2160. HIV infection, Antiretroviral Therapy, and Measures of Endothelial Function, Inflammation, Metabolism, and Oxidative Stress.
Session: Poster Abstract Session: HIV Inflammation and Immune Activation
Saturday, October 29, 2016
Room: Poster Hall
Posters
  • poster 2160.pdf (430.2 kB)
  • Background:

    People with HIV have an increased risk of cardiovascular disease (CVD). Impaired endothelial function is an early risk factor for CVD in the general population. It is presumed that HIV infection is associated with impaired endothelial function, but results have been inconsistent due to differences in methodologies. Our objectives were to determine the relationships between HIV infection, virological suppression with antiretroviral therapy (ART), in vivo measures of endothelial function, and circulating biomarkers of pathways associated with CVD.

    Methods:

    We performed a cross-sectional analysis of three prospectively enrolled groups from a single center: 28 were HIV-infected and virologically-suppressed on a regimen of FTC/TDF/EFV (HIV+ART+), 44 were HIV-infected but not on ART (HIV+ART-), and 39 were HIV-uninfected healthy volunteers (HIV-). None had diabetes, uncontrolled hypertension, known CVD, or other pro-inflammatory condition. Flow mediated dilation (FMD), nitroglycerin-mediated dilation (NTGMD), reactive hyperemia velocity time integral (RHVTI), and FMD/RHVTI of the brachial artery were measured, as well as circulating biomarkers of systemic inflammation, metabolism, oxidative stress, and endothelial activation.

    Results:

    No significant differences were found amongst the three groups in FMD (P=0.46), NTGMD (P=0.42), RHVTI (P=0.17), and FMD/RHVTI (P=0.22) in unadjusted and adjusted ANOVA models which included brachial artery diameter, demographics, and conventional CVD risk factors. In pairwise comparisons, the HIV+ART- group had significantly higher soluble tumor necrosis factor receptor II, soluble CD163, β-2 microglobulin, interferon-γ- induced protein-10, tissue inhibitor of metalloproteinase-1, and vascular cell adhesion molecule-1 compared to the other two groups (all p<0.05).

    Conclusion:

    Although untreated HIV infection was associated with elevated levels of several biomarkers of inflammation and endothelial activation, we were unable to demonstrate differences in measures of endothelial function. We did not find evidence that impaired FMD or RHVTI are underlying factors for the increased risk of CVD associated with HIV.

    Andrew Dysangco, MD, Medicine, Indiana University, School of Medicine, Indianapolis, IN, Ziyue Liu, PhD, Biostatistics, Indiana University School of Public Health and School of Medicine, Indianapolis, IN, James Stein, MD, University of Wisconsin School of Medicine and Public Health, MADISON, WI, Michael Dube, MD, Keck School of Medicine, University of Southern California, Los Angeles, CA, Lisa Kamendulis, PhD, Environmental Health, Indiana University, Bloomington, IN, Matthias Clauss, PhD, Indiana University School of Medicine, Indianapolis, IN and Samir Gupta, MD, MS, Medicine/Infectious Diseases, Indiana University School of Medicine, Indianapolis, IN

    Disclosures:

    A. Dysangco, None

    Z. Liu, None

    J. Stein, Gilead: Research Contractor , Grant recipient

    M. Dube, None

    L. Kamendulis, None

    M. Clauss, None

    S. Gupta, Gilead Sciences: Grant Investigator , Investigator and Scientific Advisor , Consulting fee , Research grant , Research support and Travel support to scientific conferences
    Bristol-Myers Squibb: Investigator , Research support and Travel support to scientific conferences
    Janssen Therapeutics: Grant Investigator and Investigator , Research grant and Research support

    Findings in the abstracts are embargoed until 12:01 a.m. CDT, Wednesday Oct. 26th with the exception of research findings presented at the IDWeek press conferences.