@article{c303dbcafb1846599e68ed98417ae842,
title = "Changes in plasma levels of oxidized lipoproteins and lipoprotein subfractions with atazanavir-, raltegravir-, darunavir-based initial antiviral therapy and associations with common carotid artery intima-media thickness: ACTG 5260s",
abstract = "Background: The role of oxidized lipoproteins (high-density [HDLox] and low-density [LDLox]) and total lipoprotein particle (Lp) number and size in HIV-related cardiovascular disease (CVD) is unclear. The goal of this study was to evaluate changes of these biomarkers and their associations with rate of carotid intima media thickness progression over 3 years (ΔCIMT) in chronic HIV infection. Methods: Prospective study of 234 HIV-infected antiretroviral treatment-naive participants without CVD who were randomized to receive tenofovir-emtricitabine plus atazanavir/ritonavir, darunavir/ritonavir or raltegravir (RAL) and achieved plasma HIV-1 RNA <50 copies/ml by week 24 and thereafter. Biomarker changes over 24, 48 or 96 weeks from baseline and pairwise treatment group comparisons were examined. Associations of these biomarkers with ΔCIMT were analysed with mixed effects linear regression. Results: HDLp number increased with both protease inhibitors (PIs) over 48 weeks, while LDLp number declined with RAL; Lp size did not change. Over 96 weeks, normalized HDLox declined with both PIs; LDLox increased in all groups. Few treatment group differences were observed across all biomarkers. Associations between ΔCIMT and oxidized lipoproteins at all time points were not apparent (P≥0.10). There was some evidence of slower ΔCIMT for higher HDLp number (P=0.06) and for lower LDLp number (P=0.08) measured at baseline. Conclusions: Unexpectedly, LDLox increased modestly in all treatment groups after ART initiation. Associations of plasma HDLox and LDLox with ΔCIMT were not apparent. While plasma levels of abnormal lipoproteins have been shown to be associated with CVD outcomes, clear associations with sub-clinical atherosclerosis progression were not apparent in our study.",
author = "Theodoros Kelesidis and Tran, {Thuy Tien T.} and Brown, {Todd T.} and Carlee Moser and Ribaudo, {Heather J.} and Dube, {Michael P.} and Yang, {Otto O.} and McComsey, {Grace A.} and Stein, {James H.} and Currier, {Judith S.}",
note = "Funding Information: ACTG 5260s Team Members: Howard Hodis (Keck School of Medicine at USC, Los Angeles, CA, USA), Catherine Godfrey (National Institute of Allergy and Infectious Disease, National Institute of Health, Bethesda, MD, USA), Bernadette Jarocki (Frontier Science and Technology Research Foundation, Inc., Amherst, NY, USA), Alex Benns (AIDS Clinical Trials Group) and Ken Braun (AIDS Clinical Trials Group). We thank the staff and patients from the following hospitals who participate in ACTG (in alphabetical order): Beth Israel Deaconess Medical Center, Brigham and Women's Hospital, Case University CRS, Duke University Medical Center, Harbor-UCLA Medical Center, Houston AIDS Research Team CRS, John Hopkins Adult AIDS CRS, Metrohealth, New Jersey Medical School, New York University HIV/AIDS CRS, Northwestern University, Rush University Medical Center ACTG, The Ohio State University, The Ponce De Leon Center CRS, UCLA Care Center, UCSF AIDS CRS, University of Cincinnati, University of Colorado, University of North Carolina AIDS CRS, University of Pittsburg CRS, University of Rochester ACTG AIDS Care, University of Southern California, University of Washington, Vanderbilt Therapeutics CRS, Washington University. This research was supported by NIH grants HL095132, HL095126, AI 068636, AI068634, AI69471, AI069501, and AI56933, NIH/NCATS Grant number UL1TR000124, NIH K08AI08272. The study received additional financial support from Gilead, Merck, Bristol-Myers Squibb and Janssen. The project described was supported by Award Number UM1 AI068634, UM1 AI068636 and UM1 AI106701 from the National Institute of Allergy and Infectious Diseases. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or any of the funders. TTB has served as a consultant for BMS, GSK, Merck, Abbott, Gilead, ViiV Healthcare and has received research funding from Merck and GSK. JSC has served as a consultant for Gilead and has received research funding from Merck. GAM has served as consultant, speaker or received research grants from BMS, Pfizer, Merck, Gilead and GSK. MPD has served as a consultant for Gilead and AstraZeneca, and receives research funding from Gilead, ViiV and Merck. HJR, JHS, TK, OOY, CM and TTTT have no competing interests. Publisher Copyright: {\textcopyright}2017 International Medical Press.",
year = "2017",
doi = "10.3851/IMP3093",
language = "English (US)",
volume = "22",
pages = "113--126",
journal = "Antiviral therapy",
issn = "1359-6535",
publisher = "International Medical Press Ltd",
number = "2",
}