Rosuvastatin slows progression of subclinical atherosclerosis in patients with treated HIV infection

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To determine the effect of statins on the progression of subclinical atherosclerosis in a population of HIV-infected adults on antiretroviral therapy.


Double-blind, randomized clinical trial.


Stopping Atherosclerosis and Treating Unhealthy Bone with RosuvastatiN in HIV infection was a 96-week double-blind, randomized clinical trial of 10 mg daily rosuvastatin (n = 72) vs. placebo (n = 75) in a population of HIV-infected subjects on stable antiretroviral therapy with LDL-cholesterol 130 mg/dl or less (≤3.36 mmol/l) and evidence of heightened T-cell activation (CD8+CD38+HLA-DR+ ≥19%) or increased inflammation [high sensitivity C-reactive protein ≥2 mg/l (≥19 mmol/l)]. Change in common carotid artery intima–media thickness (IMT) (CCA-IMT) was the primary outcome. Secondary outcomes were changes in LDL and coronary artery calcium.


Median (Q1, Q3) age was 46 (40, 53) years; 78% were man and 68% African-American; 49% were on a protease inhibitor. Mean (95% confidence interval) change in LDL was −21 (−27 to −15) mg/dl [−0.54 (−0.70 to −0.39) mmol/l] in the rosuvastatin arm. In a multivariable linear mixed-effects model, assignment to statin was associated with 0.019 mm (95% confidence interval: 0.002–0.037 mm) less progression of CCA-IMT over 96 weeks. We did not find substantial effect modification by level of inflammation or immune activation biomarkers, except for a borderline statistically significant interaction for soluble vascular cell adhesion molecule (P = 0.065). There was no difference in coronary artery calcium change (P = 0.61).


Rosuvastatin effectively lowers LDL and appears to substantially slow progression of CCA-IMT in patients with treated HIV infection. Future study is needed to determine whether subjects with higher levels of inflammation or immune activation derive greater cardiovascular benefit from statin therapy.

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