Why the study?
Recent clinical trials have shown inconsistent cardioprotective effects of omega-3 fatty acids despite imaging evidence of plaque stabilization, warranting a review of mechanistic pathways to explain these discrepancies.
This review provides mechanistic insights into the effects of omega-3 fatty acids on atherosclerosis to help explain inconsistencies in recent clinical trials.
May reconcile inconsistent omega-3 trial results via lipid and plaque mechanisms; leaves open optimal dosing and populations for future trials.
Omega-3 polyunsaturated fatty acids (PUFAs) were early established as therapeutic option for patients with high triglyceride levels. Their effects on lipoprotein particles, including a reduction in very low-density lipoprotein and a shift from small to large low-density lipoprotein, is increasingly recognised. This is coupled with their ability to be incorporated within the cellular membrane, leading to plaque stability and anti-inflammatory effects. Nonetheless, recent clinical trials have not been consistent in demonstrating the potential cardioprotective effects of omega-3 fatty acids. This is despite the circumstantial evidence from imaging studies illustrating the stabilising effects on atherosclerotic plaques and slowing of plaque progression. In this article, we will review the effects of omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on lipid biomarkers, atherosclerotic plaque features, and clinical outcome studies and provide a mechanistic role in managing residual risk of atherosclerosis. This will provide better insight into the inconsistency of the recently reported clinical outcome studies.
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Gupta et al. (2023) studied this question.
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