title: Arterial inflammation in patients with HIV.
abstract: BACKGROUND
  Cardiovascular disease is increased in patients with human immunodeficiency virus (HIV), but the specific mechanisms are unknown.
  
  
  OBJECTIVE
  To assess arterial wall inflammation in HIV, using 18fluorine-2-deoxy-D-glucose positron emission tomography (18F-FDG-PET), in relationship to traditional and nontraditional risk markers, including soluble CD163 (sCD163), a marker of monocyte and macrophage activation.
  
  
  METHODS
  A cross-sectional study of 81 participants investigated between November 2009 and July 2011 at the Massachusetts General Hospital. Twenty-seven participants with HIV without known cardiac disease underwent cardiac 18F-FDG-PET for assessment of arterial wall inflammation and coronary computed tomography scanning for coronary artery calcium. The HIV group was compared with 2 separate non-HIV control groups. One control group (n = 27) was matched to the HIV group for age, sex, and Framingham risk score (FRS) and had no known atherosclerotic disease (non-HIV FRS-matched controls). The second control group (n = 27) was matched on sex and selected based on the presence of known atherosclerotic disease (non-HIV atherosclerotic controls).
  
  
  METHODS
  Arterial inflammation was prospectively determined as the ratio of FDG uptake in the arterial wall of the ascending aorta to venous background as the target-to-background ratio (TBR).
  
  
  RESULTS
  Participants with HIV demonstrated well-controlled HIV disease (mean [SD] CD4 cell count, 641 [288] cells/μL; median [interquartile range] HIV-RNA level, <48 [<48 to <48] copies/mL). All were receiving antiretroviral therapy (mean [SD] duration, 12.3 [4.3] years). The mean FRS was low in both HIV and non-HIV FRS-matched control participants (6.4; 95% CI, 4.8-8.0 vs 6.6; 95% CI, 4.9-8.2; P = .87). Arterial inflammation in the aorta (aortic TBR) was higher in the HIV group vs the non-HIV FRS-matched control group (2.23; 95% CI, 2.07-2.40 vs 1.89; 95% CI, 1.80-1.97; P < .001), but was similar compared with the non-HIV atherosclerotic control group (2.23; 95% CI, 2.07-2.40 vs 2.13; 95% CI, 2.03-2.23; P = .29). Aortic TBR remained significantly higher in the HIV group vs the non-HIV FRS-matched control group after adjusting for traditional cardiovascular risk factors (P = .002) and in stratified analyses among participants with undetectable viral load, zero calcium, FRS of less than 10, a low-density lipoprotein cholesterol level of less than 100 mg/dL (<2.59 mmol/L), no statin use, and no smoking (all P ≤ .01). Aortic TBR was associated with sCD163 level (P = .04) but not with C-reactive protein (P = .65) or D-dimer (P = .08) among patients with HIV.
  
  
  CONCLUSIONS
  Participants infected with HIV vs noninfected control participants with similar cardiac risk factors had signs of increased arterial inflammation, which was associated with a circulating marker of monocyte and macrophage activation.
authors: MR-PET-CT Program and Department of Imaging, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
authors: Sharath
authors: S
authors: Subramanian
authors: Ahmed
authors: A
authors: Tawakol
authors: Tricia H
authors: TH
authors: Burdo
authors: Suhny
authors: S
authors: Abbara
authors: Jeffrey
authors: J
authors: Wei
authors: Jayanthi
authors: J
authors: Vijayakumar
authors: Erin
authors: E
authors: Corsini
authors: Amr
authors: A
authors: Abdelbaky
authors: Markella V
authors: MV
authors: Zanni
authors: Udo
authors: U
authors: Hoffmann
authors: Kenneth C
authors: KC
authors: Williams
authors: Janet
authors: J
authors: Lo
authors: Steven K
authors: SK
authors: Grinspoon
mesh_terms: D015703:Antigens, CD / Q000097:blood; D015214:Antigens, Differentiation, Myelomonocytic / Q000097:blood; D001011:Aorta / Q000000981:diagnostic imaging* / Q000473:pathology*; D015415:Biomarkers / Q000097:blood; D002318:Cardiovascular Diseases / Q000209:etiology*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D019788:Fluorodeoxyglucose F18; D015658:HIV Infections / Q000150:complications* / Q000276:immunology; D006801:Humans; D007249:Inflammation; D008262:Macrophage Activation; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D049268:Positron-Emission Tomography; D011956:Receptors, Cell Surface / Q000097:blood; D012307:Risk Factors; D000098902:CD163 Antigen
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D000098902:CD163 Antigen; D011956:Receptors, Cell Surface; D019788:Fluorodeoxyglucose F18