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Systemic inflammation in heart failure – The whys and wherefores
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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“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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Metadata
- 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
- Venue
- Heart Failure Reviews
- Published
- 2006-03
- Volume
- 11
- Issue
- 1
- Pages
- 83-92
- ISSN
- 1382-4147 (ISSN-L)
- 1573-7322
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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