Intestinal barrier dysfunction and microbial translocation in patients with first-diagnosed atrial fibrillation

Julian Friebel (Berlin)1, L. Blöbaum (Berlin)2, K. Jakobs (Berlin)1, M. Puccini (Berlin)1, U. Landmesser (Berlin)1, U. Rauch-Kröhnert (Berlin)2

1Charité - Universitätsmedizin Berlin CC 11: Med. Klinik für Kardiologie Berlin, Deutschland; 2Deutsches Herzzentrum der Charite (DHZC) Innere Medizin-Kardiologie Berlin, Deutschland


Background: Following the leaky-gut concept, microbial products (e.g. lipopolysaccharide, LPS) enter the circulation and mediate a pro-inflammatory immunological response. Higher plasma levels of LPS have been reported in patients with atrial fibrillation (AF) but not specifically during early AF. Methods: We studied data and blood samples from patients presenting with first- diagnosed AF (FDAF) (n = 80) and 20 controls. Results: Circulating biomarkers that are suggestive for mucosal inflammation (zonulin, mucosal adhesion molecule MAdCAM-1) and damage of the intestinal epithelium (intestinal-fatty acid binding protein) were increased in plasma of patients with FDAF compared to patients with chronic cardiovascular diseases but without AF. Surrogate plasma markers of increased intestinal permeability (LPS, CD14, LPS-binding protein, consumption of gut-derived LPS‐neutralizing IgA antibodies, EndoCAbs) were found during early AF. A reduced ratio of IgG/IgM EndoCAbs titres pointed towards chronic endotoxaemia. Biomarker of collagen turnover, that corresponded to LPS values, suggested an association of gut-derived low-grade endotoxaemia with adverse structural remodeling. LPS concentrations were higher in FDAF patients that experienced a major adverse cardiovascular event.
Conclusions: Intestinal barrier dysfunction and MT accompany FDAF. Improving gut permeability and low-grade endotoxaemia might be a potential therapeutic approach to reduce disease progression and vascular complications after FDAF.

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