Suman Srinivasa1, Michael T Lu2, Kathleen V Fitch1, Travis R Hallett2,3, Timothy K O'Malley1, Lauren A Stone1, Amanda Martin1,4, Alexandra J Coromilas1, Tricia H Burdo5, Virginia A Triant1,6, Janet Lo1, Sara E Looby1,7, Tomas G Neilan2, Markella V Zanni1. 1. Program in Nutritional Metabolism, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 2. Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 3. Boston University School of Medicine, Boston, MA, USA. 4. University of Texas at Houston, Houston, TX, USA. 5. Department of Neuroscience, Temple University School of Medicine, Philadelphia, PA, USA. 6. Division of Infectious Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 7. Yvonne L Munn Center for Nursing Research, Massachusetts General Hospital, Boston, MA, USA.
Abstract
BACKGROUND: Mechanisms underlying the heightened myocardial infarction risk among HIV-infected women (versus non-HIV-infected women) remain unclear. Our objectives were to assess epicardial adipose tissue (EAT) volume and its associations among asymptomatic women with and without HIV. METHODS: A total of 55 HIV-infected and 27 non-HIV-infected women without known cardiovascular disease who underwent cardiac CT and metabolic/immune phenotyping were included. EAT volume derived from CT was compared among women with and without HIV, and within-group EAT associations were assessed. Next, immune and atherosclerotic plaque parameters were compared among groups stratified by HIV serostatus and high/low EAT (defined in reference to median EAT for each serostatus group). RESULTS: Asymptomatic HIV-infected women and age-matched non-HIV-infected women with comparable mean body mass index (28 ±1 versus 29 ±1 kg/m2) had similar median (IQR) volumes of EAT (54 [41-79] versus 65 [41-78] cm3; P>0.05); however, different within-group associations were noted. Markers of monocyte activation/arterial inflammation differed by HIV serostatus/EAT volume subgroup (CXCL10 [P=0.02], sCD163 [P=0.004], sCD14 [P=0.03], Lp-PLA2 [P=0.04]; P for overall ANOVA) and were highest among HIV-infected women with excess EAT (versus HIV-infected women without excess EAT, non-HIV-infected women with excess EAT and non-HIV-infected women without excess EAT). The percentage of segments with non-calcified coronary plaque also differed by HIV serostatus/EAT volume subgroup and was highest among HIV-infected women with excess EAT. CONCLUSIONS: Asymptomatic women with and without HIV have similar volumes of EAT, but drivers of EAT may differ between groups. HIV-infected women with excess EAT have highest-level immune activation and the highest percentage of non-calcified plaque. Future studies are needed to determine whether EAT contributes pathogenetically to HIV-associated cardiovascular disease in women.
BACKGROUND: Mechanisms underlying the heightened myocardial infarction risk among HIV-infectedwomen (versus non-HIV-infectedwomen) remain unclear. Our objectives were to assess epicardial adipose tissue (EAT) volume and its associations among asymptomatic women with and without HIV. METHODS: A total of 55 HIV-infected and 27 non-HIV-infectedwomen without known cardiovascular disease who underwent cardiac CT and metabolic/immune phenotyping were included. EAT volume derived from CT was compared among women with and without HIV, and within-group EAT associations were assessed. Next, immune and atherosclerotic plaque parameters were compared among groups stratified by HIV serostatus and high/low EAT (defined in reference to median EAT for each serostatus group). RESULTS: Asymptomatic HIV-infectedwomen and age-matched non-HIV-infectedwomen with comparable mean body mass index (28 ±1 versus 29 ±1 kg/m2) had similar median (IQR) volumes of EAT (54 [41-79] versus 65 [41-78] cm3; P>0.05); however, different within-group associations were noted. Markers of monocyte activation/arterial inflammation differed by HIV serostatus/EAT volume subgroup (CXCL10 [P=0.02], sCD163 [P=0.004], sCD14 [P=0.03], Lp-PLA2 [P=0.04]; P for overall ANOVA) and were highest among HIV-infectedwomen with excess EAT (versus HIV-infectedwomen without excess EAT, non-HIV-infectedwomen with excess EAT and non-HIV-infectedwomen without excess EAT). The percentage of segments with non-calcified coronary plaque also differed by HIV serostatus/EAT volume subgroup and was highest among HIV-infectedwomen with excess EAT. CONCLUSIONS: Asymptomatic women with and without HIV have similar volumes of EAT, but drivers of EAT may differ between groups. HIV-infectedwomen with excess EAT have highest-level immune activation and the highest percentage of non-calcified plaque. Future studies are needed to determine whether EAT contributes pathogenetically to HIV-associated cardiovascular disease in women.
Authors: Amir A Mahabadi; Marie H Berg; Nils Lehmann; Hagen Kälsch; Marcus Bauer; Kaffer Kara; Nico Dragano; Susanne Moebus; Karl-Heinz Jöckel; Raimund Erbel; Stefan Möhlenkamp Journal: J Am Coll Cardiol Date: 2013-02-20 Impact factor: 24.094
Authors: Guido A Rosito; Joseph M Massaro; Udo Hoffmann; Frederick L Ruberg; Amir A Mahabadi; Ramachandran S Vasan; Christopher J O'Donnell; Caroline S Fox Journal: Circulation Date: 2008-01-22 Impact factor: 29.690
Authors: Mabel Toribio; Tomas G Neilan; Magid Awadalla; Lauren A Stone; Adam Rokicki; Corinne Rivard; Connor P Mulligan; Diana Cagliero; Lindsay T Fourman; Takara L Stanley; Jennifer E Ho; Virginia A Triant; Tricia H Burdo; Michael D Nelson; Lidia S Szczepaniak; Markella V Zanni Journal: J Clin Endocrinol Metab Date: 2019-12-01 Impact factor: 5.958