle area and fat-free mass. We then used data in a subset (n = 966) of a larger cohort, the COPDGene (COPD Genetic Epidemiology) Study, to explore the relationship between pectoralis muscle area and COPD-related traits. We first investigated the correlation between pectoralis muscle area and fat-free mass, using data from a subset of participants in the ECLIPSE Study. We then further investigated pectoralis muscle area in COPDGene Study participants and found that higher pectoralis muscle area values were associated with greater height, male sex, and younger age. On subsequent clinical correlation, compared with BMI, pectoralis muscle area was more significantly associated with COPD-related traits, including spirometric measures, dyspnea, and 6-minute-walk distance (6MWD). For example, on average, each 10-cm(2) increase in pectoralis muscle area was associated with a 0.8-unit decrease in the BODE (Body mass index, Obstruction, Dyspnea, Exercise) index (95% confidence interval, -1.0 to -0.6; P < 0.001). Furthermore, statistically significant associations between pectoralis muscle area and COPD-related traits remained even after adjustment for BMI. CT-derived pectoralis muscle area provides relevant indices of COPD morbidity that may be more predictive of important COPD-related traits than BMI. However, the relationship with clinically relevant outcomes such as hospitalization and death requires additional investigation. Pectoralis muscle area is a convenient measure that can be collected in the clinical setting in addition to BMI.

Assessment of RV Function in Patients of (COPD).

Chronic Obstructive Pulmonary Disease (COPD) has considerable effects on cardiac functions primarily affecting the pulmonary vasculature and then right ventricle along with left ventricle. One of the important causes of increased morbidity and mortality associated with COPD is cor pulmonale. Echocardiography provides a rapid, non-invasive method to evaluate cardiac changes. Our aim was to evaluate RVfunction in COPD as per guidelines of American Society of Echocardiography with an aim to find a simpler way of predicting cardiac morbidity. A cross sectional observational study was conducted on 17 COPD patients attending Respiratory Medicine outdoor of R. G. KAR Medical College, Kolkata, India, through history taking, clinical examination, PFT (PFT) and Echocardiography. Statistical analysis was done by using Statistical Package for the Social Sciences (SPSS) version-17. Fractional area change of RV (FAC-%) was positively correlated with Forced Expiratory Volume in One Second (FEV1) (r = 0.4879), FEV1/ Forced Vital Capacity (FVC) ratio (r = 0.5048) and Peak Expiratory Flow Rate (PEFR) (r = 0.5361). There was strong negative correlation of Systolic Pulmonary Artery Pressure (SPAP) with FEV1/FVC ratio (r = -0.5553) and PEFR (r = - 0.4604). Right Index of Myocardial Performance (RIMP) of right ventricle was negatively correlated with FEV1/FVC ratio (r = - 0.598), PEFR (r = - 0.619), Forced Expiratory Flow (FEF) 25-75 (r = -0.515). Tricuspid annular plane systolic excursion (TAPSE) did not show any association with PFT parameters though it showed strong positive correlation with RV wall thickness. This study substantiates that FAC% and RIMP can be vital prognostic factors for RV function apart from SPAP, TAPSE to define RV dysfunction and predict morbidity in COPD.

Association of OSA and Type 2 Diabetes Mellitus

Sleep disorders in chronic obstructive pulmonary disease (COPD) can occur in 60–70% of patients. They have adverse outcome in terms of both morbidity and mortality of COPD. The various sleep disorders seen in COPD are insomnia, restless leg syndrome (RLS), obstructive sleep apnea (OSA), nocturnal hypoventilation, and nocturnal oxygen desaturation (NOD). Of these disorders, insomnia and RLS can be diagnosed on history. OSA, sleep hypoventilation, and NODmay require type I polysomnography with/without transcutaneous or exhaled CO2 monitoring. Management consists of either conservative management or drug therapy for insomnia and RLS. If pharmacotherapy is required, ramelteon for insomnia and dopaminergic drug for RLS may be given. Treatment of OSA is continuous positive airway pressure, which relieves both OSA and COPD. Nocturnal hypoventilation usually requires oxygen along with noninvasive ventilator. Treatment of only NOD is controversial, but nocturnal oxygen may be given after ruling out nocturnal hypoventilation. This review emphasises the need of sleep disorders evaluation for comprehensive management of COPD.

Management, morbidity and mortality of COPD during an 11-year period: an observational retrospective epidemiological register study in Sweden (PATHOS).

Background:Chronic obstructive pulmonary disease (COPD) is one of the most common causes of mortality and a major contributor to morbidity. Longitudinal clinical practice data yielding information on the characteristics of the disease, its natural course, and management are limited.Aims:To investigate and describe the COPD population from a nationwide perspective during an 11-year period (1999–2009) with a focus on management, co-morbidity, and mortality.Methods:This observational retrospective epidemiological study linked electronic medical records data from patients with COPD in primary care to mandatory Swedish hospital, drug and Cause of Death registry data from 1999 to 2009 (PATHOS).Results:A total of 21,361 patients with a COPD diagnosis were included (mean age 68.0 years, 53% females). The proportion of patients diagnosed in primary care increased from 59% in 1999 to 81% in 2009 and the mean age at diagnosis decreased from 73 to 66 years. The number of exacerbations decreased from 3.0 to 1.3 and COPD-related hospitalisations decreased from 1.02 to 0.20 per patient per year. Prescriptions of long-acting muscarinic antagonists and fixed combinations of inhaled corticosteroid/long-acting β2-agonist inhalers increased from 0% to 36% and 37%, respectively. The most common co-morbidities were hypertension, heart failure, ischaemic heart disease, and diabetes. Overall life expectancy was 8.3±6.8 years shorter in patients with COPD than in the general population, and all-cause mortality was 3.5 times higher.Conclusions:Management of COPD in Sweden has improved during the 11-year study period. Despite this, patients with COPD have a substantially reduced life expectancy than the general population.

Comorbidities of COPD.

By 2020, chronic obstructive pulmonary disease (COPD) will be the third cause of mortality. Extrapulmonary comorbidities influence the prognosis of patients with COPD. Tobacco smoking is a common risk factor for many comorbidities, including coronary heart disease, heart failure and lung cancer. Comorbidities such as pulmonary artery disease and malnutrition are directly caused by COPD, whereas others, such as systemic venous thromboembolism, anxiety, depression, osteoporosis, obesity, metabolic syndrome, diabetes, sleep disturbance and anaemia, have no evident physiopathological relationship with COPD. The common ground between most of these extrapulmonary manifestations is chronic systemic inflammation. All of these diseases potentiate the morbidity of COPD, leading to increased hospitalisations and healthcare costs. They can frequently cause death, independently of respiratory failure. Comorbidities make the management of COPD difficult and need to be evaluated and treated adequately.

Coronary artery disease concomitant with chronic obstructive pulmonary disease

Numerous epidemiologic studies have linked the presence of chronic obstructive pulmonary disease (COPD) to coronary artery disease (CAD). However, prevalence, pathological processes, clinical manifestations and therapy are still debated, as progress towards uncovering the link between these two disorders has been hindered by the complex nature of multimorbidity. Articles targeting CAD in patients with COPD were identified from the searches of MEDLINE and EMBASE databases in July 2013. Three authors reviewed available evidence, focusing on the latest development on disease prevalence, pathogenesis, clinical manifestations and therapeutic strategies. Both clinical trial and previous reviews have been included in this work. The most accredited hypothesis asserts that the main common risk factors, that is, cigarette smoke and ageing, elicit a chronic low-grade systemic inflammatory response, which affects both cardiovascular endothelial cells and airways/lung parenchyma. The development of CAD in patients with COPD potentiates the morbidity of COPD, leading to increased hospitalizations, mortality and health costs. Moreover, correct diagnosis is challenging and therapies are not clearly defined. Evidence from recently published articles highlights the importance of multimorbidity in patient management and future research. Moreover, many authors emphasize the importance of low-grade systemic inflammation as a common pathological mechanism and a possible future therapeutic target.

Roflumilast: a green signal is yet to come.

Chronic obstructive pulmonary disease (COPD) is a disabling disease and prevalent across nations with a huge economic impact. COPD is the third leading cause of death in the United States and will become the third leading cause of death worldwide by 2030. The increasing morbidity and mortality of COPD are a major threat to public health (1,2). Epidemiological evidence has shown that a substantial proportion of COPD mortality and morbidity is related to cardiovascular disease (3-5). Multiple studies have demonstrated that systemic inflammation and release of inflammatory mediators in COPD may potentially mediate its cardiovascular complications (6).

