The DOI matches its Crossref record; 93 of the 94 references it cites were found in a registry or an index.
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]
Citations
Cites
Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure
Levine, B., Kalman, J., Mayer, L., Fillit, H. M., & Packer, M. (1990) · New England Journal of Medicine · doi:10.1056/nejm199007263230405 · Cited by 2,582 · cited 1×
“[3], numerous studies have demonstrated that HF patients have raised”
BackgroundChung, E. S., Packer, M., Lo, K. H., Fasanmade, A. A., & Willerson, J. T. (2003) · Circulation · doi:10.1161/01.cir.0000077913.60364.d2 · Cited by 1,644
Jessup, M. L., & Brozena, S. C. (2003) · New England Journal of Medicine · doi:10.1056/nejmra021498 · Cited by 1,582
Mann, D. L., McMurray, J. J. V., Packer, M., Swedberg, K., Borer, J. S., Colucci, W. S., Djian, J., Drexler, H., Feldman, A., Kober, L., et al. (2004) · Circulation · doi:10.1161/01.cir.0000124490.27666.b2 · Cited by 1,240
Torre-Amione, G., Kapadia, S., Benedict, C., Oral, H., Young, J. B., & Mann, D. L. (1996) · Journal of the American College of Cardiology · doi:10.1016/0735-1097(95)00589-7 · Cited by 1,211
Kremer, J. M., Westhovens, R., Leon, M., Giorgio, E. D., Alten, R., Steinfeld, S. D., RUSSELL, A. S., Dougados, M., Emery, P., Nuamah, I. F., et al. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa035075 · Cited by 1,053
Cytokines and Cytokine Receptors in Advanced Heart Failure
Deswal, A. M., Petersen, N. J., Feldman, A. M., Young, J. B., White, B. G., & Mann, D. L. (2001) · Circulation · doi:10.1161/01.cir.103.16.2055 · Cited by 1,014
Complexities of CD28/B7: CTLA-4 Costimulatory Pathways in Autoimmunity and Transplantation
Salomon, B. L., & Bluestone, J. A. (2001) · Annual Review of Immunology · doi:10.1146/annurev.immunol.19.1.225 · Cited by 1,001
Tumor Necrosis Factor-α and Tumor Necrosis Factor Receptors in the Failing Human Heart
Torre‐Amione, G., Kapadia, S. R., Lee, J. J., Durand, J., Bies, R. D., Young, J. B., & Mann, D. L. (1996) · Circulation · doi:10.1161/01.cir.93.4.704 · Cited by 991
Inflammatory Mediators and the Failing Heart
Mann, D. L. (2002) · Circulation Research · doi:10.1161/01.res.0000043825.01705.1b · Cited by 987
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Abel, E. D., Litwin, S. E., & Sweeney, G. (2008) · Physiological Reviews · doi:10.1152/physrev.00017.2007 · Cited by 736
Cardiovascular disease and COPD: dangerous liaisons?
Rabe, K. F., Hurst, J. R., & Suissa, S. (2018) · European Respiratory Review · doi:10.1183/16000617.0057-2018 · Cited by 426
Trøseid, M., Andersen, G. Ø., Broch, K., & Hov, J. R. (2020) · EBioMedicine · doi:10.1016/j.ebiom.2020.102649 · Cited by 416
Suthahar, N., Meijers, W. C., Silljé, H. H. W., & de Boer, R. A. (2017) · Current Heart Failure Reports · doi:10.1007/s11897-017-0343-y · Cited by 307
Left Ventricular T-Cell Recruitment Contributes to the Pathogenesis of Heart Failure
Nevers, T. A., Salvador, A. M., Grodecki‐Pena, A., Knapp, A., Velázquez, F., Aronovitz, M. J., Kapur, N. K., Karas, R. H., Blanton, R. M., & Alcaide, P. (2015) · Circulation Heart Failure · doi:10.1161/circheartfailure.115.002225 · Cited by 281
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
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