Effect of ω-3 fatty acid supplementation on endothelial function, endogenous fibrinolysis and platelet activation in male cigarette smokers
- Jehangir N Din1,
- Rachel M Archer1,
- Scott A Harding2,
- Jaydeep Sarma3,
- Karin Lyall1,
- Andrew D Flapan4,
- David E Newby1
- 1Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, UK
- 2Department of Cardiology, Wellington Hospital, Wellington, New Zealand
- 3North West Heart Centre, Wythenshawe Hospital, Manchester, UK
- 4Edinburgh Heart Centre, Royal Infirmary of Edinburgh, Edinburgh, UK
- 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;
- Received 22 August 2012
- Revised 26 October 2012
- Accepted 30 October 2012
- Published Online First 26 November 2012
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.