Prescription omega-3 acid ethyl esters plus simvastatin 20 and 80 mg: effects in mixed dyslipidemia

Effects of Prescription Omega-3-Acid Ethyl Esters on Fasting Lipid Profile in Subjects With Primary Hypercholesterolemia

“…23 POM3 lowers TG levels in part by inhibiting several enzymes involved in TG synthesis, which thereby reduces hepatic synthesis and secretion of VLDL-TG. 2,9,21 The reduction of VLDL-TG appears to be secondary to both reductions in the number and TG content of VLDL particles as well as an increase in the rate at which VLDL particles are delipidated and thus converted to LDL. 31,33,34 The increase in conversion of VLDL to LDL particles is facilitated by a reduction in Apo CIII.…”

“…1 The most common hypertriglyceridemic phenotypes encountered in clinical practice are Fredrickson Type IIb (mixed dyslipidemia, elevations of both LDL-C and TG) and Types IV and V (isolated high to very high TG). 1,2 Omega-3 fatty acids (eicosapentaenoic acid and docosahexaenoic acid) lower TG and very low-density lipoprotein cholesterol (VLDL-C) levels and also have been found to reduce the risks for cardiovascular mortality and major events in randomized clinical trials. [3][4][5] However, most of the trials examining a potential role for omega-3 fatty acids in cardiovascular disease risk reduction administered a dose lower than that which would be expected to affect lipoprotein lipids, suggesting that mechanisms other than lipid altering are involved.…”

Effects of prescription omega-3-acid ethyl esters, coadministered with atorvastatin, on circulating levels of lipoprotein particles, apolipoprotein CIII, and lipoprotein-associated phospholipase A2 mass in men and women with mixed dyslipidemia

“…[14][15][16] Recent data suggest that some statin-treated patients may experience a decrease in LDL-P size, which may be attributable to greater affinity of larger LDL-P for hepatic LDL receptors, the expression of which is up-regulated during statin therapy, resulting in a greater reduction in larger than smaller LDL-P. 17,18 The effects of lipid-altering therapies on lipoprotein particle concentration is also of interest because analyses of data from prospective studies suggest that LDL-P concentration may be a better predictor of CHD risk than lipoprotein lipid concentrations. [19][20][21][22][23][24] Results from previous studies have suggested that the addition of POM3 to statin therapy may produce a modest increase in LDL-C level but that this is not accompanied by an increase in LDL-P concentration, but rather it is attributable to a shift toward larger, less dense LDL-P. 7,11,12 Apolipoprotein (Apo) CIII may be an important modulator of LDL-P remodeling because it acts as an inhibitor of lipoprotein lipase and of remnant uptake by the liver, thus its reduction would facilitate more rapid clearance of verylow-density lipoprotein (VLDL)-TG from the circulation. 12,25,26 Reduced Apo CIII would also tend to enhance the rate of conversion of VLDL to LDL particles and reduce the substrate available for cholesteryl ester transfer protein, thereby decreasing the rate of exchange of VLDL-TG for cholesteryl esters from LDL-P and highdensity lipoprotein particles (HDL-P).…”

“…1-5 There is a substantial body of research supporting the consumption of long-chain polyunsaturated omega-3 fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), for lowering elevated TG. 6,7 Administration of the prescription form of concentrated omega-3-acid ethyl esters (POM3) in combination with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) in patients with hypertriglyceridemia has been shown to lower the circulating TG concentration and to reduce non-highdensity lipoprotein cholesterol (non-HDL-C), a measure of the cholesterol carried by all potentially atherogenic lipoprotein particles. [8][9][10][11][12][13] The effects of POM3 plus statin therapy on lipoprotein particle sizes, concentrations, and compositions has been less well characterized.…”

Understanding hypertriglyceridemia in women: clinical impact and management with prescription omega-3-acid ethyl esters

“…In an open-label extension of this study, 14 participants were treated with P-OM3 4 g/d plus simvastatin 80 mg/d for another 6 weeks 70. The increase in statin dosage led to a further reduction in non-HDL-C (51.0% with P-OM3 plus simvastatin 80 mg/d vs 40.8% with P-OM3 plus simvastatin 20 mg/d; P < 0.05) without affecting TGs (58.6% with P-OM3 plus simvastatin 80 mg/d vs 54.7% with P-OM3 plus simvastatin 20 mg/d) 70…”