title: Endothelial function in HIV-infected patients receiving protease inhibitor therapy: does immune competence affect cardiovascular risk?
abstract: BACKGROUND
  The use of HIV protease inhibitors (PIs) as a component of combination antiretroviral therapy in HIV-infected patients has been associated with dyslipidaemia, but its significance as a risk factor for cardiovascular disease is unclear. Endothelial dysfunction is an early phase of atherogenesis that may be assessed non-invasively with ultrasonography in vivo.
  
  
  OBJECTIVE
  To evaluate vascular function and investigate potential determinants of endothelial dysfunction of the peripheral circulation in PI-treated, HIV-infected men with dyslipidaemia.
  
  
  METHODS
  Observational, case-control study.
  
  
  METHODS
  We studied 24 HIV-infected, PI-treated men with dyslipidaemia and 24 normolipidaemic, healthy male controls matched for age and body mass index. Brachial artery endothelial function was studied using high-resolution ultrasound and computerized edge-detection software. This non-invasive technique measured post-ischaemic flow-mediated dilatation (FMD), and the endothelium-independent vasodilatory response to glyceryl trinitrate (GTN).
  
  
  RESULTS
  Within the HIV patient group, FMD was significantly associated with percentage of 'naïve' CD4 + 45RA + T cells (p = 0.03), while plasma lipid/lipoprotein and insulin levels, body mass, and smoking status did not correlate with endothelial function. FMD was not significantly different between the study group and the controls.
  
  
  CONCLUSIONS
  The atherogenic potential of PI-associated dyslipidaemia may be attenuated in HIV-infected patients with decreased immune competence, reflecting a possible contribution of cell-mediated immune responses to the pathogenesis of atherosclerosis.
authors.affiliation: Centre for Clinical Immunology and Biomedical Statistics, Royal Perth Hospital and Murdoch University, Western Australia, Australia.
authors.forename: D
authors.initials: D
authors.lastname: Nolan
authors.forename: G F
authors.initials: GF
authors.lastname: Watts
authors.forename: S E
authors.initials: SE
authors.lastname: Herrmann
authors.forename: M A
authors.initials: MA
authors.lastname: French
authors.forename: M
authors.initials: M
authors.lastname: John
authors.forename: S
authors.initials: S
authors.lastname: Mallal
mesh_terms: D000328:Adult; D015992:Body Mass Index; D018791:CD4 Lymphocyte Count; D002318:Cardiovascular Diseases / Q000139:chemically induced*; D016022:Case-Control Studies; D004108:Dilatation, Pathologic / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D017320:HIV Protease Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D006801:Humans; D007121:Immunocompetence / Q000502:physiology; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008297:Male; D012307:Risk Factors; D012907:Smoking; D018709:Statistics, Nonparametric; D014664:Vasodilation / Q000502:physiology
chemical_list: D017320:HIV Protease Inhibitors; D007328:Insulin; D008055:Lipids; D008074:Lipoproteins