OBJECTIVE: HIV infection is associated with an atherogenic lipoprotein profile, and ritonavir-boosted protease inhibitors exacerbate this phenotype. We evaluated the effect of 45 days of rosuvastatin versus pravastatin on the low-density lipoprotein (LDL) size and the distribution of LDL subfractions in HIV-1 patients receiving boosted protease inhibitors with elevated LDL levels. DESIGN: Substudy of the randomized double-blind multicentre ANRS 126 VIHstatine trial. SETTING:Twenty clinical centres in France. PATIENTS: HIV-infected patients receivingboosted protease inhibitors with dyslipidaemia (LDL cholesterol >; 4.1 mmol/l and triglycerides < 8.8 mmol/l). INTERVENTION: Rosuvastatin 10 mg/day (n = 39) or pravastatin 40 mg/day (n = 37) for 45 days. MAIN OUTCOME MEASURE(S): LDL size and distribution of LDL subfractions blindly assessed by gradient gel electrophoresis at baseline and at day 45. RESULTS:Rosuvastatin was more effective than pravastatin in increasing the diameter of the LDL peak. The LDL diameter change was 0.33 ± 0.59 nm in the rosuvastatin group versus -0.01 ± 0.52 nm in the pravastatin group (P = 0.021). Rosuvastatin was also more effective in increasing significantly the percentage of large LDL (LDL1, P = 0.038; LDL2, P = 0.031) and in decreasing the percentage of small LDL (LDL3, P = 0.009). CONCLUSION:Rosuvastatin was more effective than pravastatin in normalizing LDL size and LDL subfraction distributions, leading to a less atherogenic phenotype.
RCT Entities:
OBJECTIVE:HIV infection is associated with an atherogenic lipoprotein profile, and ritonavir-boosted protease inhibitors exacerbate this phenotype. We evaluated the effect of 45 days of rosuvastatin versus pravastatin on the low-density lipoprotein (LDL) size and the distribution of LDL subfractions in HIV-1patients receiving boosted protease inhibitors with elevated LDL levels. DESIGN: Substudy of the randomized double-blind multicentre ANRS 126 VIHstatine trial. SETTING: Twenty clinical centres in France. PATIENTS: HIV-infectedpatients receiving boosted protease inhibitors with dyslipidaemia (LDL cholesterol > 4.1 mmol/l and triglycerides < 8.8 mmol/l). INTERVENTION: Rosuvastatin 10 mg/day (n = 39) or pravastatin 40 mg/day (n = 37) for 45 days. MAIN OUTCOME MEASURE(S): LDL size and distribution of LDL subfractions blindly assessed by gradient gel electrophoresis at baseline and at day 45. RESULTS:Rosuvastatin was more effective than pravastatin in increasing the diameter of the LDL peak. The LDL diameter change was 0.33 ± 0.59 nm in the rosuvastatin group versus -0.01 ± 0.52 nm in the pravastatin group (P = 0.021). Rosuvastatin was also more effective in increasing significantly the percentage of large LDL (LDL1, P = 0.038; LDL2, P = 0.031) and in decreasing the percentage of small LDL (LDL3, P = 0.009). CONCLUSION:Rosuvastatin was more effective than pravastatin in normalizing LDL size and LDL subfraction distributions, leading to a less atherogenic phenotype.