title: Effect of Omega-3 fatty acid supplementation on markers of platelet and endothelial function in patients with peripheral arterial disease.
abstract: OBJECTIVE
  Omega-3 fatty acids have been shown to reduce platelet and endothelial activation in patients with or at risk of cardiac disease. We aimed to determine if Omega-3 fatty acid supplementation in addition to best medical therapy can reduce the increased platelet and endothelial activity that is present in patients with intermittent claudication.
  
  
  METHODS
  One hundred and fifty patients who were receiving aspirin and statin therapy were recruited into a randomised cross-over double blind study involving 6 week supplementation with OMACOR fish oil (850-882 mg eicosapentaenoic and docosahexaenoic acid) versus placebo. A 12 week washout period occurred between treatments. Patients with diabetes were excluded. For each outcome a random effects model was fitted in which treatment and period were fixed effects and patients were random effects.
  
  
  RESULTS
  Omega-3 supplementation had no effect on the primary outcome measure von Willebrand factor. Similarly Omega-3 supplementation resulted in no change in unstimulated or stimulated P-selectin expression and fibrinogen binding, or platelet aggregation (Ultegra point of care). Pulse wave velocity was also unchanged. High-sensitivity C-reactive protein, s-ICAM and IL-6 were also unchanged.
  
  
  CONCLUSIONS
  Supplementation with Omega-3 fatty acids had no affect on platelet and endothelial activation or markers of inflammation in patients with peripheral arterial disease.
authors.affiliation: Vascular Unit, Aberdeen Royal Infirmary, United Kingdom.
authors.forename: Ian
authors.initials: I
authors.lastname: Mackay
authors.forename: Isobel
authors.initials: I
authors.lastname: Ford
authors.forename: Frank
authors.initials: F
authors.lastname: Thies
authors.forename: Shona
authors.initials: S
authors.lastname: Fielding
authors.forename: Paul
authors.initials: P
authors.lastname: Bachoo
authors.forename: Julie
authors.initials: J
authors.lastname: Brittenden
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism; D018592:Cross-Over Studies; D019587:Dietary Supplements / Q000009:adverse effects; D004281:Docosahexaenoic Acids / Q000009:adverse effects / Q000627:therapeutic use*; D004311:Double-Blind Method; D004338:Drug Combinations; D004359:Drug Therapy, Combination; D015118:Eicosapentaenoic Acid / Q000009:adverse effects / Q000627:therapeutic use*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D018836:Inflammation Mediators / Q000097:blood; D007383:Intermittent Claudication / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D058729:Peripheral Arterial Disease / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D010919:Placebos; D015539:Platelet Activation / Q000187:drug effects*; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011673:Pulsatile Flow / Q000187:drug effects; D012606:Scotland; D013997:Time Factors; D016896:Treatment Outcome; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; D004338:Drug Combinations; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D019007:P-Selectin; D010919:Placebos; D010975:Platelet Aggregation Inhibitors; C546937:SELP protein, human; D014841:von Willebrand Factor; D004281:Docosahexaenoic Acids; D005340:Fibrinogen; D015118:Eicosapentaenoic Acid; C405603:Omacor