Copyright © 1998 by the European Society of Cardiology.
Systemic inflammation in patients with heart failure
Department of Thoracic and Cardiovascular Surgery, German Heart Institute, Berlin
Department of Medical Immunology, Charitè, Humboldt-University Berlin, Berlin, Germany
Department of Internal Medicine, Charitè, Humboldt-University Berlin, Berlin, Germany
accepted November 21, 1997
Aims
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-
) 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.
Conclusions
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.
Key Words: 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.
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