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Multicenter Study
. 2015 Aug 15;61(4):640-50.
doi: 10.1093/cid/civ325. Epub 2015 Apr 22.

HIV Infection Is Associated With Progression of Subclinical Carotid Atherosclerosis

David B Hanna  1 , Wendy S Post  2 , Jennifer A Deal  3 , Howard N Hodis  4 , Lisa P Jacobson  3 , Wendy J Mack  5 , Kathryn Anastos  6 , Stephen J Gange  3 , Alan L Landay  7 , Jason M Lazar  8 , Frank J Palella  9 , Phyllis C Tien  10 , Mallory D Witt  11 , Xiaonan Xue  1 , Mary A Young  12 , Robert C Kaplan  1 , Lawrence A Kingsley  13
Affiliations
Multicenter Study

HIV Infection Is Associated With Progression of Subclinical Carotid Atherosclerosis

David B Hanna et al. Clin Infect Dis. .

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.

Keywords: HIV infection; atherosclerosis; cardiovascular disease; intima-media thickness; viral load.

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Figures

Figure 1.
Figure 1.
Distribution of right common carotid artery intima-media thickness (CCA-IMT) by human immunodeficiency virus (HIV) serostatus, among (A) Women's Interagency HIV Study (WIHS), and (B) Multicenter AIDS Cohort Study (MACS) participants. Average years between visits: 2.5 (WIHS), 3 (MACS). White represents HIV-uninfected, grey represents HIV-infected, box represents interquartile range, dot represents mean CCA-IMT, middle line represents median CCA-IMT, vertical lines represent the interquartile range*1.5.
Figure 2.
Figure 2.
Distribution of focal carotid artery plaque by human immunodeficiency virus (HIV) serostatus, among (A) Women's Interagency HIV Study (WIHS), and (B) Multicenter AIDS Cohort Study (MACS) participants. Labels represent N (%). Abbreviations: BIF, carotid artery bifurcation; CCA, common carotid artery; ICA, internal carotid artery.
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