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Cited by 295Cardiac Fibrosis and RemodelingHeart Failure Treatment and ManagementInflammation biomarkers and pathways

Systemic inflammation in heart failure – The whys and wherefores

Yndestad, Arne, Kristian Damås, Jan, Øie, Erik, Ueland, Thor, Gullestad, Lars, Aukrust, Pål·2006·Heart Failure Reviews
DOI 10.1007/s10741-006-9196-2
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Abstract

Patients with chronic heart failure (HF) are characterized by systemic inflammation, as evident by raised circulating levels of several inflammatory cytokines with increasing levels according to the degree of disease severity. In addition to the myocardium itself, several tissues and cells can contribute to this inflammation, including leukocytes, platelets, tissue macrophages and endothelial cells. Although the mechanisms for the systemic inflammation is unknown, both infectious (e.g., endotoxins) and non-infectious (e.g., oxidative stress and hemodynamic overload) events could be operating, also including activation of Toll-like receptors as well as interaction with the neurohormone system. A growing body of evidence suggests that this systemic inflammation in chronic HF may play a role in the development and progression of this disorder, not only by promoting myocardial dysfunction, but also by inducing pathogenic consequences in other organs and tissues, thereby contributing to additional aspects of the HF syndrome such as cachexia, endothelial dysfunction and anemia. Although this inappropriate immune activation and inflammation could represent a new target for therapy in patients with chronic HF, the anti-tumor necrosis factor trials have been disappointing, and future research in this area will have to more precisely identify the most important mechanisms and actors in the immunopathogenesis of chronic HF in order to develop better immunomodulating agents for this disorder.

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  • An inflammatory state is both a causative factor in inducing MI and a primary constituent of the response to MI.

    “and an inflammatory state is both a causative factor in inducing MI and a primary constituent of the response to MI (210, 341, 385).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [385]

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Authors
Yndestad, A., Kristian Damås, J., Øie, E., Ueland, T., Gullestad, L., & Aukrust, P.
Affiliations
  • University of Oslo (NO)
  • Oslo University Hospital (NO)
Corresponding author
Aukrust, Pål
ORCID
Venue
Heart Failure Reviews
Publisher
Springer Science and Business Media LLC
Published
2006-03
Volume
11
Issue
1
Pages
83-92
ISSN
  • 1382-4147 (ISSN-L)
  • 1573-7322
DOI
10.1007/s10741-006-9196-2
OpenAlex
W2065027534
Cited by
294
References
94
Citations by year
2026: 6 · 2025: 9 · 2024: 12 · 2023: 15 · 2022: 17 · 2021: 20 · 2020: 15 · 2019: 13 · 2018: 24 · 2017: 16 · 2016: 13 · 2015: 17 · 2014: 13 · 2013: 23 · 2012: 15
FWCI
1.90
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Heart Failure Reviews (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
systemic inflammation, chronic heart failure, inflammatory cytokines, Toll-like receptors, oxidative stress, endotoxin, hemodynamic overload, endothelial dysfunction, cachexia, anemia, cardiac dysfunction, immunopathogenesis, anti-TNF therapy, immunomodulatory therapy, macrophages, platelets
MeSH terms
Anemia, Cachexia, Endothelium, Vascular, Endotoxins, Heart Failure, Humans, Immunologic Factors, Inflammation, Leukocytes, Myocardium, Tumor Necrosis Factor-alpha, Cytokines, Neurotransmitter Agents, Oxidative Stress, Disease Progression, Inflammation Mediators, Toll-Like Receptors

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