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Bronchodilator Use and the Risk of Arrhythmia in COPD: Part 2: Reassessment in the Larger Quebec Cohort.

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Bronchodilator Use and the Risk of Arrhythmia in COPD: Part 2: Reassessment in the Larger Quebec Cohort.

Chest. 2012 Aug 1;142(2):305-11

Authors: Wilchesky M, Ernst P, Brophy JM, Platt RW, Suissa S

Abstract
BACKGROUND: A previous study suggested a potential increased risk of cardiac arrhythmia with new use of long-acting β-agonists and ipratropium bromide in patients with COPD, although conclusions were limited by the small cohort size.
METHODS: We reassessed this association in a larger cohort formed from the health-care databases of the province of Quebec, Canada. We identified a cohort of patients with COPD aged ≥ 67 years who began treatment between 1990 and 1999 and followed them until December 2003. A nested case-control approach matched each subject who developed severe arrhythmia during follow-up with 20 control subjects from the cohort on age, sex, and calendar time. The rate ratio (RR) of arrhythmia associated with new use of bronchodilators was estimated using conditional logistic regression, adjusting for COPD disease severity, cardiovascular disease, and other comorbidities.
RESULTS: The cohort included 76,661 patients with COPD, of whom 5,307 developed an arrhythmia (10.3 arrhythmias per 1,000 per year), 621 of which were fatal. The rate of cardiac arrhythmias was elevated with the new use of short-acting (RR, 1.27; 95% CI, 1.03-1.57) and long-acting (RR, 1.47; 95% CI, 1.01-2.15) β-agonists. The rate was slightly elevated, although not statistically significantly, with new use of ipratropium bromide (RR, 1.23; 95% CI, 0.95-1.57) and methylxanthines (RR, 1.28; 95% CI, 0.93-1.77). These effects waned with longer-term use.
CONCLUSIONS: New use of short- and long-acting β-agonists may slightly increase the risk of cardiac arrhythmia in patients with COPD. It remains unclear whether ipratropium bromide also increases this risk, despite the use of a larger study population.From the Donald Berman Maimonides Geriatric Centre (Dr Wilchesky), the Department of Medicine (Drs Ernst, Brophy, and Suissa), the Department of Epidemiology, Biostatistics and Occupational Health (Drs Brophy, Platt, and Suissa), and the Department of Pediatrics (Dr Platt), McGill University; and the Centre for Clinical Epidemiology (Drs Wilchesky, Ernst, and Suissa), Jewish General Hospital-Lady Davis Research Institute, Montreal, QC, Canada.Correspondence to: Samy Suissa, PhD, Centre for Clinical Epidemiology, Jewish General Hospital-Lady Davis Research Institute, 3755 Côte-Ste-Catherine H-461, Montréal, QC, H3T 1E2, Canada; e-mail: samy.suissa@mcgill.caAuthor contributions: Dr Suissa had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.Dr Wilchesky: contributed to the study design, data analysis and interpretation, and writing of the manuscript.Dr Ernst: contributed to the funding acquisition, study design, data interpretation, and writing of the manuscript.Dr Brophy: contributed to the study design, data interpretation, and writing of the manuscript.Dr Platt: contributed to the study design, data interpretation, and writing of the manuscript.Dr Suissa: contributed to the funding acquisition, study design, data interpretation, and writing of the manuscript.Financial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Ernst has received speaker fees and has attended advisory boards for AstraZeneca; Boehringer Ingelheim GmbH; GlaxoSmithKline plc; Merck & Co, Inc; Novartis AG; and Nycomed GmbH. Dr Suissa has received research grants from AstraZeneca, Boehringer Ingelheim GmbH, and GlaxoSmithKline plc and has participated in advisory board meetings and as speaker for AstraZeneca; Boehringer Ingelheim GmbH; Forest Laboratories, Inc; GlaxoSmithKline plc; Merck & Co, Inc; Novartis AG; Nycomed GmbH; and Pfizer, Inc. Drs Wilchesky, Brophy, and Platt have reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.Role of sponsors: The sponsors were not involved in the design and conduct of the study; the collection, management, analysis, and interpretation of the data; or the preparation, review, or approval of the manuscript.For editorial comment see page 271For related article see page 298Funding/Support: This study was funded by the Canadian Institutes for Health Research (CIHR) [Grant 94480]. Dr Wilchesky was the recipient of a CIHR Doctoral Research Award. Dr Suissa is the recipient of the James McGill Professorship award. Drs Brophy and Platt are Research Scholars of le Fonds de Recherche en Santé du Québec.Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.

