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.
Original language | English (US) |
---|---|
Pages (from-to) | 217-227 |
Number of pages | 11 |
Journal | HIV Medicine |
Volume | 21 |
Issue number | 4 |
DOIs | |
State | Published - Apr 1 2020 |
Keywords
- AIDS
- HIV
- carotid atherosclerosis
- coronary atherosclerosis
- subclinical cardiovascular disease
ASJC Scopus subject areas
- Health Policy
- Infectious Diseases
- Pharmacology (medical)
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Subclinical cardiovascular disease in HIV controller and long-term nonprogressor populations. / Brusca, R. M.; Hanna, D. B.; Wada, N. I. et al.
In: HIV Medicine, Vol. 21, No. 4, 01.04.2020, p. 217-227.Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Subclinical cardiovascular disease in HIV controller and long-term nonprogressor populations
AU - Brusca, R. M.
AU - Hanna, D. B.
AU - Wada, N. I.
AU - Blankson, J. N.
AU - Witt, M. D.
AU - Jacobson, L. P.
AU - Kingsley, L.
AU - Palella, F. J.
AU - Budoff, M.
AU - Brown, T. T.
AU - Anastos, K.
AU - Lazar, J. M.
AU - Mack, W. J.
AU - Bacchetti, P.
AU - Tien, P. C.
AU - Golzar, Y.
AU - Plankey, M.
AU - Golub, E.
AU - Kaplan, R. C.
AU - Post, W. S.
N1 - Funding Information: Data in this manuscript related to the MACS were collected by the MACS with centres (principal investigators) at The Johns Hopkins Bloomberg School of Public Health (Joseph B. Margolick and Todd Brown), Feinberg School of Medicine, Northwestern University, and Cook County Bureau of Health Services (John Phair and Steven M. Wolinsky), University of California, Los Angeles (Roger Detels and Otto Martinez-Maza), and University of Pittsburgh (Charles R. Rinaldo), and the Data Center located at the Johns Hopkins Bloomberg School of Public Health (Lisa P. Jacobson). The website is located at http://www.aidscohortstudy.org. The MACS cardiovascular study is supported by the National Heart Lung and Blood Institute (grant RO1 HL095129 awarded to WSP), with additional support from the National Center for Advancing Translational Sciences (UL1 RR 025005), a component of the National Institutes of Health (NIH) and National Institutes of Health Roadmap for Medical Research, and the University of Washington’s CVD and Metabolic Complications of HIV/AIDS Data Coordinating Center (5R01 HL095126). Additionally, the MACS is funded by the National Center for Research Resources and National Institute of Allergy and Infectious Diseases, with additional supplemental funding from the National Cancer Institute (UO1-AI-35042, UL1-TR 001079, UL1-TR000124, UM1-AI-35043, UO1-AI-35039, UO1-AI-35040 and UO1-AI-35041). Data in this manuscript related to the WIHS were collected by the WIHS. WIHS (principal investigators): the joint University of Alabama at Birmingham and University of Mississippi WIHS site (Miriam-Colette Kempf and Deborah Konkle-Parker), U01-AI-103401; Atlanta WIHS (Ighovwerha Ofotokun and Gina Wingood), U01-AI-103408; Bronx WIHS (Kathryn Anastos and Anjali Sharma), U01-AI-035004; Brooklyn WIHS (Howard Minkoff and Deborah Gustafson), U01-AI-031834; Chicago WIHS (Mardge Cohen and Audrey French), U01-AI-034993; Metropolitan Washington WIHS (Mary Young and Seble Kassaye), U01-AI-034994; Miami WIHS (Margaret Fischl and Lisa Metsch), U01-AI-103397; UNC WIHS (Adaora Adimora), U01-AI-103390; Connie Wofsy Women’s HIV Study, Northern California (Ruth Greenblatt, Bradley Aouizerat, and Phyllis Tien), U01-AI-034989; WIHS Data Management and Analysis Center (Stephen Gange and Elizabeth Golub), U01-AI-042590; Southern California WIHS (Joel Milam), U01-HD-032632 (WIHS I–IV). The WIHS is funded primarily by the National Institute of Allergy and Infectious Diseases (NIAID), with additional co-funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the National Cancer Institute (NCI), the National Institute on Drug Abuse (NIDA) and the National Institute on Mental Health (NIMH). Targeted supplemental funding for specific projects is provided by the National Institute of Dental and Craniofacial Research (NIDCR), the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute on Deafness and other Communication Disorders (NIDCD), and the NIH Office of Research on Women's Health. WIHS data collection is supported by UL1-TR000004 (UCSF CTSA), UL1-TR000454 (Atlanta CTSA) and P30-AI-050410 (UNC CFAR). Additional funding was provided by R01-HL-083760, R01-HL-095140, R21-HL-120394, R01-HL-126543, R01-HL-132794, R01-HL-140976 and K01-HL-137557. The contents of this publication are solely the responsibility of the authors and do not represent the official views of the NIH. Conflicts of interest and source of funding: KA, PB, DH, LJ, RK, WM, WP, PT, MW and MB report grants from the NIH outside the submitted work. MB reports grants from General Electric. PT reports grants from Merck and Theratechnologies. TB reports personal fees from Merck, Gilead Sciences, ViiV Healthcare and Theratechnologies. FP reports personal fees from Gilead Sciences, Janssen Pharmaceuticals, Merck and ViiV Healthcare. MW reports grants from UCLA and Johns Hopkins University. For