Invasive Assessment of Bacterial Endotoxin and Inflammatory Cytokines in Patients with Acute Heart Failure
Open accessAbstract
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 α (TNFα 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, TNFα and IL6 were not different between these sites. At follow-up (29±6 days) endotoxin but not sCD14, TNFα 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 TNFα levels between the pulmonary artery and the left ventricle sheds doubt on the heart as a source of systemically elevated TNFα levels.
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Translocation of lipopolysaccharide from the bowel in heart failure is supported by higher endotoxin concentrations in the hepatic vein as compared to blood directly sampled from the ventricles.
“Translocation of LPS from the bowel in this setting is supported by higher endotoxin concentrations in the hepatic vei,n as compared to blood directly sampled from the ventricles26.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [26]
LPS levels are higher in blood samples recovered from the hepatic vein than from the systemic circulation, providing direct evidence that LPS can be translocated from the gut.
“Moreover, targeted sampling studies have shown that LPS levels are higher in blood samples recovered from the hepatic vein as opposed to the systemic circulation (direct sampling from the ventricles), providing direct evidence that LPS can be translocated from the gut39.”
From Dietary metabolism, the gut microbiome, and heart failure (2019) · cites this paper as [39]
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“, the digestive translocation of LPS [49].”
Background
- Authors
- Peschel, T., Schönauer, M., Thiele, H., Anker, S., Schuler, G., & Niebauer, J.
- Affiliations
- Leipzig University (DE)
- Herzzentrum der Universität Leipzig , Strümpellstraße 39, 04289, Leipzig ,
- Royal Brompton Hospital (GB)
- Corresponding author
- Niebauer, Josef
- Venue
- European Journal of Heart Failure
- Publisher
- Oxford University Press (OUP)
- Published
- 2003-10-01
- Volume
- 5
- Issue
- 5
- Pages
- 609-614
- ISSN
- 1388-9842 (ISSN-L)
- 1879-0844
- OpenAlex
- W2020604058
- Cited by
- 187
- References
- 29
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 8 · 2023: 14 · 2022: 6 · 2021: 15 · 2020: 13 · 2019: 11 · 2018: 8 · 2017: 10 · 2016: 10 · 2015: 12 · 2014: 6 · 2013: 6 · 2012: 10
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Journal of Heart Failure (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Health Sciences › Medicine › Epidemiology › Infective Endocarditis Diagnosis and Management
- Keywords
- acute heart failure, bacterial endotoxin, endotoxin translocation, hepatic vein, soluble CD14, TNF-α, interleukin-6, inflammatory cytokines, bacterial translocation, cardiac catheterization, left ventricle, pulmonary artery
- MeSH terms
- Aged, Blood Specimen Collection, Endotoxins, Heart Failure, Heart Ventricles, Hepatic Veins, Humans, Tumor Necrosis Factor-alpha, Interleukin-6, Case-Control Studies, Cytokines, Inflammation Mediators, Lipopolysaccharide Receptors, Bacterial Translocation
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