CROI 2020 Abstract eBook

Abstract eBook

Poster Abstracts

of awake periods was associated with poorer physical (p=0.01) and mental (p=0.04) health and greater sleep-related impairment (p<0.001). Greater irregularity in duration/timing and longer onset latency were both associated with greater sleep-related impairment (p<0.001 and p=0.004) and disturbance (p<0.001 and p=0.03). Irregularity in duration/timing was also associated with poorer mental health (p=0.03). Associations were generally similar to those seen among the HIV-negative controls; only the associations of onset latency and sleep-related QoL appeared to differ (p-interaction=0.01 and 0.003, Figure). Conclusion: We found seven dimensions of sleep health based on objective actigraphy measures. Whilst these dimensions have differential impacts on self-reported health, the effects are generally similar between people with and without HIV. These findings could inform targeted strategies to improve sleep health and, in turn, QoL of PWH.

700 HIV AS A RISK FACTOR FOR INCIDENT PULMONARY HYPERTENSION Meredith S. Duncan 1 , Suman Kundu 1 , Charles Alcorn 2 , Emily Epstein 1 , Grace Wallace 1 , Kaku So-Armah 3 , Amy C. Justice 4 , Kristina Crothers 5 , Matthew Freiberg 1 , Evan L. Brittain 1 1 Vanderbilt University, Nashville, TN, USA, 2 University of Pittsburgh, Pittsburgh, PA, USA, 3 Boston University, Boston, MA, USA, 4 VA Connecticut Healthcare System, West Haven, CT, USA, 5 University of Washington, Seattle, WA, USA Background: HIV is associated with prevalent pulmonary hypertension (PH). However, PH incidence based on echocardiographic measures of pulmonary artery systolic pressure (PASP) in both HIV-infected and uninfected persons remains unstudied. We hypothesized that HIV-infected individuals have higher PH incidence rates and risk versus uninfected individuals and that markers of poor HIV viral suppression would further elevate PH risk. Methods: This analysis used data from the Veterans Aging Cohort Study (VACS), an electronic health record cohort of HIV-infected veterans matched 1:2 to uninfected controls on age, sex, race/ethnicity, clinical site, and enrollment year. We evaluated 3677 VACS participants (N=1188 HIV+) referred for echocardiography with reported PASP measures at/below 35mmHg. We estimated PH incidence rates by HIV status using Poisson regression; HIV-infected individuals were further stratified by CD4 cell count and HIV viral load at the time of their first echocardiogram (baseline). We then performed Cox proportional hazards regression to estimate risk of incident PH in HIV- infected individuals as a whole, by CD4 cell count, and by HIV viral load versus uninfected. Adjusted models included age, sex, race/ethnicity, prevalent heart failure, chronic obstructive pulmonary disease, body mass index, and eGFR as covariates. PH incidence was defined as the presence of at least one subsequent echocardiogramwith PASP above 35mmHg. Individuals with a single echocardiogram or follow-up PASP measures at/below 35mmHg were censored at date of death or end of follow-up (9/30/2015). Results: Over 97% of the cohort was male with an average age of 58 years. Nearly half of the cohort was African American; another 40%was white. Median follow-up time was 3 years (Q1, Q3: 1, 7). PH incidence rates were higher among HIV-infected veterans versus uninfected veterans (Table). Accordingly, PH risk was 50% higher in HIV-infected individuals compared to uninfected; highest risk was observed in individuals with low CD4 cell counts and/or unsuppressed HIV viral load (Table). We also observed increased PH risk in African Americans versus white individuals (HR=1.38 [1.08, 1.76]). Conclusion: HIV is independently associated with higher PH incidence after adjusting for risk factors. Low CD4 cell count and high HIV viral load contribute to the increased risk of incident PH among HIV-infected veterans. Race may also contribute to differences in incident PH.

699 HIV IS ASSOCIATED WITH WORSE PULMONARY DIFFUSING CAPACITY INDEPENDENT OF EMPHYSEMA Sarath Raju 1 , Meredith C. McCormack 1 , Jacquie Astemborski 2 , M. Brad Drummond 3 , Jing Sun 2 , Robert H. Brown 2 , Gregory D. Kirk 2 1 Johns Hopkins University School of Medicine, Baltimore, MD, USA, 2 Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA, 3 University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Background: HIV is associated with accelerated decline in lung function and increased risk for Chronic Obstructive Pulmonary Disease(COPD). Recently there has been more focus on the Diffusing Capacity of the Lungs for Carbon Monoxide(DLCO), a marker of gas transfer. Studies note that HIV is associated with lower DLCO. While increased emphysema and COPD likely contribute to the DLCO impairment observed, there may be other factors that drive this association. We aimed to 1)Describe the association between HIV and DLCO independent of emphysema severity and 2)Identify the joint influence of HIV and COPD on DLCO impairment. Methods: We utilized data from the Study of HIV in the Etiology of Lung Disease(SHIELD) in Baltimore, MD. SHIELD characterized COPD, and early lung disease, among 229 HIV+(67%) and 110 HIV- participants, with lung function testing and Chest CT imaging. COPD was defined as post-bronchodilator FEV1/FVC<0.70. Emphysema severity was defined by % emphysema on CT. To examine the contribution of HIV to DLCO impairment, linear and logistic regression models were generated with % predicted DLCO(corrected for hemoglobin, age, sex) and odds of moderate-severe DLCO impairment(<60% predicted) as primary outcomes. Models were adjusted for race, emphysema, FEV1% predicted(to account for differences in COPD sampling across group), smoking status, pack-years, and injection drug use. Models were also stratified by COPD status. Results: Participants had a median age of 50.9(+/- 4.84), 235(69%) were male, 131(39%) had COPD. Of those with HIV 86(38%) had detectable viremia. After adjusting for confounders, including emphysema, HIV was associated with lower DLCO(β -3.69%; P=0.02) and higher odds of significant DLCO impairment(Odds Ratio 1.93; P=0.01). Among HIV+ participants, we did not see effect modification by CD4 count or viremia. When analyzed by COPD status(figure), a higher percentage of those with HIV and COPD(69.3%) had significant DLCO impairment versus COPD alone(54.2%)(P<0.01). Even among those without COPD, HIV was independently associated with lower DLCO(β -4.81%; P=0.04) and significant impairment(OR 2.68; P=0.01). Conclusion: HIV was associated with DLCO impairment independent of emphysema severity on CT and COPD. Our data also suggest a potentially additive influence between HIV and COPD on DLCO impairment. Future studies should investigate the other factors, including pulmonary vascular disease, that may contribute to DLCO impairment among persons living with HIV.

Poster Abstracts

CROI 2020 256