PMID: 22871756 [PubMed - in process]

Pneumococcal pneumonia: mechanisms of infection and resolution.

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Pneumococcal pneumonia: mechanisms of infection and resolution.

Chest. 2012 Aug 1;142(2):482-91

Authors: Dockrell DH, Whyte MK, Mitchell TJ

Abstract
Vaccination and antimicrobial therapy remain the cornerstones of the management of pneumococcal pneumonia. Despite significant successes, the capacity of the pneumococcus to evolve in the face of the selective pressure of anticapsular immunity challenges immunization programs. Treatment focuses on antimicrobial therapy but ignores the central role of the dysregulated inflammatory response during pneumonia. Future therapeutic approaches need to build on the considerable recent advances in our understanding of the pathogenesis of pneumococcal pneumonia, including those from models of pneumonia. Enhancement of the essential components of the host response that prevents most colonized individuals from developing pneumonia and strategies to limit inappropriate inflammatory responses to lower respiratory tract infection are approaches that could be exploited to improve disease outcome. This review highlights recent discoveries relating to the microbial and host determinants of microbial clearance and regulation of the inflammatory response, which provide clues as to how this could be achieved in the future.From the Department of Infection and Immunity (Drs Dockrell and Whyte), University of Sheffield Medical School and Sheffield Teaching Hospitals, Sheffield; and the School of Immunity and Infection (Dr Mitchell), College of Medical and Dental Sciences, University of Birmingham, Birmingham, England.Correspondence to: David H. Dockrell, MD, Department of Infection and Immunity, The University of Sheffield Medical School, Beech Hill Road, Sheffield, S10 2RX, England; e-mail: d.h.dockrell@sheffield.ac.ukFinancial/nonfinancial disclosures: The authors have reported to CHEST the following conflicts of interest: Dr Whyte has received travel support for scientific meetings from Boehringer Ingelheim GmbH. She has received competitive external grant funding from a number of noncommercial sources, including the Medical Research Council (MRC) and the Wellcome Trust. Dr Dockrell has received grant support from the Wellcome trust and the MRC. He has received financial support to attend clinical meetings from ViiV Healthcare, Gilead, Bristol-Myers Squibb, Merck Sharp & Dohme Corp and Janssen-Cilag Pty Limited, and has received grant support from Novartis AG. Dr Mitchell has reported that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.Role of sponsors: The sponsors had no role in the design of the study, the collection and analysis of the data, or in the preparation of the manuscriptFunding/Support: This work is supported by a Wellcome Trust Senior Clinical Fellowship to Dr Dockrell (076945) and by Wellcome Trust and Medical Research Council (MRC) grants to Drs Dockrell, Whyte, and Mitchell. Drs Dockrell and Whyte are also funded as part of the MRC-Association of the British Pharmaceutical Industry COPD consortium and the TJM laboratory by the European Community's Seventh Framework Programme under Grant Agreement No. HEALTH-F3-2009-223111 (CAREPNEUMO).This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Information for commercial entities is available online.

PMID: 22871758 [PubMed - in process]

Bronchial and nonbronchial systemic artery embolization in managing haemoptysis: 31 years of experience.

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The authors report on 31 years of experience with bronchial (BAE) and/or nonbronchial (NBAE) systemic artery embolisation for managing haemoptysis.

