title: Acute systemic inflammation induced by influenza A (H1N1) vaccination causes a deterioration in endothelial function in HIV-infected patients.
abstract: OBJECTIVE
  Vaccination of HIV-infected patients against the influenza A/H1N1 subtype was proposed as a mandatory precautionary measure during the 2009 pandemic. The immediate cardiovascular effects of the novel vaccine have been largely unexplored. We investigated the impact of vaccination on indices of endothelial function in a cohort of HIV-infected patients.
  
  
  METHODS
  We included 24 HIV-infected patients in a study with a randomized, sham procedure-controlled design. A monovalent, adjuvanted vaccine against influenza A/H1N1 was used in the vaccine arm (n=16); patients in the control group (n=8) were subjected to a sham procedure. Endothelial function, as assessed by flow-mediated dilatation (FMD), and inflammatory markers were assessed prior to and 8 and 48 h post vaccination.
  
  
  RESULTS
  FMD deteriorated following vaccination (baseline, 6.5 ± 1.1%; 8 h, 1.1 ± 1.5%; 48 h, 2.0 ± 1.4%; P=0.04). The white blood cell count increased at 8 h and remained elevated at 48 h. Soluble intercellular adhesion molecule-1 levels decreased after vaccination; the maximum decrease was noted at 48 h. Conversely, the sham procedure did not induce changes in endothelial function or inflammatory markers, apart from a reduction in the white blood cell count at 48 h.
  
  
  CONCLUSIONS
  Acute systemic inflammation induced by vaccination against the influenza A/H1N1 virus resulted in a deterioration in endothelial function in HIV-infected patients, and this effect was sustained for at least 48 h. Our findings may have important implications in view of the high cardiovascular risk that HIV infection carries. The effect of the novel vaccine on endothelial function should be weighed against the immunological protection that it confers.
authors.affiliation: 1st Cardiology Department, Athens Medical School, Hippokration Hospital, Athens, Greece. cvlachop@otenet.gr
authors.forename: C
authors.initials: C
authors.lastname: Vlachopoulos
authors.forename: P
authors.initials: P
authors.lastname: Xaplanteris
authors.forename: H
authors.initials: H
authors.lastname: Sambatakou
authors.forename: E
authors.initials: E
authors.lastname: Mariolis
authors.forename: A
authors.initials: A
authors.lastname: Bratsas
authors.forename: E
authors.initials: E
authors.lastname: Christoforatou
authors.forename: A
authors.initials: A
authors.lastname: Miliou
authors.forename: K
authors.initials: K
authors.lastname: Aznaouridis
authors.forename: C
authors.initials: C
authors.lastname: Stefanadis
mesh_terms: D017088:AIDS-Related Opportunistic Infections / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D000328:Adult; D018791:CD4 Lymphocyte Count; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology* / Q000503:physiopathology; D005500:Follow-Up Studies; D015658:HIV Infections / Q000150:complications / Q000276:immunology*; D006801:Humans; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology*; D007252:Influenza Vaccines / Q000009:adverse effects*; D007251:Influenza, Human / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects / Q000276:immunology*; D008297:Male
chemical_list: D007252:Influenza Vaccines; D018799:Intercellular Adhesion Molecule-1