OUP user menu

Systemic inflammation in patients with heart failure

D. Hasper, M. Hummel, F.X. Kleber, I. Reindl, H.-D. Volk
DOI: http://dx.doi.org/10.1053/euhj.1997.0858 761-765 First published online: 1 May 1998



We hypothesized that chronic heart failure as a model of systemic hypoxia may result in systemic inflammation. The signs of a systemic inflammatory response should disappear after successful mechanical circulatory support using biventricular assist device systems

Methods and Results

Plasma levels of cytokines (IL-6, IL-8, TNF-α) and soluble adhesion molecules (sVCAM, sE-, sL-, sP-Selectin) were determined in samples obtained from patients with chronic heart failure NYHA classes II–III, patients with overt cardiogenic shock before and after implantation of a mechanical assist-device system (‘Berlin Heart’) and in patients with coronary artery disease as a control. Elevated levels of cytokines and soluble adhesion molecules could be observed in patients with cardiogenic shock, although slightly decreased levels of soluble adhesion molecules were also detectable in patients with chronic heart failure NYHA classes II–III. The signs of systemic inflammation disappeared following successful mechanical circulatory support, but persisted in patients who developed infectious complications.


Our data suggest that a systemic hypoxic and inflammatory syndrome is manifested during end-stage heart failure, such as in patients with sepsis or who have suffered non-infectious insults. During mechanical circulatory support, elevated levels of inflammatory mediators may be indicative of persistent peripheral hypoxia associated with a high risk for infection or sepsis. Therefore, the monitoring of inflammatory mediators should be evaluated as markers of the effectiveness of this therapy.

  • chronic heart failure
  • cardiogenic shock
  • biventricular assist device system
  • systemic inflammatory response syndrome
  • cytokines
  • adhesion molecules


  • f1 Correspondence: Hans-Dieter Volk, Institut für Medizinische Immunologie, Universitätsklinikum Charitè, Humboldt-Universität Berlin, Schumannstr. 20/21, 10098 Berlin, Germany.

View Abstract