title: Untreated HIV infection and large and small artery elasticity.
abstract: BACKGROUND
  Untreated HIV infection may increase risk for cardiovascular disease, and arterial elasticity is a marker of cardiovascular risk and early disease.
  
  
  METHODS
  HIV-infected participants not taking antiretroviral therapy (n=32) were compared with HIV-negative controls (n=30). Large and small artery elasticity (LAE and SAE) were estimated via analysis of radial pulse waveforms. Differences in LAE and SAE by HIV status were compared using analysis of covariance, with and without adjustment for Framingham risk (model 1); covariates that differed between groups [smoking, injection drug use, hepatitis C, and high-density lipoprotein cholesterol (HDLc); model 2]; or age, sex, race/ethnicity, smoking, injection frug use, hepatitis C, HDLc, and non-HDLc (model 3).
  
  
  RESULTS
  HIV infection was associated with impaired LAE (-2.55 mL/mm Hg x 10; P=0.02) and SAE (-1.50 mL/mm Hg x 100; P=0.02). Associations with traditional risk factors were often stronger for SAE than LAE, including with Framingham score (per 1% higher; SAE -0.18, P=0.01; LAE -0.19, P=0.13). Fasting lipid levels were not significantly associated with LAE and SAE. After adjustment, differences between HIV-infected and HIV-uninfected participants were similar in model 1 (-2.36 for LAE, P=0.04; -1.31 for SAE, P=0.04), model 2 (-2.67 for LAE, P=0.02; -1.13 for SAE, P=0.07) and model 3 (-2.91 for LAE, P=0.02; -1.34 for SAE, P=0.03). CD4 count and HIV RNA level were not associated with LAE and SAE among HIV-infected participants.
  
  
  CONCLUSIONS
  Untreated HIV infection is associated with impaired arterial elasticity, of both the large and small vasculature, after controlling for additional risk factors. Pulse waveform analysis is a noninvasive technique to assess cardiovascular disease risk that should be evaluated in larger studies of HIV-infected persons.
authors.affiliation: Department of Medicine, Hennepin County Medical Center, Minneapolis, MN 55415, USA. baker459@umn.edu
authors.forename: Jason V
authors.initials: JV
authors.lastname: Baker
authors.forename: Daniel
authors.initials: D
authors.lastname: Duprez
authors.forename: Joshua
authors.initials: J
authors.lastname: Rapkin
authors.forename: Katherine Huppler
authors.initials: KH
authors.lastname: Hullsiek
authors.forename: Harrison
authors.initials: H
authors.lastname: Quick
authors.forename: Richard
authors.initials: R
authors.lastname: Grimm
authors.forename: James D
authors.initials: JD
authors.lastname: Neaton
authors.forename: Keith
authors.initials: K
authors.lastname: Henry
mesh_terms: D000328:Adult; D001158:Arteries / Q000503:physiopathology*; D001161:Arteriosclerosis / Q000503:physiopathology* / Q000821:virology*; D004548:Elasticity; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors