R M Brusca1, D B Hanna2, N I Wada3, J N Blankson1, M D Witt4, L P Jacobson3, L Kingsley5, F J Palella6, M Budoff4, T T Brown1,3, K Anastos2,7, J M Lazar8, W J Mack9, P Bacchetti10, P C Tien11,12, Y Golzar13, M Plankey14, E Golub3, R C Kaplan2,15, W S Post1,3. 1. Johns Hopkins University School of Medicine, Baltimore, MD, USA. 2. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA. 3. Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. 4. Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA. 5. University of Pittsburgh, Pittsburgh, PA, USA. 6. Northwestern University, Chicago, IL, USA. 7. Department of Medicine, Montefiore Medical Center, Bronx, NY, USA. 8. Department of Medicine, SUNY-Downstate Medical Center, Brooklyn, NY, USA. 9. Preventive Medicine, University of Southern California, Los Angeles, CA, USA. 10. Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, USA. 11. Department of Medicine and Clinical Pharmacy, University of California, San Francisco, CA, USA. 12. Department of Veterans Affairs Medical Center, San Francisco, CA, USA. 13. Cook County Health and Hospital System, Chicago, IL, USA. 14. Department of Medicine, Division of Infectious Diseases, Georgetown University Medical Center, Washington, DC, USA. 15. Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Abstract
OBJECTIVES: Elite controllers (ECs), viraemic controllers (VCs), and long-term nonprogressors (LTNPs) control HIV viral replication or maintain CD4 T-cell counts without antiretroviral therapy, but may have increased cardiovascular disease (CVD) risk compared to HIV-uninfected persons. We evaluated subclinical carotid and coronary atherosclerosis and inflammatory biomarker levels among HIV controllers, LTNPs and noncontrollers and HIV-uninfected individuals in the Multicenter AIDS Cohort Study (MACS) and the Women's Interagency HIV Study (WIHS). METHODS: We measured carotid plaque presence and common carotid artery intima-media thickness (IMT) in 1729 women and 1308 men, and the presence of coronary artery calcium and plaque in a subgroup of men. Associations between HIV control category and carotid and coronary plaque prevalences were assessed by multivariable regression analyses adjusting for demographics and CVD risk factors. Serum inflammatory biomarker concentrations [soluble CD163 (sCD163), soluble CD14 (sCD14), galectin-3 (Gal-3), galectin-3 binding protein (Gal-3BP) and interleukin (IL)-6] were measured and associations with HIV control category assessed. RESULTS: We included 135 HIV controllers (30 ECs) and 135 LTNPs in the study. Carotid plaque prevalence and carotid IMT were similar in HIV controllers, LTNPs and HIV-uninfected individuals. HIV controllers and LTNPs had lower prevalences of carotid plaque compared to viraemic HIV-infected individuals. The prevalence of coronary atherosclerosis was similar in HIV controllers/LTNPs compared to HIV-uninfected and viraemic HIV-infected men. Controllers and LTNPs had higher concentrations of sCD163 and sCD14 compared to HIV-uninfected persons. CONCLUSIONS: Subclinical CVD was similar in HIV controllers, LTNPs and HIV-uninfected individuals despite elevated levels of some inflammatory biomarkers. Future studies of HIV controllers and LTNPs are needed to characterize the risk of CVD among HIV-infected persons.
OBJECTIVES: Elite controllers (ECs), viraemic controllers (VCs), and long-term nonprogressors (LTNPs) control HIV viral replication or maintain CD4 T-cell counts without antiretroviral therapy, but may have increased cardiovascular disease (CVD) risk compared to HIV-uninfected persons. We evaluated subclinical carotid and coronary atherosclerosis and inflammatory biomarker levels among HIV controllers, LTNPs and noncontrollers and HIV-uninfected individuals in the Multicenter AIDS Cohort Study (MACS) and the Women's Interagency HIV Study (WIHS). METHODS: We measured carotid plaque presence and common carotid artery intima-media thickness (IMT) in 1729 women and 1308 men, and the presence of coronary artery calcium and plaque in a subgroup of men. Associations between HIV control category and carotid and coronary plaque prevalences were assessed by multivariable regression analyses adjusting for demographics and CVD risk factors. Serum inflammatory biomarker concentrations [soluble CD163 (sCD163), soluble CD14 (sCD14), galectin-3 (Gal-3), galectin-3 binding protein (Gal-3BP) and interleukin (IL)-6] were measured and associations with HIV control category assessed. RESULTS: We included 135 HIV controllers (30 ECs) and 135 LTNPs in the study. Carotid plaque prevalence and carotid IMT were similar in HIV controllers, LTNPs and HIV-uninfected individuals. HIV controllers and LTNPs had lower prevalences of carotid plaque compared to viraemic HIV-infected individuals. The prevalence of coronary atherosclerosis was similar in HIV controllers/LTNPs compared to HIV-uninfected and viraemic HIV-infected men. Controllers and LTNPs had higher concentrations of sCD163 and sCD14 compared to HIV-uninfected persons. CONCLUSIONS: Subclinical CVD was similar in HIV controllers, LTNPs and HIV-uninfected individuals despite elevated levels of some inflammatory biomarkers. Future studies of HIV controllers and LTNPs are needed to characterize the risk of CVD among HIV-infected persons.
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