Key result
Rosuvastatin combined with fenofibrate increased mean LDL size more than rosuvastatin monotherapy or combined with ω-3 fatty acids (p<0.05) and significantly raised HDL-C levels by 7.7%.
Why the study?
Does moderate-dose rosuvastatin combined with fenofibrate or ω-3 fatty acids improve lipoprotein subfraction profiles compared to high-dose rosuvastatin monotherapy in patients with mixed dyslipidaemia and metabolic syndrome?
RCT (n=71)
randomized
Does moderate-dose rosuvastatin combined with fenofibrate or ω-3 fatty acids improve lipoprotein subfraction profiles compared to high-dose rosuvastatin monotherapy in patients with mixed dyslipidaemia and metabolic syndrome?
p-value: p=<0.05
In patients with mixed dyslipidemia and metabolic syndrome, combining moderate-dose rosuvastatin with fenofibrate is more effective at increasing mean LDL size and raising HDL-C than high-dose rosuvastatin monotherapy or combination with omega-3 fatty acids.
Supports fenofibrate add-on to moderate rosuvastatin for LDL size and HDL-C gains; extends surrogate data versus high-dose monotherapy in metabolic syndrome.
BACKGROUND: Raised triglycerides (TG), decreased high-density lipoprotein cholesterol (HDL-C) levels and a predominance of small dense low density lipoproteins (sdLDL) are characteristics of the metabolic syndrome (MetS). OBJECTIVE: To compare the effect of high-dose rosuvastatin monotherapy with moderate dosing combined with fenofibrate or ω-3 fatty acids on the lipoprotein subfraction profile in patients with mixed dyslipidaemia and MetS. METHODS: We previously randomised patients with low-density lipoprotein cholesterol (LDL-C) > 160 and TG > 200 mg/dl to rosuvastatin monotherapy 40 mg/day (R group, n = 30) or rosuvastatin 10 mg/day combined with fenofibrate 200 mg/day (RF group, n = 30) or ω-3 fatty acids 2 g/day (Rω group, n = 30). In the present study, only patients with MetS were included (24, 23 and 24 in the R, RF and Rω groups respectively). At baseline and after 12 weeks of treatment, the lipoprotein subfraction profile was determined by polyacrylamide 3% gel electrophoresis. RESULTS: The mean LDL size was significantly increased in all groups. This change was more prominent with RF than with other treatments in parallel with its greater hypotriglyceridemic capacity (p < 0.05 compared with R and Rω). A decrease in insulin resistance by RF was also noted. Only RF significantly raised HDL-C levels (by 7.7%, p < 0.05) by increasing the cholesterol of small HDL particles. The cholesterol of larger HDL subclasses was significantly increased by R and Rω. CONCLUSIONS: All regimens increased mean LDL size; RF was the most effective. A differential effect of treatments was noted on the HDL subfraction profile.
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Agouridis et al. (2012) conducted an RCT in Mixed dyslipidaemia and metabolic syndrome (n=71). Rosuvastatin combined with fenofibrate or ω-3 fatty acids vs. Rosuvastatin monotherapy 40 mg/day was evaluated on Lipoprotein subfraction profile (mean LDL size and HDL-C levels) (p=<0.05). Rosuvastatin combined with fenofibrate increased mean LDL size more than rosuvastatin monotherapy or combined with ω-3 fatty acids (p<0.05) and significantly raised HDL-C levels by 7.7%.
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