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Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure

Rheumatoid arthritis (RA) patients have a 1.5- to twofold higher risk of developing heart failure (HF) and a twofold increased risk of HF-associated mortality compared to those without RA. HF is preceded subclinically by left ventricular (LV) remodeling in the general population. There is a relative...

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Autores principales: Park, Elizabeth, Ito, Kazato, Depender, Christopher, Giles, Jon T., Bathon, Joan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10362590/
https://www.ncbi.nlm.nih.gov/pubmed/37480064
http://dx.doi.org/10.1186/s13075-023-03113-8
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author Park, Elizabeth
Ito, Kazato
Depender, Christopher
Giles, Jon T.
Bathon, Joan
author_facet Park, Elizabeth
Ito, Kazato
Depender, Christopher
Giles, Jon T.
Bathon, Joan
author_sort Park, Elizabeth
collection PubMed
description Rheumatoid arthritis (RA) patients have a 1.5- to twofold higher risk of developing heart failure (HF) and a twofold increased risk of HF-associated mortality compared to those without RA. HF is preceded subclinically by left ventricular (LV) remodeling in the general population. There is a relative absence of prospective studies following RA patients from pre-clinical to clinical HF as well as prospective studies of LV remodeling in RA without clinical HF. In our study, 158 RA patients without clinical HF were enrolled and underwent transthoracic echocardiography (TTE) at baseline and on follow-up between 4 and 6 years. Extensive characterization of RA disease activity and cardiovascular risk factors were performed. LV remodeling was prevalent at 40% at baseline and increased to 60% over time. Higher levels of interleukin-6 (IL 6) were associated with concentric LV remodeling on follow-up. The use of tocilizumab was also significantly associated with baseline LV remodeling (relative wall thickness). These findings suggest a role for IL-6 as a biomarker for LV remodeling in RA patients without clinical HF. Future research should focus on prospective follow-up of LV remodeling and the effects of IL-6 inhibition on LV remodeling in RA patients. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13075-023-03113-8.
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spelling pubmed-103625902023-07-23 Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure Park, Elizabeth Ito, Kazato Depender, Christopher Giles, Jon T. Bathon, Joan Arthritis Res Ther Correspondence Rheumatoid arthritis (RA) patients have a 1.5- to twofold higher risk of developing heart failure (HF) and a twofold increased risk of HF-associated mortality compared to those without RA. HF is preceded subclinically by left ventricular (LV) remodeling in the general population. There is a relative absence of prospective studies following RA patients from pre-clinical to clinical HF as well as prospective studies of LV remodeling in RA without clinical HF. In our study, 158 RA patients without clinical HF were enrolled and underwent transthoracic echocardiography (TTE) at baseline and on follow-up between 4 and 6 years. Extensive characterization of RA disease activity and cardiovascular risk factors were performed. LV remodeling was prevalent at 40% at baseline and increased to 60% over time. Higher levels of interleukin-6 (IL 6) were associated with concentric LV remodeling on follow-up. The use of tocilizumab was also significantly associated with baseline LV remodeling (relative wall thickness). These findings suggest a role for IL-6 as a biomarker for LV remodeling in RA patients without clinical HF. Future research should focus on prospective follow-up of LV remodeling and the effects of IL-6 inhibition on LV remodeling in RA patients. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13075-023-03113-8. BioMed Central 2023-07-21 2023 /pmc/articles/PMC10362590/ /pubmed/37480064 http://dx.doi.org/10.1186/s13075-023-03113-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Correspondence
Park, Elizabeth
Ito, Kazato
Depender, Christopher
Giles, Jon T.
Bathon, Joan
Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
title Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
title_full Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
title_fullStr Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
title_full_unstemmed Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
title_short Left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
title_sort left ventricular remodeling in rheumatoid arthritis patients without clinical heart failure
topic Correspondence
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10362590/
https://www.ncbi.nlm.nih.gov/pubmed/37480064
http://dx.doi.org/10.1186/s13075-023-03113-8
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