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Updated: Aug 24, 2026

Isolation of Functional Cardiac Immune Cells
Published on: December 5, 2011
[Immunactivation in chronic heart failure. Inflammatory mediators]
S Genth-Zotz1, S von Haehling, S Blankenberg
1II. Medizinische Klinik und Poliklinik, Johannes-Gutenberg-Universität Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany. genth@2-med.klinik.uni-mainz.de
Inflammatory cytokines are thought to contribute to the development and progression of chronic heart failure (CHF). It has been shown that especially tumor necrosis factor-alpha (TNF) is activated in patients with CHF and exerts detrimental effects on the myocardium. Recent studies have demonstrated that circulating levels of TNF, soluble TNF receptors 1 and 2 and interleukin-6 are strong prognostic markers. The results of two randomized studies directly antagonizing TNF in CHF patients were rather disappointing. Nevertheless, TNF antagonism remains a therapeutic option and should be focussed on patients with systemic immune activation, particularly at times of exacerbation.
Inflammatory cytokines are thought to contribute to the development and progression of chronic heart failure (CHF). It has been shown that especially tumor necrosis factor-alpha (TNF) is activated in patients with CHF and exerts detrimental effects on the myocardium. Recent studies have demonstrated that circulating levels of TNF, soluble TNF receptors 1 and 2 and interleukin-6 are strong prognostic markers. The results of two randomized studies directly antagonizing TNF in CHF patients were rather disappointing. Nevertheless, TNF antagonism remains a therapeutic option and should be focussed on patients with systemic immune activation, particularly at times of exacerbation.
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