| Vascular dysfunction in chronic obstructive pulmonary disease. | |
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MedLine Citation:
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PMID: 19542477 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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RATIONALE: Cardiovascular disease is a major cause of morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), which may in part be attributable to abnormalities of systemic vascular function. It is unclear whether such associations relate to the presence of COPD or prior smoking habit. OBJECTIVES: To undertake a comprehensive assessment of vascular function in patients with COPD and healthy control subjects matched for smoking history. METHODS: Eighteen men with COPD were compared with 17 healthy male control subjects matched for age and lifetime cigarette smoke exposure. Participants were free from clinically evident cardiovascular disease. MEASUREMENTS AND MAIN RESULTS: Pulse wave velocity and pulse wave analysis were measured via applanation tonometry at carotid, radial, and femoral arteries. Blood flow was measured in both forearms using venous occlusion plethysmography during intrabrachial infusion of endothelium-dependent vasodilators (bradykinin, 100-1,000 pmol/min; acetylcholine, 5-20 microg/min) and endothelium-independent vasodilators (sodium nitroprusside, 2-8 microg/min; verapamil, 10-100 microg/min). Tissue plasminogen activator (t-PA) was measured in venous plasma before and during bradykinin infusions. Patients with COPD have greater arterial stiffness (pulse wave velocity, 11 +/- 2 vs. 9 +/- 2 m/s; P = 0.003; augmentation index, 27 +/- 10 vs. 21 +/- 6%; P = 0.028), but there were no differences in endothelium-dependent and -independent vasomotor function or bradykinin-induced endothelial t-PA release (P > 0.05 for all). CONCLUSIONS: COPD is associated with increased arterial stiffness independent of cigarette smoke exposure. However, this abnormality is not explained by systemic endothelial dysfunction. Increased arterial stiffness may represent the mechanistic link between COPD and the increased risk for cardiovascular disease associated with this condition. |
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Authors:
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John D Maclay; David A McAllister; Nicholas L Mills; Finny P Paterson; Christopher A Ludlam; Ellen M Drost; David E Newby; William Macnee |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-06-19 |
Journal Detail:
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Title: American journal of respiratory and critical care medicine Volume: 180 ISSN: 1535-4970 ISO Abbreviation: Am. J. Respir. Crit. Care Med. Publication Date: 2009 Sep |
Date Detail:
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Created Date: 2009-09-07 Completed Date: 2009-10-01 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9421642 Medline TA: Am J Respir Crit Care Med Country: United States |
Other Details:
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Languages: eng Pagination: 513-20 Citation Subset: AIM; IM |
Affiliation:
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Centre for Inflammation Research, Edinburgh University, Edinburgh, United Kingdom. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aged Arteries / physiopathology Blood Flow Velocity / physiology* Cardiovascular Diseases / physiopathology* Case-Control Studies Endothelium / physiology Fibrinolysis / physiology Forced Expiratory Volume / physiology Humans Male Middle Aged Plethysmography Pulmonary Disease, Chronic Obstructive / physiopathology* Pulsatile Flow / physiology Risk Factors Smoking Tissue Plasminogen Activator / blood Vascular Resistance / physiology |
| Grant Support | |
ID/Acronym/Agency:
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//Chief Scientist Office |
| Chemical | |
Reg. No./Substance:
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EC 3.4.21.68/Tissue Plasminogen Activator |
| Comments/Corrections | |
Comment In:
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Am J Respir Crit Care Med. 2009 Sep 15;180(6):487-8
[PMID:
19734349
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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