title: Rosuvastatin slows progression of subclinical atherosclerosis in patients with treated HIV infection.
abstract: 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 (CD8CD38HLA-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.
authors.affiliation: aCase Western Reserve University School of Medicine bUniversity Hospitals Case Medical Center, Cleveland, Ohio, USA.
authors.forename: Chris T
authors.initials: CT
authors.lastname: Longenecker
authors.forename: Abdus
authors.initials: A
authors.lastname: Sattar
authors.forename: Robert
authors.initials: R
authors.lastname: Gilkeson
authors.forename: Grace A
authors.initials: GA
authors.lastname: McComsey
mesh_terms: D000328:Adult; D019380:Anti-HIV Agents / Q000627:therapeutic use*; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000188:drug therapy* / Q000473:pathology / Q000517:prevention & control*; D002118:Calcium / Q000032:analysis; D002339:Carotid Arteries / Q000473:pathology; D008078:Cholesterol, LDL / Q000097:blood; D003331:Coronary Vessels / Q000473:pathology; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D015658:HIV Infections / Q000150:complications* / Q000188:drug therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010919:Placebos / Q000008:administration & dosage; D000068718:Rosuvastatin Calcium / Q000627:therapeutic use*; D016896:Treatment Outcome; D017539:Tunica Intima / Q000473:pathology
chemical_list: D019380:Anti-HIV Agents; D000924:Anticholesteremic Agents; D008078:Cholesterol, LDL; D010919:Placebos; D000068718:Rosuvastatin Calcium; D002118:Calcium