title: Difference in Aortic Stiffness Between Treated Middle-Aged HIV Type 1-Infected and Uninfected Individuals Largely Explained by Traditional Cardiovascular Risk Factors, With an Additional Contribution of Prior Advanced Immunodeficiency.
abstract: Patients with HIV, even with suppressed viremia on combination antiretroviral therapy, are at increased risk for cardiovascular disease. The underlying pathophysiology remains to be clarified. Aortic stiffness, known to be associated with cardiovascular disease in the general population, was investigated in a cohort of HIV type 1 (HIV 1)-infected and similar but uninfected individuals.
  
  
  
  Aortic stiffness was assessed by measuring pulse wave velocity (PWV) with an Arteriograph. Five hundred seven HIV-uninfected and 566 HIV 1-infected individuals, predominantly with suppressed viremia on combination antiretroviral therapy, aged ≥45 years, participating in the ongoing AGEhIV Cohort Study were included in the analysis. Multivariable linear regression was used to investigate whether HIV was independently associated with aortic stiffness, adjusting for traditional cardiovascular risk factors.
  
  
  
  Study groups were comparable in demographics; smoking and hypertension were more prevalent in HIV-infected participants. PWV was higher in the HIV-infected group (7.9 vs. 7.7 m/s, P = 0.004). After adjustment for mean arterial pressure, age, gender, and smoking, HIV status was not significantly associated with aortic stiffness. In HIV-infected participants, having a nadir CD4 T-cell count ≤100 cells per cubic millimeter was independently associated with a higher PWV.
  
  
  
  The increased aortic stiffness in HIV-infected participants was largely explained by a higher prevalence of traditional cardiovascular risk factors, particularly smoking. Although HIV itself was not independently associated with higher aortic stiffness, a prior greater degree of immunodeficiency was. This suggests a detrimental effect of immunodeficiency on the aortic wall, possibly mediated by inflammation.
authors: *Department of Global Health, Amsterdam Institute for Global Health and Development and Academic Medical Center, Amsterdam, the Netherlands;†Department of Neurology, Academic Medical Center, Amsterdam, the Netherlands;‡Division of Infectious Diseases, Center for Infection and Immunity Amsterdam, Academic Medical Center, Amsterdam, the Netherlands;§HIV Monitoring Foundation, Amsterdam, the Netherlands;‖Department of Experimental Immunology, Academic Medical Center, Amsterdam, the Netherlands;¶Department of Infectious Diseases, Public Health Service of Amsterdam, Amsterdam, the Netherlands;#Julius Global Health, Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands; and**Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
authors: Katherine W
authors: KW
authors: Kooij
authors: Judith
authors: J
authors: Schouten
authors: Ferdinand W N M
authors: FW
authors: Wit
authors: Marc
authors: M
authors: van der Valk
authors: Neeltje A
authors: NA
authors: Kootstra
authors: Ineke G
authors: IG
authors: Stolte
authors: Jan T M
authors: JT
authors: van der Meer
authors: Maria
authors: M
authors: Prins
authors: Diederick E
authors: DE
authors: Grobbee
authors: Bert-Jan H
authors: BJ
authors: van den Born
authors: Peter
authors: P
authors: Reiss
mesh_terms: D001011:Aorta / Q000503:physiopathology*; D016022:Case-Control Studies; D015331:Cohort Studies; D005260:Female; D015658:HIV Infections / Q000276:immunology / Q000503:physiopathology*; D015497:HIV-1; D006801:Humans; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D059289:Vascular Stiffness / Q000502:physiology*