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

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Inflammatory mediators in chronic heart failure: an overview

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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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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: bronze
doi.org
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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