David B Hanna1, Wendy S Post2, Jennifer A Deal3, Howard N Hodis4, Lisa P Jacobson3, Wendy J Mack5, Kathryn Anastos6, Stephen J Gange3, Alan L Landay7, Jason M Lazar8, Frank J Palella9, Phyllis C Tien10, Mallory D Witt11, Xiaonan Xue1, Mary A Young12, Robert C Kaplan1, Lawrence A Kingsley13. 1. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York. 2. Department of Medicine, Johns Hopkins University School of Medicine Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. 3. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland. 4. Departments of Medicine. 5. Preventive Medicine, University of Southern California, Los Angeles, California. 6. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York Department of Medicine, Montefiore Medical Center, Bronx, New York. 7. Department of Immunology and Microbiology, Rush University Medical Center, Chicago, Illinois. 8. Department of Medicine, SUNY-Downstate Medical Center, Brooklyn, New York. 9. Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois. 10. Department of Medicine, University of California-San Francisco. 11. Department of Medicine, University of California-Los Angeles. 12. Department of Medicine, Georgetown University Medical Center, Washington D.C. 13. Departments of Infectious Diseases and Microbiology Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pennsylvania.
Abstract
BACKGROUND: Individuals infected with human immunodeficiency virus (HIV) live longer as a result of effective treatment, but long-term consequences of infection, treatment, and immunological dysfunction are poorly understood. METHODS: We prospectively examined 1011 women (74% HIV-infected) in the Women's Interagency HIV Study and 811 men (65% HIV-infected) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004-2013. Outcomes included changes in right common carotid artery intima-media thickness (CCA-IMT) and new focal carotid artery plaque formation (IMT >1.5 mm) over median 7 years. We assessed the association between HIV serostatus and progression of subclinical atherosclerosis, adjusting for demographic, behavioral, and cardiometabolic risk factors. RESULTS: Unadjusted mean CCA-IMT increased (725 to 752 µm in women, 757 to 790 µm in men), but CCA-IMT progression did not differ by HIV serostatus, either in combined or sex-specific analyses. Focal plaque prevalence increased from 8% to 15% in women and 25% to 34% in men over 7 years. HIV-infected individuals had 1.6-fold greater risk of new plaque formation compared with HIV-uninfected individuals (relative risk [RR] 1.61, 95% CI, 1.12-2.32), adjusting for cardiometabolic factors; the association was similar by sex. Increased plaque occurred even among persistently virologically suppressed HIV-infected individuals compared with uninfected individuals (RR 1.56, 95% CI, 1.07-2.27). HIV-infected individuals with baseline CD4+ ≥ 500 cells/µL had plaque risk not statistically different from uninfected individuals. CONCLUSIONS: HIV infection is associated with greater increases in focal plaque among women and men, potentially mediated by factors associated with immunodeficiency or HIV replication at levels below current limits of detection.
BACKGROUND: Individuals infected with human immunodeficiency virus (HIV) live longer as a result of effective treatment, but long-term consequences of infection, treatment, and immunological dysfunction are poorly understood. METHODS: We prospectively examined 1011 women (74% HIV-infected) in the Women's Interagency HIV Study and 811 men (65% HIV-infected) in the Multicenter AIDS Cohort Study who underwent repeated B-mode carotid artery ultrasound imaging in 2004-2013. Outcomes included changes in right common carotid artery intima-media thickness (CCA-IMT) and new focal carotid artery plaque formation (IMT >1.5 mm) over median 7 years. We assessed the association between HIV serostatus and progression of subclinical atherosclerosis, adjusting for demographic, behavioral, and cardiometabolic risk factors. RESULTS: Unadjusted mean CCA-IMT increased (725 to 752 µm in women, 757 to 790 µm in men), but CCA-IMT progression did not differ by HIV serostatus, either in combined or sex-specific analyses. Focal plaque prevalence increased from 8% to 15% in women and 25% to 34% in men over 7 years. HIV-infected individuals had 1.6-fold greater risk of new plaque formation compared with HIV-uninfected individuals (relative risk [RR] 1.61, 95% CI, 1.12-2.32), adjusting for cardiometabolic factors; the association was similar by sex. Increased plaque occurred even among persistently virologically suppressed HIV-infected individuals compared with uninfected individuals (RR 1.56, 95% CI, 1.07-2.27). HIV-infected individuals with baseline CD4+ ≥ 500 cells/µL had plaque risk not statistically different from uninfected individuals. CONCLUSIONS:HIV infection is associated with greater increases in focal plaque among women and men, potentially mediated by factors associated with immunodeficiency or HIV replication at levels below current limits of detection.
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