Clinics in chest medicine

Publisher: WB Saunders

Journal description

Current impact factor: 2.17

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.168
2012 Impact Factor 2.066
2011 Impact Factor 3.284
2010 Impact Factor 3.11
2009 Impact Factor 2.505
2008 Impact Factor 2.357
2007 Impact Factor 1.858
2006 Impact Factor 1.991
2005 Impact Factor 1.456
2004 Impact Factor 1.65
2003 Impact Factor 1.308
2002 Impact Factor 2.026
2001 Impact Factor 1.891
2000 Impact Factor 1.627
1999 Impact Factor 2.042
1998 Impact Factor 1.316
1997 Impact Factor 1.307
1996 Impact Factor 1.133
1995 Impact Factor 1.105
1994 Impact Factor 1.027
1993 Impact Factor 0.972
1992 Impact Factor 1.785

Impact factor over time

Impact factor

Additional details

5-year impact 2.19
Cited half-life 8.20
Immediacy index 0.41
Eigenfactor 0.00
Article influence 0.71
Other titles Clinics in chest medicine (Online), Clinics in chest medicine
ISSN 1557-8216
OCLC 40612530
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

WB Saunders

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Authors who are required to deposit in subject-based repositories may also use Sponsorship Option
    • 'WB Saunders' is an imprint of 'Elsevier'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Diffuse cystic and nodular lung diseases have characteristic imaging findings. The most common causes of cystic lung disease are lymphangioleiomyomatosis and Langerhans cell histiocytosis. Other less common cystic lung diseases include Birt-Hogg-Dube syndrome, lymphocytic interstitial pneumonitis, and light chain deposition disease. Computed tomography is used to differentiate cystic lung disease from emphysema, honeycombing, cavities, and bronchiectasis, which mimic cystic lung disease. Diffuse nodular lung disease are categorized as centrilobular, perilymphatic, and random types. In diffuse nodular lung disease, a specific diagnosis is achieved through a combination of history, physical examination, and imaging findings. Copyright © 2015 Elsevier Inc. All rights reserved.
    Clinics in chest medicine 04/2015; 36(2). DOI:10.1016/j.ccm.2015.02.011
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    ABSTRACT: High-resolution chest computed tomography (CT) is one of the most useful techniques available for imaging bronchiolitis because it shows highly specific direct and indirect imaging signs. The distribution and combination of these various signs can further classify bronchiolitis as either cellular/inflammatory or fibrotic/constrictive. Emphysema is characterized by destruction of the airspaces, and a brief discussion of imaging findings of this class of disease is also included. Typical CT findings include destruction of airspace, attenuated vasculatures, and hyperlucent as well as hyperinflated lungs. Copyright © 2015 Elsevier Inc. All rights reserved.
    Clinics in chest medicine 04/2015; 36(2). DOI:10.1016/j.ccm.2015.02.013
  • [Show abstract] [Hide abstract]
    ABSTRACT: Computed tomography (CT) is central to the detection and diagnosis of a wide variety of pulmonary, cardiovascular, and other diseases of the chest. Successful interpretation of thoracic CT requires both an appreciation of the spectrum of normal appearances of the chest and a systematic approach to the characterization of thoracic pathology. This article provides an introduction to basic CT techniques and protocols, a review of normal CT anatomy, and an overview of commonly encountered abnormalities. Copyright © 2015 Elsevier Inc. All rights reserved.
    Clinics in chest medicine 04/2015; 36(2). DOI:10.1016/j.ccm.2015.02.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Occupational and environmental lung disease remains a major cause of respiratory impairment worldwide. Despite regulations, increasing rates of coal worker's pneumoconiosis and progressive massive fibrosis are being reported in the United States. Dust exposures are occurring in new industries, for instance, silica in hydraulic fracking. Nonoccupational environmental lung disease contributes to major respiratory disease, asthma, and COPD. Knowledge of the imaging patterns of occupational and environmental lung disease is critical in diagnosing patients with occult exposures and managing patients with suspected or known exposures. Copyright © 2015 Elsevier Inc. All rights reserved.
    Clinics in chest medicine 04/2015; 36(2). DOI:10.1016/j.ccm.2015.02.008
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although primarily a lung disease, chronic obstructive pulmonary disease (COPD) is now recognized to have extrapulmonary effects on distal organs, the so-called systemic effects and comorbidities of COPD. Skeletal muscle dysfunction, nutritional abnormalities including weight loss, cardiovascular complications, metabolic complications, and osteoporosis, among others, are all well-recognized associations in COPD. These extrapulmonary effects add to the burden of mortality and morbidity in COPD and therefore should be actively looked for, assessed, and treated.