MATERIALS AND METHODS: A total of 534 patients who underwent bronchial artery angiography for haemoptysis between 1979 and 2010 were retrospectively evaluated. Of these patients, 477 (89%) had active bleeding and underwent BAE and/or NBAE (295 males and 182 females, aged between 12 and 71 years). Embolisation techniques, materials, major and minor complications and relapses were recorded.

RESULTS: Complete resolution of haemoptysis was achieved within 24 h in 458/477 (96%) cases and within 48 h in 2% of cases. The aetiology of haemoptysis was as follows: cystic fibrosis (23%), bronchiectasis (13%), tuberculosis sequelae (8%), chronic obstructive pulmonary disease (COPD) (6%) and no apparent cause (21%). Major complications were recorded in 3/477 (0.6%): stroke (n=1), transient ischaemic attack (TIA) (n=1) and transient quadriplegia (n=1). Minor complications were recorded in 143/477 (30%): chest pain 86/143 (60%) and dysphagia 29/143 (20%). During a mean follow-up period of 14 (8-36) months, haemoptysis recurrence was observed in 42/110 cases (38%) of cystic fibrosis and in 77/367 cases of other diseases (21%).

CONCLUSIONS: BAE and NBAE are effective and safe for acute treatment of haemoptysis, with low recurrence and complication rates. Interventional radiologist experience is crucial to the successful haemoptysis control and preventing complications.

Effects of Active Smoking on Airway and Systemic Inflammation Profiles in Patients with Chronic Obstructive Pulmonary Disease.

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The markers that characterize local and systemic inflammation in chronic obstructive pulmonary disease (COPD) remain unclear, as do their correlations with smoking status and presence of disease. The aim of this study was to assess markers of inflammation in the peripheral blood and airways of current smokers without COPD, of current smokers with COPD and of ex-smokers with COPD.

METHODS:: In this study, 17 current smokers with COPD (mean age: 58.2 ± 9.6 years; mean forced expiratory volume in 1 second [FEV1]: 56.1 ± 15.9%), 35 ex-smokers with COPD (mean age: 66.3 ± 7.3 years; mean FEV1: 47.9 ± 17.2%) and 20 current smokers without COPD (mean age: 49.1 ± 6.2 years; mean FEV1: 106.5 ± 15.8%) were evaluated. Spirometry findings, body composition and serum/induced sputum concentrations of tumor necrosis factor α (TNF-α), interleukin (IL)-6, IL-8 and IL-10, together with serum C-reactive protein (CRP) levels, were assessed.

RESULTS:: Serum TNF-α concentration was higher in all current smokers than in ex-smokers with COPD. In current smokers without COPD, serum CRP level was lower than in ex-smokers with COPD and significantly lower than in current smokers with COPD. Sputum TNF-α concentration was higher in current and ex-smokers with COPD than in current smokers without COPD. Multiple regression analyses showed that serum TNF-α was associated with active smoking, and serum CRP and sputum TNF-α were associated with COPD diagnosis.

CONCLUSIONS:: Smoking is associated with higher systemic inflammation in patients with COPD. Current findings also support the hypothesis that smoking and COPD have different effects on the regulation of airway and systemic inflammatory processes.

Epigenetics in asthma and COPD.

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Epigenetic mechanisms are likely to play a role in many complex diseases, the extent of which we only beginning to understand. COPD and asthma are two respiratory diseases subject to strong environmental influences depending on underlying genetic susceptibility. Epigenetic mechanisms such as DNA methylation, histone modification and microRNA may be involved in these processes by modulating environmental effects to influence disease development. Given their demonstrated modifiable nature, epigenetic mechanisms may open new possibilities for therapeutic intervention.

Here we give an overview of recent developments in the field of respiratory epigenetics in relation to asthma and COPD in the context of our current understanding of mechanisms leading to such diseases.

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