title: Soluble markers of inflammation are associated with Framingham scores in HIV-infected patients on suppressive antiretroviral therapy.
abstract: OBJECTIVE
  To evaluate the association between biomarkers of inflammation and endothelial dysfunction and Framingham scores (FS) for risk of coronary heart disease (FS-CHD), stroke (FS-Stroke) or any cardiovascular event (FS-CVE) in HIV-infected on suppressive highly active antiretroviral therapy (HAART).
  
  
  METHODS
  A cross-sectional study was conducted in 73 HIV-infected patients and 23 healthy controls. Inflammatory molecules and endothelial dysfunction markers were measured using a multiplex immunoassay (plasminogen activator inhibitor type 1 (PAI-1), soluble TNF receptor type 1 (sTNF-R1), soluble CD40 ligand (sCD40L), soluble E-selectin (sE-selectin), soluble P-selectin (sP-selectin), soluble intercellular adhesion molecules (sICAM-1) and soluble vascular cell adhesion molecule (sVCAM-1). Outcome variables were FS-CHD ≥10%, FS-Stroke ≥5% and FS-CVE ≥10%.
  
  
  RESULTS
  Significant differences (p < 0.05) were found comparing controls and HIV patients for PAI-1 (5.4 vs. 13.5 ng/dL), sTNF-R1 (0.85 vs. 1.09 ng/dL), sICAM-1 (529 vs. 858 ng/dL), sE-selectin (73.7 vs. 120 ng/dL), sP-selectin (676 vs. 1511 ng/dL) sCD40L (76 vs. 307 ng/dL), FS-CHD (4% vs. 7.8% L), FS-Stroke (2% vs. 2.8%) and FS-CVE (5% vs. 11%). In HIV-infected patients, the adjusted logistic regression analysis revealed that sTNF-R1 levels were significantly associated with increased FS-CHD>10% (OR: 11.51 (95% CI: 1.14; 115.84); p = 0.038) and FS-CVE (OR: 12.41 (95% CI: 1.25; 123.23); p = 0.031).
  
  
  CONCLUSIONS
  HIV-infected patients show higher levels of soluble inflammatory and endothelial dysfunction markers than controls and have a two-fold increased FS of presenting coronary heart disease, stroke or cardiovascular events at 10 years. Furthermore, sTNF-R1 displayed the best association with FS of coronary heart disease and any cardiovascular event in our patients.
authors.affiliation: Laboratory of Molecular Epidemiology of Infectious Diseases, Centro Nacional de Microbiología, Instituto de Salud Carlos III (Campus Majadahonda), Carretera Majadahonda-Pozuelo, Km 2.2, 28220 Majadahonda, Madrid, Spain.
authors.forename: María
authors.initials: M
authors.lastname: Guzmán-Fulgencio
authors.forename: Jose
authors.initials: J
authors.lastname: Medrano
authors.forename: Norma
authors.initials: N
authors.lastname: Rallón
authors.forename: Amaya
authors.initials: A
authors.lastname: Echeverria-Urabayen
authors.forename: Jose
authors.initials: J
authors.lastname: Miguel Benito
authors.forename: Clara
authors.initials: C
authors.lastname: Restrepo
authors.forename: Mónica
authors.initials: M
authors.lastname: García-Álvarez
authors.forename: Eugenia
authors.initials: E
authors.lastname: Vispo
authors.forename: Jesus
authors.initials: J
authors.lastname: San Roman
authors.forename: Carlos
authors.initials: C
authors.lastname: Sánchez-Piedra
authors.forename: Vicente
authors.initials: V
authors.lastname: Soriano
authors.forename: Salvador
authors.initials: S
authors.lastname: Resino
mesh_terms: D000328:Adult; D023241:Antiretroviral Therapy, Highly Active / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood*; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000503:physiopathology; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D015658:HIV Infections / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D018570:Risk Assessment / Q000379:methods; D012307:Risk Factors; D013030:Spain
chemical_list: D015415:Biomarkers