HIV Infection Is Associated with Progression of Subclinical Carotid Atherosclerosis

David B. Hanna, Wendy S Post, Jennifer A Deal, Howard N. Hodis, Lisa Paula Jacobson, Wendy J. Mack, Kathryn Anastos, Stephen J Gange, Alan L. Landay, Jason M. Lazar, Frank J. Palella, Phyllis C. Tien, Mallory D. Witt, Xiaonan Xue, Mary A. Young, Robert C. Kaplan, Lawrence A. Kingsley

Research output: Contribution to journalArticle

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.

Original languageEnglish (US)
Pages (from-to)640-650
Number of pages11
JournalClinical Infectious Diseases
Volume61
Issue number4
DOIs
StatePublished - Aug 15 2015

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Carotid Artery Diseases
Virus Diseases
HIV
Carotid Intima-Media Thickness
Common Carotid Artery
Carotid Stenosis
Virus Replication
Carotid Arteries
Limit of Detection
Ultrasonography
Atherosclerosis
Acquired Immunodeficiency Syndrome
Cohort Studies
Demography

Keywords

  • atherosclerosis
  • cardiovascular disease
  • HIV infection
  • intima-media thickness
  • viral load

ASJC Scopus subject areas

  • Infectious Diseases
  • Microbiology (medical)

Cite this

HIV Infection Is Associated with Progression of Subclinical Carotid Atherosclerosis. / Hanna, David B.; Post, Wendy S; Deal, Jennifer A; Hodis, Howard N.; Jacobson, Lisa Paula; Mack, Wendy J.; Anastos, Kathryn; Gange, Stephen J; Landay, Alan L.; Lazar, Jason M.; Palella, Frank J.; Tien, Phyllis C.; Witt, Mallory D.; Xue, Xiaonan; Young, Mary A.; Kaplan, Robert C.; Kingsley, Lawrence A.

In: Clinical Infectious Diseases, Vol. 61, No. 4, 15.08.2015, p. 640-650.

Research output: Contribution to journalArticle

Hanna, DB, Post, WS, Deal, JA, Hodis, HN, Jacobson, LP, Mack, WJ, Anastos, K, Gange, SJ, Landay, AL, Lazar, JM, Palella, FJ, Tien, PC, Witt, MD, Xue, X, Young, MA, Kaplan, RC & Kingsley, LA 2015, 'HIV Infection Is Associated with Progression of Subclinical Carotid Atherosclerosis', Clinical Infectious Diseases, vol. 61, no. 4, pp. 640-650. https://doi.org/10.1093/cid/civ325
Hanna, David B. ; Post, Wendy S ; Deal, Jennifer A ; Hodis, Howard N. ; Jacobson, Lisa Paula ; Mack, Wendy J. ; Anastos, Kathryn ; Gange, Stephen J ; Landay, Alan L. ; Lazar, Jason M. ; Palella, Frank J. ; Tien, Phyllis C. ; Witt, Mallory D. ; Xue, Xiaonan ; Young, Mary A. ; Kaplan, Robert C. ; Kingsley, Lawrence A. / HIV Infection Is Associated with Progression of Subclinical Carotid Atherosclerosis. In: Clinical Infectious Diseases. 2015 ; Vol. 61, No. 4. pp. 640-650.
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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.",
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T1 - HIV Infection Is Associated with Progression of Subclinical Carotid Atherosclerosis

AU - Hanna, David B.

AU - Post, Wendy S

AU - Deal, Jennifer A

AU - Hodis, Howard N.

AU - Jacobson, Lisa Paula

AU - Mack, Wendy J.

AU - Anastos, Kathryn

AU - Gange, Stephen J

AU - Landay, Alan L.

AU - Lazar, Jason M.

AU - Palella, Frank J.

AU - Tien, Phyllis C.

AU - Witt, Mallory D.

AU - Xue, Xiaonan

AU - Young, Mary A.

AU - Kaplan, Robert C.

AU - Kingsley, Lawrence A.

PY - 2015/8/15

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N2 - 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.

AB - 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.

KW - atherosclerosis

KW - cardiovascular disease

KW - HIV infection

KW - intima-media thickness

KW - viral load

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