© 2004 European Society of Cardiology
Selective intestinal decontamination in advanced chronic heart failure: a pilot trial
a Department of Cardiology, University Hospital Antwerp Wilrijkstraat 10, 2650 Edegem, Belgium
b Department of Intensive Care Medicine, University Hospital Antwerp Wilrijkstraat 10, 2650 Edegem, Belgium
c Department of Immunology, University Hospital Antwerp Wilrijkstraat 10, 2650 Edegem, Belgium
d Department of Medical Microbiology, University of Liverpool UK
e Department of Microbiology, University Hospital Antwerp Wilrijkstraat 10, 2650 Edegem, Belgium
f Department of Medical Statistics, University Hospital Antwerp Wilrijkstraat 10, 2650 Edegem, Belgium
g Department of Cardiology, Franz-Volhard-Klinik, Charité Medical School Campus Berlin-Buch, Berlin, Germany
h Department of Cardiology, Universitätsklinik und Poliklinik für Innere Medizin III Halle, Germany
* Corresponding author. Tel.: +32-3-821-46-72; fax: +32-3-825-08-48. E-mail address: Viviane.Conraads{at}uza.be
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Abstract |
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Background and aims: Endotoxin, derived from intestinal aerobic Gram-negative bacilli (AGNB), could be an important monocyte activator in chronic heart failure (CHF). The effect of selective decontamination of the digestive tract (SDD) on intracellular monocyte cytokine production, monocyte CD14 expression, circulating endotoxin and cytokines, and flow-mediated dilation (FMD) was studied in patients with severe CHF.
Methods and results: Ten patients with CHF (NYHA class III–IV) were enrolled in a non-placebo controlled pilot trial involving the administration of SDD (polymyxin B, tobramycin) for 8 weeks. One patient was later excluded due to cardiac transplantation. Before treatment, after 4 and 8 weeks therapy, and 6 weeks post-treatment, monocyte CD14 expression, intracellular monocyte production of interleukin-1β [IL-1β], interleukin-6 [IL-6], tumour necrosis factor (TNF)-
with and without lipopolysaccharide (LPS) stimulation were measured. Concentrations of endotoxin and cytokines (IL-1β, IL-6, TNF-) were also determined. AGNB in faeces, intestinal endotoxin and FMD were assessed at baseline, after 4 weeks of treatment and 6 weeks post-treatment. SDD eradicated intestinal AGNB (P<0.00001) and decreased faecal endotoxin concentrations (P<0.00001). There was a significant decline in monocyte CD14 expression (P=0.03) and in IL-1β (P=0.0001), IL-6 (P=0.02) and TNF- (P=0.0002) production after 4 and 8 weeks of treatment in the basal state and for IL-1β (P=0.008) and IL-6 (P=0.005) after LPS stimulation. FMD significantly improved at 4 weeks and returned to baseline after treatment discontinuation (P=0.002). Circulating concentrations of endotoxin and cytokines remained unchanged.
Conclusion: Reduction of the intestinal endotoxin pool led to a decrease in monocyte CD14 expression and intracellular cytokine production in patients with severe CHF. The improvement of peripheral endothelial function could be a marker of the anti-inflammatory effect of SDD.
Key Words: Chronic heart failure • Inflammation • Endotoxin • Selective digestive decontamination • Endothelial dysfunction
Received June 30, 2003; Revised October 10, 2003; Accepted December 7, 2003
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