title: Increased carotid intima-media thickness in HIV patients treated with protease inhibitors as compared to non-nucleoside reverse transcriptase inhibitors.
abstract: BACKGROUND
  Prolonged exposure to protease inhibitor (PI)-, but not non-nucleoside reverse transcriptase inhibitor (NNRTI)-containing combination antiretroviral therapy (CART) has been associated with an increased cardiovascular risk, partly explained by the different effects of these drugs on plasma lipids. Most markedly, NNRTIs have been associated with increases in high density lipoprotein cholesterol (HDL-C), which may be atheroprotective.
  
  
  METHODS
  In a cross-sectional study we investigated the impact of PI- vs. NNRTI-based CART in 130 HIV-1-infected patients with plasma virus suppressed to below the limit of detection, whom had been continuously exposed for at least 2 years to either one of such regimens, but not both. Carotid intima-media thickness (C-IMT) and fasting metabolic parameters were measured.
  
  
  RESULTS
  Mean (+/-S.D.) C-IMT in patients treated with PI-based CART was 0.81 (+/-0.17) mm as compared to 0.71 (+/-0.14)mm in NNRTI treated patients (p=0.0003). HDL-C and apolipoprotein A-I (apoA-I) levels were higher in the NNRTI than in the PI group (1.39 mmol/L vs. 1.03 mmol/L; p<0.0001, and 1.44 mmol/L vs. 1.33 mmol/L; p=0.0008, respectively). Framingham Risk Score, body mass index, duration of CART, and use of PI-based CART were positively correlated with C-IMT whereas HDL-C and apoA-I were inversely correlated with C-IMT.
  
  
  CONCLUSIONS
  Treatment of HIV-1-infected patients for 2 years or more with PI-based compared to NNRTI-based CART is associated with greater C-IMT, consistent with the reported higher risk of CVD in patients using PI. However, this difference seems not fully explained by a more favorable impact of NNRTI-based CART on HDL-C and apoA-I levels.
authors.affiliation: Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Raaj R
authors.initials: RR
authors.lastname: Sankatsing
authors.forename: Ferdinand W
authors.initials: FW
authors.lastname: Wit
authors.forename: Martin
authors.initials: M
authors.lastname: Vogel
authors.forename: Eric
authors.initials: E
authors.lastname: de Groot
authors.forename: Kees
authors.initials: K
authors.lastname: Brinkman
authors.forename: Juergen K
authors.initials: JK
authors.lastname: Rockstroh
authors.forename: John J P
authors.initials: JJ
authors.lastname: Kastelein
authors.forename: Erik S G
authors.initials: ES
authors.lastname: Stroes
authors.forename: Peter
authors.initials: P
authors.lastname: Reiss
mesh_terms: D000328:Adult; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000453:epidemiology*; D008076:Cholesterol, HDL / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000453:epidemiology*; D017320:HIV Protease Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D015497:HIV-1; D006801:Humans; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D018894:Reverse Transcriptase Inhibitors / Q000008:administration & dosage / Q000009:adverse effects*; D012307:Risk Factors; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography
chemical_list: D008076:Cholesterol, HDL; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors