© 2003 European Society of Cardiology
Invasive assessment of bacterial endotoxin and inflammatory cytokines in patients with acute heart failure
a Herzzentrum der Universität Leipzig Strümpellstraße 39, 04289 Leipzig, Germany
b Royal Brompton Hospital London, UK and Franz Volhard Klinik, Charité Berlin-Buch Berlin, Germany
* Corresponding author. Tel.: +49-341-8650; fax: +49-341-865-1461. E-mail address: j.niebauer{at}medizin.uni-leipzig.de
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Abstract |
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Aims: To test the hypothesis that during acute heart failure endotoxin might be increased in hepatic veins as a sign of bacterial or endotoxin translocation from the bowel into the blood stream.
Methods and results: In patients with acute heart failure (NYHA IV; n=17) levels of endotoxin, soluble (s) CD14, tumor necrosis factor 
(TNF and interleukin 6 (IL6)) were measured in blood drawn from an antecubital vein on admission and compared with age-matched patients with stable chronic heart failure (n=21) and healthy volunteers (n=9). All levels were systemically elevated during acute heart failure (all P<0.05); once patients were stable enough to undergo cardiac catheterization, endotoxin was found to be significantly higher in hepatic veins (0.62±0.05 EU/ml) than left ventricles (0.46±0.04 EU/ml; P<0.05), whereas sCD14, TNF and IL6 were not different between these sites. At follow-up (29±6 days) endotoxin but not sCD14, TNF or IL-6 was significantly lower as compared to baseline (P<0.05).
Conclusions: Higher levels of endotoxin in hepatic veins as compared to the left ventricle during acute heart failure are suggestive of bacterial or endotoxin translocation from the bowel into the blood stream. This may lead to new treatment strategies. The lack of difference in TNF levels between the pulmonary artery and the left ventricle sheds doubt on the heart as a source of systemically elevated TNF levels.
Key Words: Cytokines • Edema • Heart failure • Inflammation
Received November 12, 2002; Revised February 3, 2003; Accepted June 16, 2003
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