title: Vascular dysfunction in chronic obstructive pulmonary disease.
abstract: 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.
authors: Centre for Inflammation Research, Edinburgh University, Edinburgh, United Kingdom.
authors: John D
authors: JD
authors: Maclay
authors: David A
authors: DA
authors: McAllister
authors: Nicholas L
authors: NL
authors: Mills
authors: Finny P
authors: FP
authors: Paterson
authors: Christopher A
authors: CA
authors: Ludlam
authors: Ellen M
authors: EM
authors: Drost
authors: David E
authors: DE
authors: Newby
authors: William
authors: W
authors: Macnee
mesh_terms: 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
chemical_list: D010959:Tissue Plasminogen Activator