Cytokines released by epicardial fat are implicated in the pathogenesis of atherosclerosis. HIV infection and antiretroviral therapy have been associated with changes in body fat distribution and coronary artery disease. We sought to determine whether HIV infection is associated with greater epicardial fat and whether epicardial fat is associated with subclinical coronary atherosclerosis.
We studied 579 HIV-infected and 353 HIV-uninfected men aged 40–70 years with noncontrast computed tomography to measure epicardial adipose tissue (EAT) volume and coronary artery calcium (CAC). Total plaque score (TPS) and plaque subtypes (noncalcified, calcified, and mixed) were measured by coronary computed tomography angiography in 706 men.
We evaluated the association between EAT and HIV serostatus, and the association of EAT with subclinical atherosclerosis, adjusting for age, race, and serostatus and with additional cardiovascular risk factors and tested for modifying effects of HIV serostatus.
HIV-infected men had greater EAT than HIV-uninfected men (P = 0.001). EAT was positively associated with duration of antiretroviral therapy (P = 0.02), specifically azidothymidine (P < 0.05). EAT was associated with presence of any coronary artery plaque (P = 0.006) and noncalcified plaque (P = 0.001), adjusting for age, race, serostatus, and cardiovascular risk factors. Among men with CAC, EAT was associated with CAC extent (P = 0.006). HIV serostatus did not modify associations between EAT and either CAC extent or presence of plaque.
Greater epicardial fat volume in HIV-infected men and its association with coronary plaque and antiretroviral therapy duration suggest potential mechanisms that might lead to increased risk for cardiovascular disease in HIV.
aJohns Hopkins University School of Medicine, Baltimore, Maryland
bLos Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California
cJohns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
dNorthwestern University, Chicago, Illinois
eUniversity of Pittsburgh, Pittsburgh, Pennsylvania, USA.
*Michael Brener and Kerunne Ketlogetswe contributed equally to this work.
Correspondence to Wendy S. Post, MD, MS, The Ciccarone Center for the Prevention of Heart Disease, The Johns Hopkins Hospital, 600 N. Wolfe St., Carnegie 568, Baltimore, MD 21287, USA. Tel: +1 410 955 7376; fax: +1 443 287 0121; e-mail: email@example.com
Received 16 July, 2013
Revised 16 October, 2013
Accepted 16 October, 2013
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