the remaining authors, no conflicts of interest are declared. Primary sources of funding include the National Institutes of Health, National Heart, Lung, and Blood Institute, National Institute of Allergy and Infectious Diseases, and American Heart Association. Funding Information: Data in this manuscript related to the MACS were collected by the MACS with centres (principal investigators) at The Johns Hopkins Bloomberg School of Public Health (Joseph B. Margolick and Todd Brown), Feinberg School of Medicine, Northwestern University, and Cook County Bureau of Health Services (John Phair and Steven M. Wolinsky), University of California, Los Angeles (Roger Detels and Otto Martinez‐Maza), and University of Pittsburgh (Charles R. Rinaldo), and the Data Center located at the Johns Hopkins Bloomberg School of Public Health (Lisa P. Jacobson). The website is located at http://www.aidscohortstudy.org . The MACS cardiovascular study is supported by the National Heart Lung and Blood Institute (grant RO1 HL095129 awarded to WSP), with additional support from the National Center for Advancing Translational Sciences (UL1 RR 025005), a component of the National Institutes of Health (NIH) and National Institutes of Health Roadmap for Medical Research, and the University of Washington’s CVD and Metabolic Complications of HIV/AIDS Data Coordinating Center (5R01 HL095126). Additionally, the MACS is funded by the National Center for Research Resources and National Institute of Allergy and Infectious Diseases, with additional supplemental funding from the National Cancer Institute (UO1‐AI‐35042, UL1‐TR 001079, UL1‐TR000124, UM1‐AI‐35043, UO1‐AI‐35039, UO1‐AI‐35040 and UO1‐AI‐35041). Data in this manuscript related to the WIHS were collected by the WIHS. WIHS (principal investigators): the joint University of Alabama at Birmingham and University of Mississippi WIHS site (Miriam‐Colette Kempf and Deborah Konkle‐Parker), U01‐AI‐103401; Atlanta WIHS (Ighovwerha Ofotokun and Gina Wingood), U01‐AI‐103408; Bronx WIHS (Kathryn Anastos and Anjali Sharma), U01‐AI‐035004; Brooklyn WIHS (Howard Minkoff and Deborah Gustafson), U01‐AI‐031834; Chicago WIHS (Mardge Cohen and Audrey French), U01‐AI‐034993; Metropolitan Washington WIHS (Mary Young and Seble Kassaye), U01‐AI‐034994; Miami WIHS (Margaret Fischl and Lisa Metsch), U01‐AI‐103397; UNC WIHS (Adaora Adimora), U01‐AI‐103390; Connie Wofsy Women’s HIV Study, Northern California (Ruth Greenblatt, Bradley Aouizerat, and Phyllis Tien), U01‐AI‐034989; WIHS Data Management and Analysis Center (Stephen Gange and Elizabeth Golub), U01‐AI‐042590; Southern California WIHS (Joel Milam), U01‐HD‐032632 (WIHS I–IV). The WIHS is funded primarily by the National Institute of Allergy and Infectious Diseases (NIAID), with additional co‐funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the National Cancer Institute (NCI), the National Institute on Drug Abuse (NIDA) and the National Institute on Mental Health (NIMH). Targeted supplemental funding for specific projects is provided by the National Institute of Dental and Craniofacial Research (NIDCR), the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Institute on Deafness and other Communication Disorders (NIDCD), and the NIH Office of Research on Women's Health. WIHS data collection is supported by UL1‐TR000004 (UCSF CTSA), UL1‐TR000454 (Atlanta CTSA) and P30‐AI‐050410 (UNC CFAR). Additional funding was provided by R01‐HL‐083760, R01‐HL‐095140, R21‐HL‐120394, R01‐HL‐126543, R01‐HL‐132794, R01‐HL‐140976 and K01‐HL‐137557. The contents of this publication are solely the responsibility of the authors and do not represent the official views of the NIH. Funding Information: KA, PB, DH, LJ, RK, WM, WP, PT, MW and MB report grants from the NIH outside the submitted work. MB reports grants from General Electric. PT reports grants from Merck and Theratechnologies. TB reports personal fees from Merck, Gilead Sciences, ViiV Healthcare and Theratechnologies. FP reports personal fees from Gilead Sciences, Janssen Pharmaceuticals, Merck and ViiV Healthcare. MW reports grants from UCLA and Johns Hopkins University. For the remaining authors, no conflicts of interest are declared. Primary sources of funding include the National Institutes of Health, National Heart, Lung, and Blood Institute, National Institute of Allergy and Infectious Diseases, and American Heart Association. Conflicts of interest and source of funding: Publisher Copyright: © 2019 British HIV Association
PY - 2020/4/1
Y1 - 2020/4/1
N2 - 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.
AB - 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.
KW - AIDS
KW - HIV
KW - carotid atherosclerosis
KW - coronary atherosclerosis
KW - subclinical cardiovascular disease
UR - http://www.scopus.com/inward/record.url?scp=85075421242&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85075421242&partnerID=8YFLogxK
U2 - 10.1111/hiv.12820
DO - 10.1111/hiv.12820
M3 - Article
C2 - 31729142
AN - SCOPUS:85075421242
SN - 1464-2662
VL - 21
SP - 217
EP - 227
JO - HIV Medicine
JF - HIV Medicine
IS - 4
ER -