However, in those species with atherosclerotic lesions most similar to humans, the effects of omega-3 fatty acids on atherogenesis have generally been beneficial. The effects of omega-3 fatty acids in human atherosclerosis have not yet been studied, but recent preliminary reports have suggested that coronary artery restenosis after angioplasty was reduced in patients given omega-3 fatty acids. In contrast, a study from Australia found no differences in the incidence of restenosis. Source
The mechanism(s) by which omega-3 fatty acids might impede atherogenesis remain speculative. Although a reduction in cholesterol levels by diet or medication has been observed to retard atherogenesis, the effects of dietary omega-3 fatty acid supplementation on lipid levels have been inconsistent in humans. As noted previously, experimental atherosclerosis was inhibited without changes in plasma lipids, so it is unlikely that the beneficial effects of omega-3 fatty acids on experimental atherosclerosis are substantially related to changes in total or LDL cholesterol levels. Platelet function and platelet-vessel wall interactions are impaired by the ingestion of omega-3 fatty acids. The contribution of platelets to atherosclerotic plaque development via their release of platelet-derived growth factor or other substances may be important, so that a reduction in the interaction between platelets and the vessel wall could contribute to the inhibition of atherogenesis.
Macrophages and monocytes have also been postulated to play an early and critical role in the evolution of the atherosclerotic plaque. Dietary omega-3 fatty acid supplementation has been observed to inhibit monocyte production of the pro-inflammatory substance, leukotriene B4. Additionally, monocyte generation of free radicals, important mediators of cellular injury, is reduced in humans receiving dietary omega-3 fatty acid supplementation. Thus, the ability of omega-3 fatty acids to reduce monocyte interactions with vessel walls could also contribute to inhibition of atherogenesis.