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Vascular Dysfunction in Chronic Obstructive Pulmonary Disease

¹ Centre for Inflammation Research, and ² Centre for Cardiovascular Science, Edinburgh University, Edinburgh, United Kingdom; and ³ Wellcome Trust Clinical Research Facility, and ⁴ Department of Haematology, Royal Infirmary of Edinburgh, Edinburgh, United Kingdom

Correspondence and requests for reprints should be addressed to Professor William MacNee, M.D., F.R.C.P., ELEGI Colt Laboratory, Queen's Medical Research Institute, The University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK. E-mail: w.macnee{at}ed.ac.uk

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 µg/min) and endothelium-independent vasodilators (sodium nitroprusside, 2–8 µg/min; verapamil, 10–100 µg/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.

Key Words: pulmonary disease, chronic obstructive • cardiovascular diseases • arterial stiffness • endothelial function

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Previous studies have shown that chronic obstructive pulmonary disease (COPD) is associated with increased arterial stiffness and suggested that this is caused by systemic endothelial impairment, which may explain the excess cardiovascular risk in COPD. What This Study Adds to the Field Men with COPD do not have impairment of endothelial vasomotor or fibrinolytic function in comparison with age-matched control subjects with similar cigarette smoke exposure. Therefore, increased arterial stiffness in COPD is unlikely to be caused by abnormal endothelial function. Abnormalities of the vascular extracellular matrix may be an independent systemic feature of COPD.

 

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