In-Home Air Pollution Is Linked to Respiratory Morbidity in Former Smokers with Chronic Obstructive Pulmonary Disease

The effect of indoor air pollutants on respiratory morbidity among patients with chronic obstructive pulmonary disease (COPD) in developed countries is uncertain. The first longitudinal study to investigate the independent effects of indoor particulate matter (PM) and nitrogen dioxide (NO(2)) concentrations on COPD morbidity in a periurban community. Former smokers with COPD were recruited and indoor air was monitored over a 1-week period in the participant's bedroom and main living area at baseline, 3 months, and 6 months. At each visit, participants completed spirometry and questionnaires assessing respiratory symptoms. Exacerbations were assessed by questionnaires administered at clinic visits and monthly telephone calls. Participants (n = 84) had moderate or severe COPD with a mean FEV1 of 48.6% predicted. The mean (± SD) indoor PM(2.5) and NO(2) concentrations were 11.4 ± 13.3 µg/m(3) and 10.8 ± 10.6 ppb in the bedroom, and 12.2 ± 12.2 µg/m(3) and 12.2 ± 11.8 ppb in the main living area. Increases in PM(2.5) concentrations in the main living area were associated with increases in respiratory symptoms, rescue medication use, and risk of severe COPD exacerbations. Increases in NO(2) concentrations in the main living area were independently associated with worse dyspnea. Increases in bedroom NO(2) concentrations were associated with increases in nocturnal symptoms and risk of severe COPD exacerbations. Indoor pollutant exposure, including PM(2.5) and NO(2), was associated with increased respiratory symptoms and risk of COPD exacerbation. Future investigations should include intervention studies that optimize indoor air quality as a novel therapeutic approach to improving COPD health outcomes.

Uso de beta-bloqueadores en pacientes con enfermedad pulmonar obstructiva crónica

La enfermedad pulmonar obstructiva crónica (EPOC) es un síndrome sistémico con múltiples fenotipos, en el que la enfermedad cardiovascular contribuye significativamente a la morbilidad y la mortalidad por su causa. El tabaquismo, la clase socioeconómica baja y un estilo de vida sedentario contribuyen a la historia natural de cada una de estas condiciones. La mayoría de las enfermedades cardiovasculares requieren tratamiento con beta-bloqueadores, que tradicionalmente se han contraindicado en los pacientes con EPOC; sin embargo el uso de estos fármacos se asocia a beneficios y mejores resultados en pacientes con enfermedades cardiovasculares, hipertensión, insuficiencia cardiaca, enfermedad coronaria y enfermedad pulmonar obstructiva crónica.

Enhanced cytotoxic function of natural killer and natural killer T‐like cells associated with decreased CD94 (Kp43) in the chronic obstructive pulmonary disease airway

Natural killer (NK) and natural killer T (NKT)-like cells represent a small but important proportion of effector lymphocytes that we have previously shown to be major sources of pro-inflammatory cytokines and granzymes. We hypothesized that these cells would be increased in the airway in chronic obstructive pulmonary disease (COPD), accompanied by reduced expression of the inhibitory receptor CD94 (Kp43) and increased expression of cytotoxic mediators granzyme B and perforin. We measured NK and NKT-like cells and their expression of CD94 in the blood of COPD patients (n = 71; 30 current and 41 ex-smokers), smokers (16) and healthy controls (25), and bronchoalveolar lavage fluid (BALF) from a cohort of subjects (19 controls, 12 smokers, 33 COPD). Activation was assessed by measuring CD69 in blood and the cytotoxic potential of NK cells by measuring granzymes A and B, and using a cytotoxicity assay in blood and BALF. In blood in COPD, there were no significant changes in the proportion of NK or NKT-like cells or expression of granzyme A or NK cytotoxic potential versus controls. There was, however, increased expression of granzyme B and decreased expression of CD94 by both cell types versus controls. The proportion of NK and NKT-like cells were increased in BALF in COPD, associated with increased NK cytotoxicity, increased expression of granzyme B and decreased expression of the inhibitory receptor CD94 by both cell types. Treatment strategies that target NK and NKT-like cells, their cytotoxicity and production of inflammatory mediators in the airway may improve COPD morbidity.

