Basic Research in Cardiology

, Volume 99, Issue 1, pp 18–28 | Cite as

Tumour necrosis factor-α and the failing heart

Pathophysiology and therapeutic implications
  • Stephan von Haehling
  • Ewa A. Jankowska
  • Stefan D. Anker
JOINT SESSION OF THE INTERNATIONAL SOCIETY FOR HEART RESEARCH EUROPE AND THE GERMAN CARDIAC SOCIETY: TNFα IN HEART FAILURE

Abstract.

Immune activation plays a significant role in the development and progression of chronic heart failure (CHF). Indeed, pro-inflammatory cytokines, especially tumour necrosis factor-α (TNFα) are activated in this condition and exert direct detrimental actions on the myocardium. Physiological dampeners of TNFα production, such as interleukin-10, catecholamines, cortisol, and others fail in the course of the disease. However, the outcomes of two large-scale clinical trials with etanercept and infliximab, which directly antagonise TNFα have been rather disappointing. Nevertheless, TNFα antagonism remains a major target of CHF therapy, although counterbalancing this cytokine alone may not be sufficient.

Key words

Heart failure cytokines tumour necrosis factor therapy 

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Copyright information

© Steinkopff Verlag 2003

Authors and Affiliations

  • Stephan von Haehling
    • 1
    • 4
  • Ewa A. Jankowska
    • 1
    • 2
  • Stefan D. Anker
    • 1
    • 3
  1. 1.Imperial College School of MedicineNational Heart & Lung Institute, Department of Clinical CardiologyLondonUK
  2. 2.Cardiac DepartmentMilitary HospitalWroclawPoland
  3. 3.Applied Cachexia Research, Department of CardiologyChartité Medical School Campus Virchow-KlinikumBerlinGermany
  4. 4.National Heart and Lung Institute, Department of Clinical CardiologyLondonU. K.

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