Fish oil omega-3 fatty acids reduces left ventricular remodelling after acute MIHeydari et al., Circulation. 2016
Effect of Omega-3 Acid Ethyl Esters on Left Ventricular Remodeling After Acute Myocardial Infarction. The OMEGA-REMODEL Randomized Clinical Trial
Heydari B, Abdullah S, Pottala JV, et al.
BackgroundThe use of omega-3 fatty acids from fish oil (O-3FA) has been related to favourable clinical outcomes [1,2], but it is unclear whether it affects the cardiac structure and function after an acute myocardial infarction (MI) in the context of current guideline-based therapy.
In the prospective, multicentre, double-blind, placebo-controlled OMEGA-REMODEL trial, 358 patients with an acute MI on guideline-based therapy, were randomised to 4g/d O-3FA or placebo. At baseline and after 6 months, left ventricular (LV) structure and function, infarct size, and extracellular matrix expansion were quantified with cardiac MRI (CMR) , to assess the effects of high-dose O-3FA on LV remodelling.
- O-3FA treatment was associated with a mean reduction in LV end-systolic volume indexed to body surface area (LVESVI) by intention-to-treat analysis: –5.8% (95%CI: –10.3% to –1.1%; P=0.017) as compared with placebo, and with –6.6% (95%CI: –11.3% to –1.8%; P=0.007) in the per-protocol analysis
- A mean reduction in non-infarct myocardial fibrosis of –5.6% (95%CI: –10.4% to –0.9%; P=0.022) was seen in intention-to-treat analysis and by –5.5% (95%CI: –10.4% to –0.6%; P=0.026) in a per-protocol analysis.
- No significant difference was seen between groups in change in infarct size or LV ejection fraction (LVEF) in the intention-to-treat or per-protocol analyses.
- In patients who completed both study visits per-protocol, a dose-response relationship was seen, such that with increasing O-3FA exposure, reductions in LVESVI and non-infarct myocardial fibrosis were observed, and an increasing LVEF.
- By intention-to-treat analysis, O-3FA treatment was associated with 8.1% reduction in myeloperoxidase (inflammation biomarker) and 7.9% reduction in ST-2 (fibrosis biomarker). By per-protocol analysis, O-3FA treatment was associated with 9.3% reduction of myeloperoxidase and 8.3% reduction of ST-2.
- There were no adverse events associated with high-dose O-3FA therapy.
ConclusionIn 358 patients with an acute MI on guideline-based therapy, high-dose O-3FA treatment for 6 months was safe and had a beneficial effect on adverse LV remodelling, non-infarct myocardial fibrosis, and serum biomarkers of systemic inflammation. The authors propose that the observations may be the consequence of suppression of inflammation at both systemic and myocardial levels during the healing phase after acute MI.
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