Peschel Thomas, Schönauer Martin, Thiele Holger, Anker Stefan D, Schuler Gerhard, Niebauer Josef
Herzzentrum der Universität Leipzig, Strümpellstrasse 39, 04289 Leipzig, Germany.
Eur J Heart Fail. 2003 Oct;5(5):609-14. doi: 10.1016/s1388-9842(03)00104-1.
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.
In patients with acute heart failure (NYHA IV; n=17) levels of endotoxin, soluble (s) CD14, tumor necrosis factor alpha (TNFalpha 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, TNFalpha and IL6 were not different between these sites. At follow-up (29+/-6 days) endotoxin but not sCD14, TNFalpha or IL-6 was significantly lower as compared to baseline (P<0.05).
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 TNFalpha levels between the pulmonary artery and the left ventricle sheds doubt on the heart as a source of systemically elevated TNFalpha levels.
