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

AIDS

aDivision 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.

Published: June 2017

Objective: HIV-positive (HIV+) individuals experience an increased burden of coronary artery disease (CAD) not adequately accounted for by traditional CAD risk factors. Coronary endothelial function (CEF), a barometer of vascular health, is depressed early in atherosclerosis and predict future events but has not been studied in HIV+ individuals. We tested whether CEF is impaired in HIV+ patients without CAD as compared with an HIV-negative (HIV-) population matched for cardiac risk factors.

Design/methods: In this observational study, CEF was measured noninvasively by quantifying isometric handgrip exercise-induced changes in coronary vasoreactivity with MRI in 18 participants with HIV but no CAD (HIV+CAD-, based on prior imaging), 36 age-matched and cardiac risk factor-matched healthy participants with neither HIV nor CAD (HIV-CAD-), 41 patients with no HIV but with known CAD (HIV-CAD+), and 17 patients with both HIV and CAD (HIV+CAD+).

Results: CEF was significantly depressed in HIV+CAD- patients as compared with that of risk-factor-matched HIV-CAD- patients (P < 0.0001) and was depressed to the level of that in HIV- participants with established CAD. Mean IL-6 levels were higher in HIV+ participants (P < 0.0001) and inversely related to CEF in the HIV+ patients (P = 0.007).

Conclusion: Marked coronary endothelial dysfunction is present in HIV+ patients without significant CAD and is as severe as that in clinical CAD patients. Furthermore, endothelial dysfunction appears inversely related to the degree of inflammation in HIV+ patients as measured by IL-6. CEF testing in HIV+ patients may be useful for assessing cardiovascular risk and testing new CAD treatment strategies, including those targeting inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5626458PMC
http://dx.doi.org/10.1097/QAD.0000000000001469DOI Listing

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