[Non-ST-elevation acute coronary syndrome. Comparison of effects of atorvastatin and rosuvastatin on blood levels of lipids and markers of inflammation]

Abstract

Data on rapid effects of statins in patients (pts) with acute coronary syndrome (ACS) are mostly from trials of atorvastatin (ATO). We hypothesized that due to high potency 10 mg of rosuvastatin (ROS) would produce same changes of lipids and inflammation markers as 40 mg ATO.

Methods: We openly randomized 53 pts (69.7+/-10.1 years, 58.5% - man) within 36 h of non ST elevation (NSTE) ACS (56.6% NSTE myocardial infarction) to ROS 10 (n=19), ATO 40 (n=19) mg/day or no statin (n=15). Pts with low density lipoprotein cholesterol (LDL-C) >6, triglycerides (TG) >4.5 mmol/l, C-reactive protein (CRP) >10 mg/l (non-fasting sample) were not included. LDL-C, high density lipoprotein (HDL)-C, TG, apolipoproteins A-1 (apoA), and B (apoB), high sensitivity CRP, tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6) were measured in fasting blood sampled at randomization and 2 weeks later.

Results: Both statins caused similar decreases of LDL-C (-44.0% ROS, -50% ATO; both p<0.00001 vs control [-4%]). TG significantly rose in ROS (p=0.042) and control (p=0.008) groups but not in ATO group (p=0.615). HDL-C decreased similarly in 3 groups. ApoA-1 did not differ between 3 groups at all time points. ApoB decreased more in ATO (-32.6%), than in ROS (-24%) group (p=0.049). CRP and IL-6 changes from baseline were insignificant. In ROS group CRP had tendency to decrease but same tendency took place in control. TNFalpha significantly increased in all groups. There were no significant differences between 3 groups in inflammation markers.

Conclusion: In pts with NSTEACS effect on lipids of ROS 10 mg was somewhat inferior to ATO 40 mg/day. Unexpectedly ATO and ROS during first 14 days of NSTEACS produced no significant effect on inflammation markers possibly because of insufficient dose of both.