Katherine W Kooij1, Judith Schouten, Ferdinand W N M Wit, Marc van der Valk, Neeltje A Kootstra, Ineke G Stolte, Jan T M van der Meer, Maria Prins, Diederick E Grobbee, Bert-Jan H van den Born, Peter Reiss. 1. *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.
Abstract
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: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. METHODS: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. RESULTS: Study groups were comparable in demographics; smoking and hypertension were more prevalent in HIV-infectedparticipants. 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-infectedparticipants, having a nadir CD4 T-cell count ≤100 cells per cubic millimeter was independently associated with a higher PWV. CONCLUSIONS: The increased aortic stiffness in HIV-infectedparticipants 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: C I Hatleberg; L Ryom; A d'Arminio Monforte; E Fontas; P Reiss; O Kirk; W El-Sadr; A Phillips; S de Wit; F Dabis; R Weber; M Law; J D Lundgren; C Sabin Journal: HIV Med Date: 2018-07-18 Impact factor: 3.180
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