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Dietary metabolism, gut microbiota and acute heart failure
  1. WH Wilson Tang1,2,
  2. Stanley L Hazen1,2
  1. 1Department of Cardiovascular Disease, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio, USA
  2. 2Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA
  1. Correspondence to Dr WH Wilson Tang, Department of Cardiovascular Disease, Heart and Vascular Institute, Cleveland Clinic, 9500 Euclid Avenue, Desk J3-4, Cleveland OH 44195, USA; tangw{at}

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The human gut harbours trillions of microbial organisms. The overall architecture of the microbial community is remarkably stable over time within an individual and his/her family members. However, gut microbial composition and function are also profoundly influenced by dietary exposure and the local intestinal environment. Thus, the combined functions of the gut microbiome and host genotype together determine global physiological responses to varied nutrient inputs, with both dynamic and adaptive functional components from gut microbiome and host participating. Furthermore, the gut microbiome has been increasingly appreciated to play important physiological and metabolic roles in our overall health and disease.

It has long been recognised that heart failure (HF) is associated with altered intestinal function, likely as a consequence of ischaemia and/or congestion within the intestines. There is enhanced gut bacterial translocation due to impaired intestinal barrier function, as well as release and detection of heightened levels of endotoxin-like compounds within the circulation, accompanied by heightened inflammatory responses and increased indices of oxidative stress. On the other hand, metabolic derangements as a result of altered gut microbial metabolism may also influence the overall host metabolic processes. Our group has discovered that gut microbiota, via specific microbial choline trimethylamine-lyases, play an obligatory role in the generation of trimethylamine N-oxide (TMAO), a bioactive metabolite of choline or L-carnitine that contributes to cardiovascular disease pathogenesis.1 ,2 In recent studies, we further observed that patients with HF have significantly …

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  • Contributors WHWT drafted the editorial and SLH critically reviewed and edited the final version.

  • Funding Supported by grants from the National Institutes of Health and the Office of Dietary Supplements (R01HL103866, P20HL113452 and R01DK10600).

  • Competing interests SLH are named as coinventor on pending patents held by the Cleveland Clinic relating to cardiovascular diagnostics and therapeutics. SLH reports having been paid as a consultant for the following companies: Esperion and P&G. SLH reports receiving research funds from Abbott, P&G, Pfizer, Roche Diagnostics and Takeda. SLH reports having the right to receive royalty payments for inventions or discoveries related to cardiovascular diagnostics or therapeutics from the following companies: Cleveland Heart Lab, Siemens, Esperion and Frantz Biomarkers LLC.

  • Provenance and peer review Commissioned; internally peer reviewed.

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