Micaela Iantorno1, Sahar Soleimanifard2, Michael Schär3, Todd T Brown4, Gabriele Bonanno3, Patricia Barditch-Crovo5, Lena Mathews6, Shenghan Lai7, Gary Gerstenblith6, Robert G Weiss6, Allison G Hays8. 1. Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, MD, USA; Critical Care Medicine Department, National Institutes of Health, Bethesda, MD, USA. 2. Department of Radiology, Division of Magnetic Resonance Research, Johns Hopkins University, Baltimore, MD, USA; Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD, USA. 3. Department of Radiology, Division of Magnetic Resonance Research, Johns Hopkins University, Baltimore, MD, USA. 4. Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University, Baltimore, MD, USA. 5. Department of Medicine, Division of Infectious Diseases, Johns Hopkins University, Baltimore, MD, USA. 6. Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, MD, USA. 7. Department of Pathology, Johns Hopkins University, Baltimore, MD, USA. 8. Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, MD, USA. Electronic address: ahays2@jhmi.edu.
Abstract
BACKGROUND AND AIMS: Coronary artery disease (CAD) is now an important cause of premature death in people with HIV but the causes of accelerated CAD are poorly understood. Epicardial adipose tissue (EAT) is metabolically-active and thought to contribute to CAD development. We tested the hypothesis that abnormal coronary endothelial function (CEF), an early marker and mediator of atherosclerosis, is related to the amount of local pericoronary EAT in HIV. METHODS: We studied 36 participants with HIV and no CAD (HIV+ CAD-), 15 participants with HIV and known CAD (HIV+ CAD+), and 14 age-matched, healthy participants without HIV (HIV-CAD-). To measure CEF, coronary MRI was performed before and during isometric handgrip exercise (IHE), an endothelial-dependent stressor. EAT was measured with MRI at the same imaging plane as CEF. RESULTS: CEF was significantly depressed, as measured by IHE-induced % coronary cross sectional area (CSA) change, in HIV+ CAD- and HIV+ CAD+ as compared to HIV-CAD-participants (p<0.0001). EAT thickness was significantly greater in HIV+ CAD- and HIV+ CAD+ participants as compared to HIV-CAD-participants (p=0.001). There was a significant inverse relationship between CEF and local EAT thickness and area (R = -0.48 and R = -0.51 respectively, p<0.0001 for both) among participants with HIV even after adjustment for cardiovascular risk factors. In participants with multiple CEF measures, CEF was lower in segments with higher EAT, other factors being equivalent. CONCLUSIONS: There is a significant relationship between increased metabolically-active EAT and depressed local CEF in people with HIV, consistent with the hypothesis that increased epicardial fat contributes to accelerated CAD in persons with HIV.
BACKGROUND AND AIMS: Coronary artery disease (CAD) is now an important cause of premature death in people with HIV but the causes of accelerated CAD are poorly understood. Epicardial adipose tissue (EAT) is metabolically-active and thought to contribute to CAD development. We tested the hypothesis that abnormal coronary endothelial function (CEF), an early marker and mediator of atherosclerosis, is related to the amount of local pericoronary EAT in HIV. METHODS: We studied 36 participants with HIV and no CAD (HIV+ CAD-), 15 participants with HIV and known CAD (HIV+ CAD+), and 14 age-matched, healthy participants without HIV (HIV-CAD-). To measure CEF, coronary MRI was performed before and during isometric handgrip exercise (IHE), an endothelial-dependent stressor. EAT was measured with MRI at the same imaging plane as CEF. RESULTS:CEF was significantly depressed, as measured by IHE-induced % coronary cross sectional area (CSA) change, in HIV+ CAD- and HIV+ CAD+ as compared to HIV-CAD-participants (p<0.0001). EAT thickness was significantly greater in HIV+ CAD- and HIV+ CAD+participants as compared to HIV-CAD-participants (p=0.001). There was a significant inverse relationship between CEF and local EAT thickness and area (R = -0.48 and R = -0.51 respectively, p<0.0001 for both) among participants with HIV even after adjustment for cardiovascular risk factors. In participants with multiple CEF measures, CEF was lower in segments with higher EAT, other factors being equivalent. CONCLUSIONS: There is a significant relationship between increased metabolically-active EAT and depressed local CEF in people with HIV, consistent with the hypothesis that increased epicardial fat contributes to accelerated CAD in persons with HIV.
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