TY - JOUR
T1 - Regional coronary endothelial dysfunction is related to the degree of local epicardial fat in people with HIV
AU - Iantorno, Micaela
AU - Soleimanifard, Sahar
AU - Schär, Michael
AU - Brown, Todd T.
AU - Bonanno, Gabriele
AU - Crovo, Patricia
AU - Mathews, Lena
AU - Lai, Shenghan
AU - Gerstenblith, Gary
AU - Weiss, Robert G.
AU - Hays, Allison G.
N1 - Funding Information:
Work supported by NHLBI grants HL120905 and HL125059, American Heart Association (17GRNT33670943) and Johns Hopkins University Center for AIDS Research (P30AI094189).
Funding Information:
Work supported by NHLBI grants HL120905 and HL125059 , American Heart Association ( 17GRNT33670943 ) and Johns Hopkins University Center for AIDS Research ( P30AI094189 ).
Publisher Copyright:
© 2018 Elsevier B.V.
PY - 2018/11
Y1 - 2018/11
N2 - 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.
AB - 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.
KW - Coronary endothelial function
KW - Epicardial fat
KW - HIV
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U2 - 10.1016/j.atherosclerosis.2018.08.002
DO - 10.1016/j.atherosclerosis.2018.08.002
M3 - Article
C2 - 30227267
AN - SCOPUS:85053317863
VL - 278
SP - 7
EP - 14
JO - Atherosclerosis
JF - Atherosclerosis
SN - 0021-9150
ER -