Add-on fish oil lowers lipid levels in rosuvastatin-treated patients
Supplementation with omega-3 fatty acids in combination with rosuvastatin may yield significant reductions in triglycerides and nonhigh-density lipoprotein (HDL) cholesterol as compared with rosuvastatin monotherapy, according to data from the ROMANTIC (rosuvastatin-omacor in residual hypertriglyceridemia) trial.
The trial randomized 201 patients (mean age 58.1 years; 62.7 percent male) to receive rosuvastatin 20 mg/d plus ω-3 fatty acids 4 g/d (ROSUMEGA group) or rosuvastatin 20 mg/d (rosuvastatin group) alone for 8 weeks. All patients had residual hypertriglyceridemia following a 4-week run-in period of rosuvastatin treatment.
Compared with those in the rosuvastatin group, patients in the ROSUMEGA group showed a significantly greater percentage change from baseline in triglycerides (–26.3 vs –11.4 percent; p<0.001) and non-HDL cholesterol (–10.7 vs –2.2 percent; p=0.001) following 8 weeks of treatment.
Linear regression analysis found that the lipid-lowering effect of omega-3 fatty acids was more pronounced when baseline triglycerides or non-HDL cholesterol levels were high and body mass index was low.
In terms of safety, the incidence of adverse events did not significantly differ between the two treatment groups.
Researchers pointed out that additional work must be conducted to determine whether the lipid-lowering effect of omega-3 fatty acids actually leads to the prevention of cardiovascular event.
Omega-3 fatty acids are derived from fatty fish and other seafood, and their consumption has been previously reported to decrease plasma triglycerides, resting heart rate, and blood pressure, as well as also improve myocardial filling and efficiency, lower inflammation, and improve vascular function. Omega-3 fatty acids affect multiple molecular pathways, including alteration of physical and chemical properties of cellular membranes, direct interaction with and modulation of membrane channels and proteins, regulation of gene expression via nuclear receptors and transcription factors, changes in eicosanoid profiles, and conversion of n-3 PUFA to bioactive metabolites. [J Am Coll Cardiol 2011;58:2047–2067]