Statin-Treated Patients with Mixed Dyslipidemia Benefit from Concomitant Omega-3 Fatty Acids
NEW ORLEANS, LA— The addition of omega-3 fatty acids (POM3) to atorvastatin increased low-density lipoprotein particle (LDL-P) size without altering LDL-P concentration in patients with mixed dyslipidemia, results of a post-hoc analysis demonstrated at a ACC.11, the American College of Cardiology's 60th Annual Scientific Session.
Recent data suggest that a substantial number of statin-treated patients may experience a decrease in LDL-P size, which might contribute to residual atherosclerotic risk. Thus, Kevin C. Maki, PhD from Provident Clinical Research, Glen Ellyn, IL, and colleagues evaluated the effect of POM3 + atorvastatin on LDL-P size and concentration in mixed dyslipidemic patients. This double-blind, randomized, 8-week trial compared escalating doses of open-label atorvastatin (10, 20, and 40mg/d) + matching placebo capsules (corn oil) with escalating atorvastatin + POM3 4g/d. Funding for this study was provided by GlaxoSmithKline.
Following a 4-week diet lead-in period without any lipid-lowering agents, 237 patients aged 18 to 79 years with elevated fasting triglyceride levels (as defined as ≥250mg/dL and <600 mg/dL) and non-HDL-C (≥160mg/dL) were randomized into either a placebo + atorvastatin group (n=118) or a POM3 + atorvastatin group (n=119). Baseline characteristics were similar between the two groups; mean age was 56 years and the majority of patients were male. Patients received dietary counseling on the National Cholesterol Education Program Therapeutic Lifestyle Changes diet with reinforcement throughout the study. After 8 weeks, patients continued their blinded study drug with atorvastatin 20mg for 4 additional weeks followed by atorvastatin 40mg for a final 4-week treatment period.
The addition of 10mg/d POM3 significantly increased median change from baseline LDL-P size (P=0.0011) without altering the total LDL-P concentration (P=0.1813). POM3-treated subjects showed significant shifts in LDL subclass distribution, including reduction in small LDL-P concentration (P=0.0255 vs. placebo) and an increase in large LDL-P concentration (P<0.0001 vs. placebo). Also, a significantly larger fraction of subjects in the POM3 group switched from pattern B (predominance of small LDL-P) to pattern A (predominance of large LDL-P) vs. placebo(18.5% vs. 8.5%; P=0.0241). Findings were consistent as the atorvastatin dose was escalated.
The addition of 4g/d POM3 to atorvastatin 10mg/d improved LDL subclass distribution compared to placebo, without altering LDL-P concentration in patients with mixed dyslipidemia.