This randomised, double-blind, placebo-controlled trial, enrolled 40 HIV-infected participants (aged between 18 and 60) with subclinical coronary atherosclerosis, evidence of arterial inflammation in the aorta by fluorodeoxyglucose (FDG)-PET, and LDL-cholesterol < 3.37 mmol/L (130 mg/dL), and stable antiretroviral therapy in the past 6 months. Patients were randomly assigned (1:1), with stratification by sex, to 1 year of atorvastatin (20 mg/day, escalating to 40mg/d at M3 if good tolerance, n=19) or placebo (n=21). The pre-specified primary endpoint was arterial inflammation as assessed by FDG-PET of the aorta. Additional endpoints were non-calcified and calcified plaque measures and high risk plaque features assessed with coronary CT angiography and biochemical measures. Analysis was done by ITT with all available data and without imputation for missing data. Baseline characterics were similar between groups; 37 participants completed the study. After 12 months, change in FDG-PET uptake of the most diseased segment of the aorta was not different between atorvastatin and placebo, but technically adequate results comparing longitudinal changes in identical regions could be assessed in only 21 patients. Atorvastatin reduced non-calcified coronary plaque volume relative to placebo: median change -19.4% (IQR -39.2 to 9.3) versus 20.4% (-7.1 to 94.4; p=0.009, n=37). The number of high-risk plaques was significantly reduced in the atorvastatin group compared with the placebo group: change in number of low attenuation plaques -0.2 (95% CI -0.6 to 0.2) vs 0.4 (0.0, 0.7; p=0.03; n=37); and change in number of positively remodeled plaques -0.2 (-0.4 to 0.1) vs 0.4 (-0.1 to 0.8; p=0.04; n=37). Direct LDL-cholesterol (-1.00 mmol/L, 95% CI -1.38 to 0.61 vs 0.30 mmol/L, 0.04 to 0.55, p<0.0001) and lipoprotein-associated phospholipase A2 (-52.2 ng/mL, 95% CI -70.4 to -34.0, vs -13.3 ng/mL, -32.8 to 6.2; p=0.005; n=37) decreased significantly with atorvastatin relative to placebo. Statin therapy was well tolerated, with a low incidence of clinical adverse events.
In summary, although statin therapy had no effects on arterial inflammation of aorta (FDG-PET), it reduced non-calcified plaque volume and high risk coronary plaque features in HIV-infected patients.
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