title: Perivascular fat, inflammation, and cardiovascular risk in HIV-infected patients on antiretroviral therapy.
abstract: BACKGROUND
  HIV-infection is characterized by chronic immune activation that persists despite effective antiretroviral therapy (ART) and is associated with elevated cardiovascular risk. Whether specific perivascular fat depots are associated with inflammation in HIV is unknown.
  
  
  METHODS
  In a cross-sectional study, epicardial (EAT) and thoracic periaortic (TAT) adipose tissue volumes were measured by computed tomography in 100 HIV-infected adults, on stable ART, with LDL-cholesterol ≤130 mg/dL and evidence of heightened T-cell activation (CD8+CD38+HLA-DR+ ≥19%) or increased inflammation (high sensitivity C-reactive protein ≥2 mg/L).
  
  
  RESULTS
  Overall, 77% were males and 70% African American. Mean (standard deviation) age and body mass index were 47 (10) years and 28 (6.4) kg/m(2), respectively. All subjects had HIV-1 RNA <1000 copies/mL with mean (standard deviation) CD4+ T cell count of 665 (280) cells/μL; 50% were on a protease inhibitor. EAT and TAT were correlated with each other (r = 0.766, p < 0.0001). Both were associated with metabolic syndrome, atherogenic lipid profile, insulin resistance, total and central body fat, serum biomarkers of inflammation, and soluble CD163, but not with cellular immune activation markers. In multivariable models that adjusted for age, sex, and other measures of adiposity, both perivascular fat depots were independently associated with the presence of coronary calcium.
  
  
  CONCLUSIONS
  Perivascular fat is associated with soluble CD163, biomarkers of inflammation, insulin resistance, and subclinical atherosclerosis in this population of virologically suppressed HIV-infected patients on ART. The association of perivascular fat with coronary artery calcification appears to be independent of other measures of adiposity.
authors.affiliation: University Hospitals Harrington Heart & Vascular Institute, Division of Cardiology, Case Western Reserve University, Cleveland, OH, USA. Electronic address: chris.longenecker@uhhospitals.org.
authors.forename: Chris T
authors.initials: CT
authors.lastname: Longenecker
authors.forename: Ying
authors.initials: Y
authors.lastname: Jiang
authors.forename: Chun-Ho
authors.initials: CH
authors.lastname: Yun
authors.forename: Sara
authors.initials: S
authors.lastname: Debanne
authors.forename: Nicholas T
authors.initials: NT
authors.lastname: Funderburg
authors.forename: Michael M
authors.initials: MM
authors.lastname: Lederman
authors.forename: Norma
authors.initials: N
authors.lastname: Storer
authors.forename: Danielle E
authors.initials: DE
authors.lastname: Labbato
authors.forename: Hiram G
authors.initials: HG
authors.lastname: Bezerra
authors.forename: Grace A
authors.initials: GA
authors.lastname: McComsey
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000473:pathology*; D000328:Adult; D044966:Anti-Retroviral Agents / Q000009:adverse effects* / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000175:diagnosis / Q000453:epidemiology*; D003430:Cross-Sectional Studies; D004311:Double-Blind Method; D005260:Female; D015658:HIV Infections / Q000188:drug therapy* / Q000453:epidemiology*; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000175:diagnosis / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000187:drug effects / Q000473:pathology; D012307:Risk Factors; D061205:Vascular Calcification / Q000139:chemically induced / Q000175:diagnosis / Q000453:epidemiology
chemical_list: D044966:Anti-Retroviral Agents
keywords: Adipose tissue; Atherosclerosis; HIV; Inflammation; Macrophages