Abstract P1064: Central Vascular Implication in Neurocognitive Functioning among Men Living with and without HIV
Abstract
Background: Neurocognitive impairment is linked to aging, vascular stiffness, and HIV infection. The role of vascular stiffness in neurocognitive functioning among men with HIV (MWH) remains unclear. This study examined the relationship between carotid artery distensibility and neurocognitive decline in MWH and men without HIV (MWoH), while exploring whether HIV serostatus and age influenced the association. Methods: Baseline vascular and cognitive assessments (2004-2013) were measured in the Multicenter AIDS Cohort Study. Carotid distensibility was measured using B-mode ultrasound. Neurocognitive function was assessed via executive function (Trail Making B) and psychomotor/information processing speed (Trail Making A, Symbol Digit Modalities Test) over a 6.5-year follow-up. Mixed effects linear regression was used to evaluate the association between baseline stiffness and the progression of neurocognitive function, with time operationalized as participant age. Models were adjusted for demographic, behavioral, and cardiometabolic risk factors. Results: Among 717 men, (mean age 49.9 years, 62.9% non-Hispanic White), 459 (64%) were MWH. In MWH, lower distensibility (higher stiffness) at baseline was associated with greater neurocognitive decline with increasing age in Trail Making A (β=-0.03, p <0.001) and Trail Making B (β=-0.02, p =0.02), but not in Symbol Digit Modalities Test. Among MWoH, lower distensibility at baseline was associated with greater neurocognitive decline with increasing age in Trail Making B (β=-0.03, p=0.002) only. The longitudinal association of distensibility with neurocognition only differed by HIV serostatus for Trail Making A ( p <0.05), when assessing the three-way interaction of serostatus, age, and distensibility. Conclusions: Increased vascular stiffness was linked to significant neurocognitive decline in both MWH and MWoH after adjusting for confounding factors. Addressing cardiovascular risk factors may help prevent neurocognitive decline in this population.
Article Details
Authors (18)
Ray Jones
University of Alabama at Birmingham, Birmingham, Alabama, United States
Jessica Blair
University of Alabama at Birmingham, Columbiana, Alabama, United States
Zenoria Causey Pruitt
University of Alabama at Birmingham, Birmingham, Alabama, United States
Michael Hankes
University of Alabama at Birmingham, Birmingham, Alabama, United States
David Vance
University of Alabama at Birmingham, Birmingham, Alabama, United States
Amanda Willig
University of Alabama at Birmingham, Birmingham, Alabama, United States
Daniel Huck
Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States
Wendy Post
JOHNS HOPKINS UNIVERSITY, Baltimore, Maryland, United States
Mary Masters
Northwestern University, Chicago, Illinois, United States
Frank Palella
Northwestern University, Chicago, Illinois, United States
Matthew Mimiaga
UCLA, Los Angeles, California, United States
Mallory Witt
Harbor-UCLA, Torrance, California, United States
Jamie Peven
University of Pittsburgh, Pittsburgh, Pennsylvania, United States
Sabina Haberlen
Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States
Mariam Aziz
Roland Thorpe
Johns Hopkins University, Baltimore, Maryland, United States
Emily Levitan
UNIVERSITY ALABAMA AT BIRMINGHAM, Birmingham, Alabama, United States
Thomas Buford
University of Alabama at Birmingham, Birmingham, Alabama, United States