SYSTEMIC INFLAMMATION IN PATIENTS WITH HEART-FAILURE

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 cir culatory support using biventricular assist device systems Methods and Results Plasma levels of cytokines (IL-6, IL-8, TNF-alpha) and solubl e adhesion molecules (sVCAM, sE-, sL-, sP-Selectin) were determined in samples obtained from patients with chronic heart failure NYHA classe s II-III, patients with overt cardiogenic shock before and after impla ntation of a mechanical assist-device system ('Berlin Heart') and in p atients 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 hear t failure NYHA classes II-III. The signs of systemic inflammation disa ppeared following successful mechanical circulatory support, but persi sted in patients who developed infectious complications. Conclusions O ur data suggest that a systemic hypoxic and inflammatory syndrome is m anifested during end-stage heart failure, such as in patients with sep sis or who have suffered non-infectious insults. During mechanical cir culatory support, elevated levels of inflammatory mediators may be ind icative of persistent peripheral hypoxia associated with a high risk f or infection or sepsis. Therefore, the monitoring of inflammatory medi ators should be evaluated as markers of the effectiveness of this ther apy.