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Summary Aims:  To evaluate the efficacy of switching from a previous statin monotherapy to ezetimibe/simvastatin (EZE/SIMVA) 10/20 mg vs. rosuvastatin (ROSUVA) 10 mg. Methods:  In this randomised, double‐blind study, 618 patients with documented hypercholesterolaemia [low‐density lipoprotein cholesterol (LDL‐C) ≥ 2.59 and ≤ 4.92 mmol/l] and with high cardiovascular risk who were taking a stable daily dose of one of several statin medications for ≥ 6 weeks prior to the study randomisation visit entered a 6‐week open‐label stabilisation/screening period during which they continued to receive their prestudy statin dose. Following stratification by study site and statin dose/potency, patients were randomised to EZE/SIMVA 10/20 mg (n = 314) or ROSUVA 10 mg (n = 304) for 6 weeks. Results:  EZE/SIMVA produced greater reductions in LDL‐C (−27.7% vs. −16.9%; p ≤ 0.001), total cholesterol (−17.5% vs. −10.3%; p ≤ 0.001), non‐high‐density lipoprotein cholesterol (HDL‐C) (−23.4% vs. −14.0%; p ≤ 0.001) and apolipoprotein B (−17.9% vs. −9.8%; p ≤ 0.001) compared with ROSUVA, while both treatments were equally effective at increasing HDL‐C (2.1% vs. 3.0%; p = 0.433). More patients achieved LDL‐C levels < 2.59 mmol/l (73% vs. 56%), < 2.00 mmol/l (38% vs. 19%) and < 1.81 mmol/l (25% vs. 11%) with EZE/SIMVA than ROSUVA (p ≤ 0.001). A borderline significantly greater reduction in triglycerides (p = 0.056) was observed for EZE/SIMVA (−11.0%) vs. ROSUVA (−5.3%). There were no between‐group differences in the incidences of adverse events or liver transaminase and creatine kinase elevations. Conclusion:  EZE/SIMVA 10/20 mg produced greater improvements in LDL‐C, total cholesterol, non‐HDL‐C and apoB with a similar safety profile as for ROSUVA 10 mg.

Hyperuricemia has been described as associated with the risk of development metabolic syndrome; however the relationship between the uric acid level and particular parameters of metabolic syndrome remained unclear. We performed a cross-sectional study on a cohort of 833 dyslipidemic patients and correlated their levels of uric acid with parameters of insulin resistance, lipid metabolism, C-reactive protein, anthropometric parameters. We also defined patients with hypertriglyceridemic waist phenotype and compered their uric acid levels with those without this phenotype. We found that levels of uric acid are associated with parameters of metabolic syndrome. Specifically, dyslipidemia characteristic for metabolic syndrome (low HDL cholesterol and high triglycerides) correlates better with uric acid levels than parameters of insulin resistance. Also waist circumference correlates better with uric acid levels than body mass index. Patients with hypertriglyceridemic waist phenotype had higher levels of uric acid when compared with patients without this phenotype. Serum uric acid levels are even in low levels linearly correlated with parameters of metabolic syndrome (better with typical lipid characteristics than with parameters of insulin resistance) and could be associated with higher cardiovascular risk.

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