# Relationship Between Level of Trimethylamine Oxide and the Risk of Recurrent Cardiovascular Events in Patients with Acute Myocardial Infarction

**Authors:** Wenjun Ji, Bin Zhang, Jiahui Liu, Kaiyin Li, Jia Jia, Fangfang Fan, Jie Jiang, Xingang Wang, Yan Zhang

PMC · DOI: 10.3390/nu17101664 · 2025-05-14

## TL;DR

High levels of trimethylamine oxide (TMAO) and choline are linked to higher risks of heart events in patients who had a heart attack.

## Contribution

This study shows choline has better predictive power than TMAO for cardiovascular risk in acute myocardial infarction patients.

## Key findings

- TMAO levels were associated with increased risk of MACE, cardiac death, and recurrent MI.
- Choline showed stronger predictive power for all-cause mortality than TMAO.
- A choline pathway independent of TMAO contributes to cardiovascular risk.

## Abstract

Background: This study investigated the value of trimethylamine oxide (TMAO) and its precursors in secondary prevention for patients with acute myocardial infarction (AMI). Methods: We retrospectively enrolled patients diagnosed with AMI. The associations of TMAO and its precursors with endpoint events were estimated by Cox proportional hazards models. Results: During a median follow-up of 6.4 years, 319 (32.0%) major adverse cardiovascular event (MACE) occurred in the 996 patients enrolled. After adjusting for traditional risk factors, the risk of MACE, cardiac death, and recurrent MI increased by 28% (HR 1.28, 95% CI 1.10–1.49), 44% (HR 1.44, 95% CI 1.12–1.84), and 27% (HR 1.27, 95% CI 1.04–1.55), respectively, per one increment in ln-transformed TMAO. After adjustment for the levels of its precursors, the relationship between TMAO and MACE was still significant. Choline was associated with MACEs, all-cause mortality, cardiac death, and risk of recurrent MI after adjusting for the levels of the remaining metabolites, in addition to traditional risk factors. The overall ability to predict all-cause mortality was better for the choline model than for the TMAO model (continuous NRI 0.185, p = 0.007; IDI 0.030, p = 0.020). Mediation effect analysis showed that the mediating effect of TMAO on choline and the risk of all-cause mortality was 11.39% (95% CI 0.0209–0.2200, p = 0.016), suggesting the existence of a choline activity pathway that is independent of the TMAO pathway. Conclusions: TMAO and choline were associated with an increased risk of MACE in patients with AMI, and choline had better predictive power.

## Linked entities

- **Chemicals:** trimethylamine oxide (PubChem CID 1145), choline (PubChem CID 305)
- **Diseases:** acute myocardial infarction (MONDO:0004781)

## Full-text entities

- **Diseases:** AMI (MESH:D009203), MACE (MESH:D002318), cardiac death (MESH:D003643)
- **Chemicals:** TMAO (MESH:C005855), Choline (MESH:D002794)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12114086/full.md

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Source: https://tomesphere.com/paper/PMC12114086