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Cited by 627Cardiac Fibrosis and RemodelingHeart Failure Treatment and ManagementInflammation biomarkers and pathways

The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.

Inflammatory mediators in chronic heart failure: an overview

Open access
Anker, Stefan D, von Haehling, Stephan·2004·Heart
DOI 10.1136/hrt.2002.007005PMC PMC1768165
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Abstract

hronic heart failure (CHF) represents a major public health burden, and its prognosis is comparable to that of different malignant diseases.Our understanding of CHF has developed from the rather simplistic model of mere pump failure to that of a multisystem disorder which affects not only the cardiovascular system but also the musculoskeletal, renal, neuroendocrine, and immune systems.Thus, the pathophysiology of CHF is exceedingly complex.Therapies to block excessive neuroendocrine activation have become a cornerstone of treatment.CHF progresses because of activation of neurohormones and pro-inflammatory cytokines following an initial cardiac injury or a mutation of the genetic programme.1 Virtually any heart disease can ultimately lead to heart failure, although the initial event leading to the development of this syndrome is in many cases unknown.However, CHF is always the result of some underlying process and the diagnosis cannot stand alone.The activation of the aforementioned systems maintains and worsens CHF.In particular, the activation of the immune system has received considerable interest in the last decade.There are several different components to this system which interact with each other in a complex manner.It is becoming increasingly apparent that inflammatory mediators play a crucial role in the development of CHF, and several strategies to counterbalance different aspects of the inflammatory response are considered.Possible targets involve pro-and anti-inflammatory cytokines and their receptors, endotoxin, adhesion molecules, nitric oxide and nitric oxide synthase, reactive oxygen species, and different types of leucocytes.The purpose of this review is to give a brief overview of the current understanding of the role of inflammation in CHF.Furthermore, we will discuss recent advances in the development of new therapeutic strategies in this field.

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Metadata

Authors
Anker, S. D., & von Haehling, S.
Affiliations
  • Imperial College London (GB)
  • Department of Clinical Cardiology, Imperial College School of Medicine, National Heart & Lung Institute, London, UK
Corresponding author
Anker, Stefan D
ORCID
Anker, Stefan D
Venue
Heart
Publisher
BMJ
Published
2004-03-12
Volume
90
Issue
4
Pages
464-470
ISSN
  • 1355-6037 (ISSN-L)
  • 1468-201X
DOI
10.1136/hrt.2002.007005
PMC
PMC1768165
OpenAlex
W2104179458
Cited by
627
References
33
Citations by year
2026: 21 · 2025: 14 · 2024: 23 · 2023: 17 · 2022: 27 · 2021: 26 · 2020: 23 · 2019: 36 · 2018: 43 · 2017: 43 · 2016: 34 · 2015: 18 · 2014: 35 · 2013: 30 · 2012: 32
FWCI
16.81
Type
journal article
Language
en
Open access
Locations
  • Heart (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
Deutsche Herzstiftung
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
chronic heart failure, inflammation, inflammatory mediators, inflammatory cytokines, anti-inflammatory cytokines, neuroendocrine activation, neurohormones, endotoxin, adhesion molecules, nitric oxide, reactive oxygen species, leukocytes, immune system, heart failure pathophysiology, anti-inflammatory therapy
MeSH terms
Etanercept, Infliximab, Anti-Inflammatory Agents, Non-Steroidal, Antibodies, Monoclonal, C-Reactive Protein, Heart Failure, Humans, Immunoglobulin G, Leukocytes, Myocarditis, Nitric Oxide, Tumor Necrosis Factor-alpha, Cell Adhesion Molecules, Lymphocyte Subsets, Cytokines, Receptors, Tumor Necrosis Factor, Hydroxymethylglutaryl-CoA Reductase Inhibitors

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