What is the clinical evidence from this study?

Study design: Cohort. Population: High atherosclerotic risk (n=134). Intervention: Plasma Trimethylamine-N-oxide (TMAO). Primary outcome: Subclinical myocardial damage (hs-cTnT ≥ 14 ng/L) (OR 1.58, 95% CI 1.24-2.08, p=0.0007).

July 22, 2021Open Access

Gut microbiota-generated metabolite, trimethylamine-N-oxide, and subclinical myocardial damage: a multicenter study from Thailand

Key Result

Elevated fasting plasma TMAO levels were independently associated with subclinical myocardial damage (OR 1.58) in stable patients at high risk of cardiovascular events.

Study Design

Type

Cohort (n=134)

Multicenter

Yes

Structured PICO

Does elevated plasma TMAO predict subclinical myocardial damage in patients at high risk of cardiovascular events?

Population

134 patients from the CORE-Thailand registry at high risk of cardiovascular events, mean age 64 ± 8.9 years, 61% men, including 123 (92%) with established atherosclerotic disease and 11 (8%) with multiple risk factors.

Intervention

Elevated plasma Trimethylamine-N-oxide (TMAO) levels

Outcome

Subclinical myocardial damage (SMD), defined as high-sensitivity cardiac troponin-T (hs-cTnT) ≥ 14 ng/Lsurrogate

Elevated fasting plasma TMAO is an independent predictor of subclinical myocardial damage in stable patients at high risk of cardiovascular events.

Main Result

Effect estimate: OR 1.58 (95% CI 1.24-2.08)

p-value: p=0.0007

Limitations

Only patients with available TMAO data were included, potentially leading to selection bias
Could not exclude the potential for dietary intake of phosphatidylcholine or TMAO within 24 hours before blood sampling
Plasma TMAO and hs-cTnT were measured at only one point in time, preventing evaluation of prognostic value of changes
Relatively low number of patients with multiple risk factors were included

Abstract

Plasma Trimethylamine-N-oxide (TMAO), a gut microbiota metabolite from dietary phosphatidylcholine, is mechanistically linked to cardiovascular disease (CVD) and adverse cardiovascular events. We aimed to examine the relationship between plasma TMAO levels and subclinical myocardial damage using high-sensitivity cardiac troponin-T (hs-cTnT). We studied 134 patients for whom TMAO data were available from the Cohort Of patients at a high Risk of Cardiovascular Events-Thailand (CORE-Thailand) registry, including 123 (92%) patients with established atherosclerotic disease and 11 (8%) with multiple risk factors. Plasma TMAO was measured by NMR spectroscopy. In our study cohort (mean age 64 ± 8.9 years; 61% men), median TMAO was 3.81 μM (interquartile range IQR 2.89-5.50 μM), and median hs-cTnT was 15.65 ng/L (IQR 10.17-26.67). Older patients and those with diabetic or hypertension were more likely to have higher TMAO levels. Plasma TMAO levels correlated with those of hs-cTnT (r = 0.54; p < 0.0001) and were significantly higher in patients with subclinical myocardial damage (hs-cTnT ≥ 14 ng/L; 4.48 μM vs 2.98 μM p < 0.0001). After adjusting for traditional risk factors, elevated TMAO levels remained independently associated with subclinical myocardial damage (adjusted odds ratio OR: 1.58; 95% CI 1.24-2.08; p = 0.0007). This study demonstrated that plasma TMAO was an independent predictor for subclinical myocardial damage in this study population.

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