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Published on: December 5, 2011
Inflammatory and anti-inflammatory cytokines in chronic heart failure: potential therapeutic implications
Pål Aukrust1, Lars Gullestad, Thor Ueland
1Research Institute for Internal Medicine, University of Oslo, N-0027 Oslo, Norway. pal.aukrust@rikshospitalet.no
Insights
Persistent inflammation contributes to chronic heart failure (HF) by affecting heart function. While targeting inflammation shows promise, current immunomodulatory therapies face challenges in improving cardiac performance effectively.
Area of Science:
- Cardiology
- Immunology
- Pathophysiology
Background:
- Persistent inflammation, marked by elevated inflammatory cytokines, is implicated in chronic heart failure (HF) pathogenesis.
- This inflammation influences cardiac contractility, hypertrophy, and apoptosis, contributing to myocardial remodeling.
- Various stimuli like heat shock proteins, microbial antigens, and oxidative stress may trigger this inflammatory response, representing a common pathway in HF.
Purpose of the Study:
- To explore the role of inflammation and immunomodulatory therapy in chronic heart failure.
- To evaluate the potential of targeting the cytokine network for HF treatment.
- To understand the challenges and future directions in developing effective immunomodulating agents for HF.
Main Methods:
- Review of existing animal and clinical studies on inflammation in chronic heart failure.
- Analysis of results from placebo-controlled anti-tumor necrosis factor (TNF) studies.
- Assessment of the impact of immunomodulatory therapy on cardiac performance.
Main Results:
- Downregulation of inflammation has shown potential to improve cardiac performance in some studies.
- Placebo-controlled anti-TNF therapy studies yielded no improvement or even adverse effects.
- Current immunomodulatory therapies face challenges in achieving beneficial net effects in HF patients.
Conclusions:
- The 'cytokine hypothesis' in HF remains relevant despite challenges with current anti-TNF therapies.
- Developing effective immunomodulating agents for HF requires overcoming significant therapeutic challenges.
- Further research is crucial to identify key players in HF immunopathogenesis for targeted therapy development.
Abstract:
Persistent inflammation, involving increased levels of inflammatory cytokines, seems to play a pathogenic role in chronic heart failure (HF) by influencing heart contractility, inducing hypertrophy and promoting apoptosis, contributing to myocardial remodeling. While several stimuli may be operating such as heat shock proteins, microbial antigens and oxidative stress, it seems that the inflammatory response to these stimuli may represent a common final pathogenic pathway in HF regardless of the initial event. Traditional cardiovascular drugs appear to have little influence on the cytokine network, and immunomodulatory therapy has emerged as a possible new treatment modality in HF. Several animal studies and also some clinical studies have suggested that downregulation of inflammation may improve cardiac performance. However, the results from the placebo-controlled anti-tumor necrosis factor studies suggest no improvement or even adverse effects of such therapy. Although somewhat disappointing, these negative results do not necessarily argue against the 'cytokine hypothesis'. These studies just underscore the challenges in developing treatment modalities that can modulate the cytokine network in HF patients resulting in beneficial net effects. Further research will have to identify more precisely the most important actors in the immunopathogenesis of chronic HF in order to develop more specific immunomodulating agents for this disorder.
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