title: Carotid intimal medial thickness in human immunodeficiency virus-infected women: effects of protease inhibitor use, cardiac risk factors, and the metabolic syndrome.
abstract: BACKGROUND
  Little is known regarding carotid intimal medial thickness (IMT) in HIV-infected women and the risk factors for subclinical atherosclerosis in this population, including antiretroviral therapy and the metabolic syndrome.
  
  
  OBJECTIVE
  Our objective was to assess carotid IMT in relationship to HIV status and antiretroviral therapy in HIV-infected women in comparison with healthy age- and body mass index (BMI)-matched control subjects.
  
  
  METHODS
  The study took place at an academic medical center and included 97 HIV-infected women compared with 86 age- and BMI-matched healthy control subjects.
  
  
  METHODS
  We assessed carotid IMT, metabolic syndrome, and risk factors for increased IMT.
  
  
  RESULTS
  Carotid IMT was not increased in HIV-infected women [0.62 mm (0.57-0.68); median (IQR)] compared with non-HIV-infected women [0.61 mm (0.55-0.68)] matched for age and BMI (P = 0.07) but was increased significantly among HIV patients receiving a protease inhibitor (PI) [0.65 (0.59-0.71) mm] vs. non-PI-treated patients [0.61 (0.57-0.66) mm] (P < 0.05) and vs. control subjects [0.61 (0.55-0.68) mm] (P < 0.05). The prevalence of metabolic syndrome was significantly increased among the HIV-infected women compared with control subjects and particularly in PI- vs. non-PI-treated HIV patients (45 vs. 19%, P = 0.001). Metabolic syndrome score correlated with IMT among non-HIV patients but not among the HIV group. Individual risk factors most strongly associated with IMT in multivariate regression modeling in the control group were age and waist-to-hip ratio, and among the HIV group age and waist circumference.
  
  
  CONCLUSIONS
  These data demonstrate increased carotid IMT in HIV-infected women receiving PI therapy, which may be due to associated metabolic abnormalities related to PI therapy or more direct effects of this medication class on the vasculature. Additional studies of the mechanisms by which PI uses results in subclinical atherosclerosis are needed.
authors.affiliation: Program in Nutritional Metabolism, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
authors.forename: Stine
authors.initials: S
authors.lastname: Johnsen
authors.forename: Sara E
authors.initials: SE
authors.lastname: Dolan
authors.forename: Kathleen V
authors.initials: KV
authors.lastname: Fitch
authors.forename: Jenna R
authors.initials: JR
authors.lastname: Kanter
authors.forename: Linda C
authors.initials: LC
authors.lastname: Hemphill
authors.forename: Jean M
authors.initials: JM
authors.lastname: Connelly
authors.forename: Robert S
authors.initials: RS
authors.lastname: Lees
authors.forename: Hang
authors.initials: H
authors.lastname: Lee
authors.forename: Steve
authors.initials: S
authors.lastname: Grinspoon
mesh_terms: D000328:Adult; D044966:Anti-Retroviral Agents / Q000494:pharmacology / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000150:complications; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D001823:Body Composition / Q000187:drug effects; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy / Q000473:pathology*; D006801:Humans; D024821:Metabolic Syndrome / Q000150:complications*; D008875:Middle Aged; D015999:Multivariate Analysis; D011480:Protease Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D011859:Radiography; D012307:Risk Factors; D017539:Tunica Intima / Q000187:drug effects / Q000473:pathology; D017540:Tunica Media / Q000187:drug effects / Q000473:pathology
chemical_list: D044966:Anti-Retroviral Agents; D015415:Biomarkers; D011480:Protease Inhibitors