title: Serum oxidized low-density lipoprotein decreases in response to statin therapy and relates independently to reductions in coronary plaque in patients with HIV.
abstract: OBJECTIVE
  Circulating oxidized low-density lipoprotein (oxLDL) levels are elevated in HIV-infected patients and have been associated with atherosclerosis. Statins have been shown to reduce plaque on coronary computed tomography angiography (cCTA) in HIV-infected individuals. Thus, we investigated the effect of statins on serum oxLDL levels and the relationship between changes in oxLDL and coronary atherosclerosis on cCTA in patients with HIV.
  
  
  METHODS
  We previously conducted a 12-month randomized, placebo-controlled trial with atorvastatin in 40 HIV-infected patients on stable antiretroviral therapy with subclinical coronary atherosclerosis and low-density lipoprotein (LDL)-cholesterol less than 130 mg/dl.
  
  
  METHODS
  In the current analysis, patients underwent cCTA and measurements of serum oxLDL, sCD14, sCD163, lipoprotein phospholipase-A2, and fasting lipids at baseline and end of the study.
  
  
  RESULTS
  Nineteen patients were randomized to atorvastatin and 21 patients to placebo. Serum oxLDL decreased -22.7% (95% CI -28.7 to -16.7) in the atorvastatin group and increased 7.5% (95% CI -3.3 to 18.4) in the placebo group (P < 0.0001). Change in oxLDL significantly correlated with changes in noncalcified plaque volume, total plaque volume, positively remodeled plaque, and low attenuation plaque. The association between changes in oxLDL and noncalcified plaque volume was independent of the baseline 10-year Framingham risk, LDL, CD4 cell count, and viral load.
  
  
  CONCLUSIONS
  Statins lower oxLDL levels in HIV-infected patients, and reductions in oxLDL are related to improvements in coronary atherosclerosis, independent of traditional cardiovascular risk factors. Reductions in oxLDL may be one mechanism through which statins exert beneficial effects on reducing atherosclerosis in HIV-infected individuals.
authors.affiliation: aProgram in Nutritional Metabolism bCardiovascular Imaging Section, Department of Radiology cBiostatistics Center, Massachusetts General Hospital, Boston, Massachusetts, USA.
authors.forename: Eric
authors.initials: E
authors.lastname: Nou
authors.forename: Michael T
authors.initials: MT
authors.lastname: Lu
authors.forename: Sara E
authors.initials: SE
authors.lastname: Looby
authors.forename: Kathleen V
authors.initials: KV
authors.lastname: Fitch
authors.forename: Elli A
authors.initials: EA
authors.lastname: Kim
authors.forename: Hang
authors.initials: H
authors.lastname: Lee
authors.forename: Udo
authors.initials: U
authors.lastname: Hoffmann
authors.forename: Steven K
authors.initials: SK
authors.lastname: Grinspoon
authors.forename: Janet
authors.initials: J
authors.lastname: Lo
mesh_terms: D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin / Q000008:administration & dosage*; D003324:Coronary Artery Disease / Q000473:pathology* / Q000517:prevention & control*; D005260:Female; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D008077:Lipoproteins, LDL / Q000032:analysis*; D008297:Male; D008875:Middle Aged; D010919:Placebos / Q000008:administration & dosage; D044967:Serum / Q000737:chemistry*; D016896:Treatment Outcome
chemical_list: D000924:Anticholesteremic Agents; D008077:Lipoproteins, LDL; D010919:Placebos; C099252:oxidized low density lipoprotein; D000069059:Atorvastatin