AB 94. Burden of COPD and SDB

Most of the information available on COPD prevalence, morbidity and mortality come from high-income countries. Even in those countries, accurate epidemiologic data on COPD are difficult and expensive to collect. It is known that almost 90% of COPD deaths occur in low and middle-income countries. WHO recognizes that chronic obstructive pulmonary disease (COPD) is of major public health importance. Unfortunately, there is no accurate epidemiological data for Serbia, but from everyday situation, we note the dominance of these patients in ambulatory and hospital work. By far the largest number of hospital admissions during the pulmonologist duty is exacerbations of COPD. We are preparing COPD register, which would improve our work. Untreated obstructive sleep apnea (OSA) and other similar sleep breathing disorders (SDB) increases healthcare utilization and are associated with reduced work performance and occupational injuries. The economic burden related to untreated OSA is substantial, accounting for billions of euros per year. Furthermore, therapy of OSA is an extremely cost-efficient use of healthcare resources, comparing highly favorably with other commonly funded medical therapies. Governments need to be better informed concerning the economic impact of untreated OSA and the benefits of therapy. In Serbia, health insurance covers the cost of polysomnography, but devices for non-invasive ventilation, which treat respiratory disorders during sleep, are not covered. The coexistence of SDB and COPD is associated with a definite increase in morbidity and a probable reduction in survival. Successful treatment of SDB through the application of positive pressure to the upper airway via nasal mask has led to the application of nocturnal positive-pressure ventilation as therapy for chronic respiratory failure due to multiple causes, including COPD. Clearly, more studies are required before valid conclusions can be made about the efficacy of noninvasive ventilation in patients with advanced COPD. In theory, noninvasive ventilation could have a role in the treatment of patients with the overlap syndrome by eliminating both upper-airway obstruction and nocturnal hypoventilation. We hope that some kind of regional cooperation will be implemented in the future, especially at projects linked with respiratory disorders during sleep.

Combined effect of lung function level and decline increases morbidity and mortality risks

Lung function level and decline are each predictive of morbidity and mortality. Evaluation of the combined effect of these measurements may help further identify high-risk groups. Using Copenhagen City Heart Study longitudinal spirometry data (n = 10,457), 16-21 year risks of chronic obstructive pulmonary disease (COPD) morbidity, COPD or coronary heart disease mortality, and all-cause mortality were estimated from combined effects of level and decline in forced expiratory volume in one second (FEV(1)). Risks were evaluated using Cox proportional hazards models for individuals grouped by combinations of baseline predicted FEV(1) and quartiles of slope. Hazard ratios (HR) and 95 % confidence intervals (CI) were estimated using stratified analysis by gender, smoking status, and baseline age (≤45 and >45). For COPD morbidity, quartiles of increasing FEV(1) decline increased HRs (95 % CI) for individuals with FEV(1) at or above the lower limit of normal (LLN) but below 100 % predicted, reaching 5.11 (2.58-10.13) for males, 11.63 (4.75-28.46) for females, and 3.09 (0.88-10.86) for never smokers in the quartile of steepest decline. Significant increasing trends were also observed for mortality and in individuals with a baseline age ≤45. Groups with 'normal' lung function (FEV(1) at or above the LLN) but excessive declines (fourth quartile of FEV(1) slope) had significantly increased mortality risks, including never smokers and individuals with a baseline age ≤45.

Future impact of various interventions on the burden of COPD in Canada: a dynamic population model.

BackgroundChronic obstructive pulmonary disease (COPD) is a growing economic burden worldwide. Smoking cessation is thought to be the single most effective way of reducing the economic burden of COPD. The impact of other strategies such as interventions that predict risk of disease, reduce progression of disease, or reduce exacerbations has not been systematically studied.ObjectivesWe estimated the economic and clinical burden of COPD over the next 25 years in Canada and the impact of three potential interventions (screening test for predisposition to COPD, new drugs to avoid progression into more severe disease stages, and predictive test for exacerbations) on COPD burden.MethodsUsing a dynamic simulation model, we projected the total burden of COPD (cost, morbidity, and mortality) from 2011 to 2035 using the population of Canada as a case study. The model stratified population based on sex, age, smoking status, respiratory symptoms, and their COPD stage. The cost and quality adjusted life years (QALYs) associated with each intervention were estimated.ResultsThe model indicates that annual societal cost of COPD is $4.52 billion (B) Canadian dollars in 2011 and will reach $3.61B ($7.33B undiscounted) per year in 2035. Over the next 25 years, COPD will be responsible for approximately $101.4B in societal costs ($147.5B undiscounted) and 12.9 million QALYs lost (19.0 million undiscounted). Our results suggested that the best strategy to reduce the financial burden of COPD is by reducing exacerbations. Smoking cessation, while it is the cornerstone of COPD prevention, has only a modest effect in attenuating the financial burden of COPD over the next 25 years in Western countries such as Canada.ConclusionOur data suggest that any intervention that can reduce the number of exacerbations has a substantial impact on morbidity and costs of COPD and should be considered in conjunction with the ongoing efforts to reduce smoking rates.