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Effect of ω-3 fatty acid supplementation on endothelial function, endogenous fibrinolysis and platelet activation in male cigarette smokers
  1. Jehangir N Din1,
  2. Rachel M Archer1,
  3. Scott A Harding2,
  4. Jaydeep Sarma3,
  5. Karin Lyall1,
  6. Andrew D Flapan4,
  7. David E Newby1
  1. 1Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, UK
  2. 2Department of Cardiology, Wellington Hospital, Wellington, New Zealand
  3. 3North West Heart Centre, Wythenshawe Hospital, Manchester, UK
  4. 4Edinburgh Heart Centre, Royal Infirmary of Edinburgh, Edinburgh, UK
  1. Correspondence to Dr Jehangir N Din, Centre for Cardiovascular Sciences, University of Edinburgh, The Chancellor's Building, 49 Little France Crescent, Edinburgh EH16 4SB, UK; jehangirdin{at}


Objective The effects of ω-3 fatty acids on endothelial function, fibrinolysis and platelet function are uncertain. We investigated the effects of ω-3 fatty acid supplementation on endothelial vasomotor function, endogenous fibrinolysis, and platelet and monocyte activation in healthy cigarette smokers; a group at increased risk of myocardial infarction.

Design, setting, participants Twenty cigarette smokers were recruited into a randomised, double-blind, placebo-controlled, crossover trial of ω-3 fatty acid supplementation.

Intervention ω-3 fatty acid supplements (2 g/day) or placebo for a 6-week period.

Main outcome measures Peripheral blood was taken for analysis of platelet and monocyte activation, and forearm blood flow (FBF) was assessed in a subset of 12 smokers during intrabrachial infusions of acetylcholine, substance P and sodium nitroprusside. Stimulated plasma tissue plasminogen activator (t-PA) concentrations were measured during substance P infusion.

Results All vasodilators caused dose-dependent increases in FBF (p<0.0001). Compared with placebo, ω-3 fatty acid supplementation led to greater endothelium-dependent vasodilatation with acetylcholine and substance P (p=0.0032 and p=0.056). Substance P caused a dose-dependent increase in plasma t-PA concentrations (p<0.0001) that was greater after ω-3 fatty acid supplementation compared with placebo (8.8±2.3 IU ml−1 vs 3.6±1.1 IU ml−1; p=0.029). ω-3 fatty acids did not affect platelet-monocyte aggregation, platelet P-selectin or CD40L, or monocyte CD40.

Conclusions We have demonstrated for the first time that ω-3 fatty acids augment acute endothelial t-PA release and improve endothelial vasomotor function in cigarette smokers. Improved endogenous fibrinolysis and endothelial function may represent important mechanisms through which ω-3 fatty acids confer potential cardiovascular benefits.

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