Coronary artery endothelial dysfunction is present in HIV-positive individuals without significant coronary artery

Micaela Iantorno1, Michael Schär, Sahar Soleimanifard

  • 1aDivision of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore bCritical Care Medicine Department, National Institutes of Health, Bethesda cDivision of Magnetic Resonance Research, Department of Radiology, Johns Hopkins University, Baltimore, Maryland dDepartment of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, Maryland eDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Johns Hopkins University, Baltimore, Maryland fDivision of Infectious Diseases, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA gDepartment of Radiology, Centre Hospitalier Universitaire Vaudois, Center for Biomedical Imaging (CIBM) and University of Lausanne, Lausanne, Switzerland hDepartment of Pathology, Johns Hopkins University, Baltimore, Maryland, USA.

AIDS (London, England)
|March 30, 2017
PubMed

Insights

Coronary endothelial dysfunction is significantly present in HIV-positive individuals without coronary artery disease, similar to patients with established disease. This dysfunction is linked to inflammation, suggesting new treatment avenues.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Vascular Biology

Background:

  • Individuals with HIV (HIV+) have a higher burden of coronary artery disease (CAD) than expected by traditional risk factors.
  • Coronary endothelial function (CEF) is a key indicator of vascular health, declining early in atherosclerosis and predicting cardiovascular events.
  • CEF has not been previously studied in HIV+ individuals.

Purpose of the Study:

  • To investigate whether CEF is impaired in HIV+ individuals without diagnosed CAD.
  • To compare CEF in HIV+ individuals without CAD to a matched HIV-negative (HIV-) population with similar cardiac risk factors.

Main Methods:

  • An observational study measured CEF noninvasively using MRI-quantified coronary vasoreactivity during isometric handgrip exercise.
  • Participants included HIV+ individuals without CAD (HIV+CAD-), HIV- individuals without CAD (HIV-CAD-), HIV- individuals with CAD (HIV-CAD+), and HIV+ individuals with CAD (HIV+CAD+).
  • Interleukin-6 (IL-6) levels were measured as a marker of inflammation.

Main Results:

  • CEF was significantly depressed in HIV+CAD- patients compared to risk-factor-matched HIV-CAD- patients (P < 0.0001).
  • The CEF impairment in HIV+CAD- patients was comparable to that observed in HIV- participants with established CAD.
  • Higher IL-6 levels were found in HIV+ participants (P < 0.0001) and were inversely correlated with CEF in this group (P = 0.007).

Conclusions:

  • Significant coronary endothelial dysfunction exists in HIV+ patients even without substantial CAD, mirroring dysfunction seen in patients with clinical CAD.
  • Endothelial dysfunction in HIV+ patients appears to be inversely related to inflammation, as indicated by IL-6 levels.
  • CEF assessment in HIV+ patients could aid cardiovascular risk stratification and the development of novel CAD treatments, potentially targeting inflammation.
Abstract

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