Vascular dysfunction in chronic obstructive pulmonary disease.
BACKGROUND
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.


OBJECTIVE
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.


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.
Maclay
John D
JD
Centre for Inflammation Research, Edinburgh University, Edinburgh, United Kingdom.
McAllister
David A
DA
Mills
Nicholas L
NL
Paterson
Finny P
FP
Ludlam
Christopher A
CA
Drost
Ellen M
EM
Newby
David E
DE
Macnee
William
W
D000368:Aged; D001158:Arteries / Q000503:physiopathology; D001783:Blood Flow Velocity / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D016022:Case-Control Studies; D004727:Endothelium / Q000502:physiology; D005342:Fibrinolysis / Q000502:physiology; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010991:Plethysmography; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology*; D011673:Pulsatile Flow / Q000502:physiology; D012307:Risk Factors; D012907:Smoking; D010959:Tissue Plasminogen Activator / Q000097:blood; D014655:Vascular Resistance / Q000502:physiology
D010959:Tissue Plasminogen Activator