    Clinics in chest medicine 03/2014; 35(1):101-130. DOI:10.1016/j.ccm.2013.10.007
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    ABSTRACT: Alpha1-antitrypsin (AAT) deficiency was first described in 1963 together with its associations with severe early-onset basal panacinar emphysema. The genetic defects leading to deficiency have been elucidated and the pathophysiologic processes, clinical variation in phenotype, and the role of genetic modifiers have been recognized. Strategies to increase plasma (and hence tissue) concentrations of AAT have been developed. The only recognized specific therapeutic strategy is regular infusions of the purified plasma protein, and evidence confirms its efficacy in protecting the lung (at least partially). Early detection and modification of lifestyle remains crucial to the management of AAT deficiency.
    Clinics in chest medicine 03/2014; 35(1):39-50. DOI:10.1016/j.ccm.2013.10.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is currently defined as a common preventable and treatable disease that is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Exacerbations and comorbidities contribute to the overall severity in individual patients. The evolution of this definition and the diagnostic criteria currently in use are discussed. COPD is increasingly divided in subgroups or phenotypes based on specific features and association with prognosis or response to therapy, the most notable being the feature of frequent exacerbations.
    Clinics in chest medicine 03/2014; 35(1):1-6. DOI:10.1016/j.ccm.2013.10.010
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease is associated with chronic inflammation affecting predominantly lung parenchyma and peripheral airways and results in largely irreversible and progressive airflow limitation. This inflammation is characterized by increased numbers of alveolar macrophages, neutrophils, and T lymphocytes, which are recruited from the circulation. Oxidative stress plays a key role in driving this inflammation. The pulmonary inflammation may enhance the development and growth of lung cancer. The peripheral inflammation extends into the circulation, resulting in systemic inflammation with the same inflammatory proteins. Systemic inflammation may worsen comorbidities. Treatment of pulmonary inflammation may therefore have beneficial effects.
    Clinics in chest medicine 03/2014; 35(1):71-86. DOI:10.1016/j.ccm.2013.10.004
  • Clinics in chest medicine 03/2014; 35(1):xiii. DOI:10.1016/j.ccm.2013.11.003
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    ABSTRACT: Cigarette smoking is a major preventable cause of morbidity and mortality. It is the major risk factor for chronic obstructive pulmonary disease in the developed world. Smoking is a chronic relapsing disease. Optimal treatment includes nonpharmacologic support, together with pharmacotherapy. All clinicians should be comfortable with the use of nicotine replacement therapy, bupropion, and varenicline. Second-line therapies can be used by those familiar with their use. Effective use of these medications requires their integration into an effective management plan, which is likely to be a long-term undertaking, involving several cycles of remission and relapse.
    Clinics in chest medicine 03/2014; 35(1):165-176. DOI:10.1016/j.ccm.2013.11.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: This article represents a review of the current literature on the role of infection in the pathogenesis of chronic obstructive pulmonary disease (COPD), in stable disease, exacerbations, and pneumonia. It outlines the complex interactions between respiratory pathogens and host immune defenses that underlie the clinical manifestations of infection in COPD.
    Clinics in chest medicine 03/2014; 35(1):87-100. DOI:10.1016/j.ccm.2013.09.012
  • [Show abstract] [Hide abstract]
    ABSTRACT: Why only 20% of smokers develop clinically relevant chronic obstructive pulmonary disease (COPD) was a puzzle for many years. Now, epidemiologic studies point clearly toward a large heritable component. The combination of genome-wide association studies and candidate gene analysis is helping to identify those genetic variants responsible for an individual's susceptibility to developing COPD. In this review, the current data implicating specific loci and genes in the pathogenesis of COPD are examined.
    Clinics in chest medicine 03/2014; 35(1):29-38. DOI:10.1016/j.ccm.2013.10.008
  • [Show abstract] [Hide abstract]
