Effect of Two Intensive Statin Regimens on Progression of Coronary Disease
What is the relative efficacy of maximal approved doses of atorvastatin and rosuvastatin on coronary disease regression?
In the SATURN (Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin versus Atorvastatin) trial, serial intravascular ultrasonography (IVUS) was performed in 1,039 patients with coronary disease, at baseline and after 104 weeks of treatment with either atorvastatin, 80 mg daily, or rosuvastatin, 40 mg daily. Patients ages 18-75 years were eligible if they had at least one vessel with a 20% stenosis and a target vessel for IVUS with <50% stenosis. Entry low-density lipoprotein cholesterol (LDL-C) levels were required to be >100 mg/dl off statins and >80 mg/dl on statins. Primary efficacy endpoint was the change in percent atheroma volume, and secondary endpoint was normalized total atheroma volume. Other measures included change in lipids, high-sensitivity C-reactive protein, safety and side-effect profiles, and cardiovascular events.
Groups were similar for: mean age 57.5 years, >70% male, 95% white, >70% hypertension, and about 60% had prior use of statins. Mean LDL-C was 120 mg/dl, high-density lipoprotein cholesterol (HDL-C) 45 mg/dl, apolipoprotein (apo) B 105 mg/dl, apo A-1 127 mg/dl, and apoB/apoA-2 0.9 mg/dl. After 104 weeks of therapy, the rosuvastatin group had lower levels of LDL-C than the atorvastatin group (62.6 vs. 70.2 mg/dl, p < 0.001), and higher levels of HDL-C (50.4 vs. 48.6 mg/dl, p = 0.01). The primary endpoint of percent atheroma volume decreased by 0.99% (95% confidence interval [CI], -1.19 to -0.63) with atorvastatin and by 1.22% (95% CI, -1.52 to -0.90) with rosuvastatin (p = 0.17). The normalized total atheroma volume was more favorable with rosuvastatin than with atorvastatin: -6.39 mm3 (95% CI, -7.52 to -5.12), as compared with -4.42 mm3 (95% CI, -5.98 to -3.26) (p = 0.01). Both agents induced regression in the majority of patients: 63.2% with atorvastatin and 68.5% with rosuvastatin for percent atheroma volume (p = 0.07) and 64.7% and 71.3%, respectively, for total atheroma volume (p = 0.02). Both agents had acceptable side-effect profiles, with a low incidence of laboratory abnormalities and cardiovascular events.
The authors concluded that maximal doses of rosuvastatin and atorvastatin resulted in significant regression of coronary atherosclerosis. Despite the lower level of LDL-C and the higher level of HDL-C achieved with rosuvastatin, a similar degree of regression of percent atheroma volume was observed in the two treatment groups.
This elegant study adds to the evidence that intensed statin dosing can be associated with regression of atherosclerotic plaque, and that the high-dose very potent statins are safe. The study size and duration were not adequate to determine whether the better lipid profile achieved with rosvastatin compared to atorvastatin would provide any clinical benefit.
Keywords: Fluorobenzenes, Coronary Artery Disease, Apolipoprotein A-II, Plaque, Atherosclerotic, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Apolipoprotein A-I, Pyrimidines, Heptanoic Acids, Constriction, Pathologic, Pyrroles, Incidence, Cholesterol, C-Reactive Protein, Confidence Intervals, Ultrasonography, Interventional, Hypertension, Sulfonamides
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