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Carotid atherosclerosis in patients with untreated chronic obstructive pulmonary disease

Authors
Kim, S. J.Yoon, D. W.Lee, E. J.Hur, G. Y.Jung, K. H.Lee, S. Y.Lee, S. Y.Shin, C.Shim, J. J.In, K. H.Kang, K. H.Yoo, S. H.Kim, J. H.
Issue Date
9월-2011
Publisher
INT UNION AGAINST TUBERCULOSIS LUNG DISEASE (I U A T L D)
Keywords
cardiovascular diseases; COPD; C-reactive protein
Citation
INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE, v.15, no.9, pp.1265 - 1270
Indexed
SCIE
SCOPUS
Journal Title
INTERNATIONAL JOURNAL OF TUBERCULOSIS AND LUNG DISEASE
Volume
15
Number
9
Start Page
1265
End Page
1270
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/111680
DOI
10.5588/ijtld.10.0680
ISSN
1027-3719
Abstract
BACKGROUND: Chronic obstructive pulmonary disease (COPD) is associated with systemic inflammation. OBJECTIVE: To evaluate carotid artery intima-media thickness (IMT), high sensitivity C-reactive protein (hsCRP) and their correlation in newly diagnosed untreated patients with COPD. DESIGN: Post-bronchodilator spirometry, carotid artery IMT and blood tests were measured in patients with COPD (COPD group). Age, sex, body mass index, smoking status and smoking amount were compared with matched healthy subjects (non-COPD group). Participants taking medications and/or with a history of hypertension, diabetes mellitus, dyslipidaemia, COPD or cardiovascular disease were excluded. RESULTS: A total of 126 patients (COPD group 42, non-COPD group 84) were enrolled. The IMT and hsCRP of the COPD group were significantly higher than in the non-COPD group (P < 0.05). The decrease in the forced expiratory volume in 1 second/forced vital capacity (FEV(1)/FVC) ratio and FEV(1) was significantly correlated with an increase in the hsCRP and IMT (P < 0.05); there was no correlation between the IMT and hsCRP (P = 0.152). CONCLUSION: In newly diagnosed untreated patients with COPD, the carotid artery IMT and hsCRP were significantly higher than in healthy subjects. These findings suggest that systemic inflammation may play a potential role in preclinical atherosclerosis in COPD.
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