Document Detail


Airflow limitation in smokers is associated with subclinical atherosclerosis.
MedLine Citation:
PMID:  18931335     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
RATIONALE: Chronic obstructive pulmonary disease (COPD) is associated with increased morbidity and mortality from cardiovascular disease. Although a close association between COPD and atherosclerosis has been speculated, such scientific information is limited. OBJECTIVES: To evaluate subclinical atherosclerosis in smokers with airflow limitation. METHODS: The subjects of this study were healthy middle-aged men. Smokers with airflow limitation (n = 61) and age-matched control smokers (n = 122) and control never-smokers (n = 122) without airflow limitation were included in the present study. Subjects with diabetes, acute infection, and respiratory disease other than COPD were excluded beforehand. All subjects underwent chest radiogram, spirometry, blood sampling, and carotid ultrasonography. We determined carotid intima-media thickness and focal atheromatous plaque as indicators of subclinical atherosclerosis. MEASUREMENTS AND MAIN RESULTS: Mean carotid intima-media thickness was greater in smokers with airflow limitation than in control smokers (P < 0.01) and control never-smokers (P < 0.005). Focal carotid plaque was significantly more prevalent in smokers with airflow limitation than in control never-smokers (P < 0.005). Multivariate analyses showed significant associations between thickened intima-media thickness and decreased percent predicted FEV(1) (P = 0.001) and between plaque and log(10) C-reactive protein (P = 0.013) independent of age, pack-years of smoking, body mass index, peripheral mean arterial pressure, heart rate, glucose, and low-density lipoprotein cholesterol. CONCLUSIONS: Smokers with airflow limitation had exaggerated subclinical atherosclerosis. This study suggests that middle-aged men who are susceptible to COPD may also be susceptible to vascular atherosclerosis by smoking, and atherosclerotic change starts early in the disease process of COPD.
Authors:
Hiroshi Iwamoto; Akihito Yokoyama; Yoshihiro Kitahara; Nobuhisa Ishikawa; Yoshinori Haruta; Kiminori Yamane; Noboru Hattori; Hitoshi Hara; Nobuoki Kohno
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-10-17
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  179     ISSN:  1535-4970     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2008-12-22     Completed Date:  2009-02-03     Revised Date:  2009-06-18    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  35-40     Citation Subset:  AIM; IM    
Affiliation:
Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
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MeSH Terms
Descriptor/Qualifier:
Carotid Arteries / ultrasonography
Carotid Artery Diseases / epidemiology*,  physiopathology
Case-Control Studies
Disease Susceptibility / physiopathology
Humans
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive / epidemiology*,  physiopathology*
Smoking / epidemiology*,  physiopathology*
Comments/Corrections
Comment In:
Am J Respir Crit Care Med. 2009 Jul 1;180(1):103; author reply 103-4   [PMID:  19535670 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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