Research progress on the relationship between trimethylamine oxide and atrial fibrillation

CHEN Xianhui; MA Yulan

doi:10.16766/j.cnki.issn.1674-4152.003560

Volume 22 Issue 6

Jun. 2024

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Article Navigation > Chinese Journal of General Practice > 2024 > 22(6): 1033-1037

CHEN Xianhui, MA Yulan. Research progress on the relationship between trimethylamine oxide and atrial fibrillation[J]. Chinese Journal of General Practice, 2024, 22(6): 1033-1037. doi: 10.16766/j.cnki.issn.1674-4152.003560

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CHEN Xianhui, MA Yulan. Research progress on the relationship between trimethylamine oxide and atrial fibrillation[J]. Chinese Journal of General Practice, 2024, 22(6): 1033-1037. doi: 10.16766/j.cnki.issn.1674-4152.003560

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Research progress on the relationship between trimethylamine oxide and atrial fibrillation

doi: 10.16766/j.cnki.issn.1674-4152.003560

CHEN Xianhui¹
, MA Yulan^{2
,
,}

1.
Graduate School of Qinghai University, Xi' ning, Qinghai 810016, China

Funds:

81760084

Received Date: 2023-11-16
Available Online: 2024-07-22

Abstract

Abstract

The gut microbiota is a complex community that interacts with the dynamic functions of the host, and proper gut microbiota structure and metabolite function are essential for maintaining homeostasis. In recent years, a large number of studies have demonstrated that the gut microbiota and its derived metabolites influence the development of cardiovascular diseases, including cardiac arrhythmias, of which atrial fibrillation is one of the most common. Trimethylamine oxide (TMAO) is one of the most studied gut microbiota-derived metabolites, and TMAO has been found to be strongly associated with the development of atrial fibrillation. Many epidemiological studies have shown that TMAO plays a role in the onset, development and prognosis of atrial fibrillation (AF). TMAO increases the susceptibility to AF by contributing to the development of multiple cardiovascular risk factors. In addition, TMAO promotes atrial structural remodeling by stimulating inflammatory responses, causing cardiac fibrosis and atrial pyroptosis. Elevated levels of TMAO also increase atrial electrophysiological instability, triggering ectopic activity that leads to electrophysiological remodeling, and directly or indirectly activate the autonomic nervous system to cause neural remodeling that induces atrial fibrillation. In addition, elevated levels of TMAO induce platelet hyper-reactivity, which promotes arterial thrombosis, increases the incidence of thromboembolism in AF, and is also significantly associated with AF recurrence after ablation. TMAO has been shown to have some potential values in the prevention and treatment of AF. The composition of the gut microbiota can be modulated through dietary habits by reducing the intake of trimethylamine-producing dietary precursors and thereby reducing circulating levels of TMAO, by increasing the excretion of TMAO from the kidneys through certain drugs, and by directly taking prebiotics, probiotics, or through fecal flora transplantation, which can in turn alter the levels of gut microbiota -derived metabolites. In this paper, we review the above aspects based on the findings of the related literature, with the aim of providing a theoretical basis for future related studies.
- Trimethylamine oxide,
- Atrial fibrillation,
- Gut microbiota

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References(44)

References

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Research progress on the relationship between trimethylamine oxide and atrial fibrillation

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