    ABSTRACT: As parenchymal lung disease in chronic obstructive pulmonary disease becomes increasingly severe there is a diminishing prospect of drug therapies conferring clinically useful benefit. Lung volume reduction surgery is effective in patients with heterogenous upper zone emphysema and reduced exercise tolerance, and is probably underused. Rapid progress is being made in nonsurgical approaches to lung volume reduction, but use outside specialized centers cannot be recommended presently. Noninvasive ventilation given to patients with acute hypercapnic exacerbation of chronic obstructive pulmonary disease reduces mortality and morbidity, but the place of chronic non-invasive ventilatory support remains more controversial.
    Clinics in chest medicine 03/2014; 35(1):251-269. DOI:10.1016/j.ccm.2013.10.011
  • [Show abstract] [Hide abstract]
    ABSTRACT: Bronchodilators are central in the symptomatic treatment of chronic obstructive pulmonary disease (COPD), although there is often limited reversibility of airflow obstruction. Three classes of bronchodilators (β2-agonists, antimuscarinic agents, methylxanthines) are currently available, which can be used individually, or in combination with each other or inhaled corticosteroids. Novel classes of bronchodilators have proved difficult to develop. The muscarinic β2-agonist molecules approach likely provides the best opportunity to develop combinations that combine corticosteroids with dual-bronchodilator activities, and thus potentially achieve better efficacy than is apparent with the current combination products that dominate the treatment of COPD.
    Clinics in chest medicine 03/2014; 35(1):191-201. DOI:10.1016/j.ccm.2013.10.005
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    ABSTRACT: Current international guidelines recommend that roflumilast be added on to an inhaled corticosteroid/long-acting β2-adrenoceptor agonist (LABA) combination therapy in high-risk patients with severe, bronchitic chronic obstructive pulmonary disease who have frequent acute exacerbations. This article presents evidence that a glucocorticoid, LABA, and phosphodiesterase (PDE) 4 inhibitor in combination can interact in a complex manner to induce a panel of genes that could act collectively to suppress inflammation and improve lung function. The possibility that multivalent ligands may deliver superior efficacy is also being explored. Single molecules that inhibit PDE4 and activate β2-adrenoceptors at similar concentrations have been described.
    Clinics in chest medicine 03/2014; 35(1):203-217. DOI:10.1016/j.ccm.2013.09.007
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    ABSTRACT: Clinical trials with new drugs for chronic obstructive pulmonary disease (COPD) have been performed. Viruses exacerbate COPD and bacteria may play a part in severe COPD; therefore, antibiotic and antiviral approaches have a sound rationale. Antiinflammatory approaches have been studied. Advances in understanding the molecular basis of other processes have resulted in novel drugs to target reactive oxidant species, mucus, proteases, fibrosis, cachexia, and muscle wasting, and accelerated aging. Studies with monoclonal antibodies have been disappointing, highlighting the tendency for infections and malignancies during treatment. Promising future directions are lung regeneration with retinoids and stem cells.
    Clinics in chest medicine 03/2014; 35(1):219-239. DOI:10.1016/j.ccm.2013.10.003
  • [Show abstract] [Hide abstract]
    ABSTRACT: The development of chronic obstructive pulmonary disease (COPD) is multifactorial, and the risk factors include both genetic and environmental factors. Although tobacco smoking is an established risk factor for COPD, many other associated factors remain underappreciated or neglected. Upto 50% of cases of COPD can be attributed to nonsmoking risk factors. This article describes the role of tobacco smoking and the various environmental risk factors associated with the development of COPD.
    Clinics in chest medicine 03/2014; 35(1):17-27. DOI:10.1016/j.ccm.2013.09.011
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) represents one of the main causes of morbidity and mortality worldwide. According to the World Health Organization, approximately 3 million people in the world die as a consequence of COPD every year. Tobacco use remains the main factor associated with development of disease in the industrialized world, but other risk factors are important and preventable causes of COPD, particularly in the developing world. The purpose of this review is to summarize the literature on the subject and to provide an update of the most recent advances in the field.
    Clinics in chest medicine 03/2014; 35(1):7-16. DOI:10.1016/j.ccm.2013.10.002