HIV- and HCV-specific markers and echocardiographic pulmonary artery systolic pressure among United States veterans

Courtney E. Zola, Meredith S. Duncan, Kaku So-Armah, Kristina A. Crothers, Adeel A. Butt, Cynthia L. Gibert, Joon Woo W. Kim, Joseph K. Lim, Vincent Lo Re, Hilary A. Tindle, Matthew S. Freiberg, Evan L. Brittain

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Hepatitis C virus (HCV) may increase pulmonary hypertension (PH) risk among people living with HIV (PLWH). Prior studies on this topic have been relatively small and examined selected populations. We determine whether HIV/HCV coinfection is associated with higher pulmonary artery systolic pressure (PASP) and prevalent echocardiographic PH. We performed a cross-sectional analysis of 6032 (16% HIV/HCV coinfected) Veterans Aging Cohort Study participants enrolled 4/1/2003–9/30/2012 with echocardiographic PASP measures. We performed multiple linear and logistic regression analyses to determine whether HIV/HCV mono- or co-infection were associated with PASP and PH compared to uninfected individuals. Individuals with HIV/HCV coinfection displayed a higher PASP than uninfected individuals (β^ =1.10, 95% CI 0.01, 2.20) but there was no association between HIV/HCV coinfection and prevalent PH. Subset analyses examined HIV and HCV disease severity markers separately and jointly. Among PLWH, HCV coinfection (β^ =1.47, 95% CI 0.26, 2.67) and CD4 + cell count (β^ = − 0.68, 95% CI − 1.10, − 0.27), but not HIV viral load nor ART regimen, were associated with PASP. Among people with HCV, neither HIV coinfection nor HCV biomarkers were associated with PASP. Among US veterans referred for echocardiography, HIV/HCV coinfection was not associated with a clinically significant elevation in pulmonary pressure. Lower absolute CD4 + T-cell count was inversely associated with PASP which warrants further investigation in prospective studies.

Original languageEnglish
Article number18729
JournalScientific Reports
Issue number1
StatePublished - Dec 1 2020

Bibliographical note

Funding Information:
The Veterans Aging Cohort Study acknowledges the support of contracts AA020794, AA020790, AA020795, AA020799, and AA013566 from the NIAAA for this research. This work was supported by grants HL146588-01, HL146588-01S1 (Drs. Brittain and Freiberg), and HL125212-01 (Dr. Brittain). Dr Freiberg is supported by the Dorothy and Laurence Grossman Chair in Cardiology. Dr. Tindle is supported by the William Anderson Spick-ard, Jr, M.D., Chair in Medicine. Disclaimer The views expressed in this article are those of the authors and do not necessarily reflect the position or policies of the Department of Veterans Affairs. Additional information Dr. Tindle has consulted for Achieve Life Sciences on a phase III clinical trial for cytisine. Dr. Tindle is a multiple PI on a cessation study of non-daily smokers donated by the manufacturer. Dr. Tindle is the project lead for a Cancer Center Support Grant Supplement (PI: Pietenpol; 3 P30 CA068485 22S3) for which Chantix (varenicline) was donated by the manufacturer. The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication. None of the other contributing authors have any disclosures to make.

Publisher Copyright:
© 2020, The Author(s).

ASJC Scopus subject areas

  • General


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