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Gut microbiota-derived metabolites in atrial fibrillation: risk markers or modifiable risk factors?
  1. Dominik Linz1,
  2. Renate B Schnabel2
  1. 1Klinik für Innere Medizin III Kardiologie, Angiologie und Internistische Intensivmedizin, Maastricht UMC+, Maastricht, The Netherlands
  2. 2Cardiology, University Heart Center Hamburg, Hamburg, Germany
  1. Correspondence to Dr Dominik Linz, Klinik für Innere Medizin III Kardiologie, Angiologie und Internistische Intensivmedizin, Maastricht UMC+, Maastricht, 6229 HX, The Netherlands; Dominik.Linz{at}gmx.de

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Most cardiovascular risk factors such as diabetes, hypertension and obesity have been shown to be associated with alterations in the composition of the gut microbiota (dysbiosis). Dysbiosis determines the production of metabolite derived from the gut microbiota.1 2 One of the best studied gut microbiota-derived metabolites is trimethylamine N-oxide (TMAO). Dietary L-Carnitine (eg, in red meat) is converted to trimethylamine (TMA) by the intestinal microbiota, and is then oxidised to TMAO by flavin-containing mono-oxygenases in the liver. Increased TMAO levels have been shown to be associated with increased risk of cardiovascular mortality and cerebral infarction in several previous studies, but the role of TMAO levels in preselected susceptible populations, such as patients with atrial fibrillation (AF), remains unclear. Although clinical data evaluating the association between AF and TMAO are inconclusive,3 marked increases in the microbial genes underlying TMA formation and TMA-microbial producers are observed in the intestines of patients with AF,4 and small studies showed that elevated serum TMAO levels were predictive of thromboembolic events in patients with AF.5 However, data from larger populations are missing.

Luciani et al6 assessed the association of plasma TMAO and adverse events in 2379 subjects with AF from the ongoing Swiss Atrial Fibrillation (Swiss-AF) cohort. Cox models, adjusting for baseline covariates, showed increased total mortality (HR 1.65, 95% CI 1.17 to 2.32, p<0.01) as well as cardiovascular mortality (HR 1.86, 95% …

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Footnotes

  • Contributors Both authors contributed to the draft and completion of this editorial.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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