Trimethylamine-N as a Novel Biomarker in Acute Decompensated Heart Failure: A Comparative Study with Stable Heart Failure Patients

Abstract

Trimethylamine-N-oxide (TMAO), a metabolite produced by gut microbiota, has been linked to cardiovascular disease; however, its role in acute decompensated heart failure (ADHF) remains unclear. In this prospective observational study involving 102 ADHF and 60 stable heart failure (SHF) patients, plasma TMAO levels were correlated with clinical, echocardiographic, and laboratory parameters. TMAO levels were higher in ADHF compared with SHF (median 452.9 vs 372.4 ng/mL; P < .001), showing a positive correlation with B-type natriuretic peptide (BNP) and creatinine, and an inverse correlation with left ventricular ejection fraction (LVEF), estimated glomerular filtration rate (eGFR), hemoglobin, and high-density lipoprotein (HDL) cholesterol. TMAO demonstrated fair diagnostic ability for identifying ADHF (area under the curve [AUC] = 0.751), although weaker (P = .006) than BNP (AUC = 0.875). Multivariate analysis identified both TMAO and BNP as important discriminators. Additionally, TMAO levels were higher in ischemic than in non-ischemic heart failure (P = .047). These findings suggest that elevated TMAO is associated with ADHF and markers of disease severity. Because TMAO levels are influenced by renal function and anemia, it may be a context-dependent adjunct to natriuretic peptides rather than a standalone diagnostic marker. Further studies are needed to determine any additional value for diagnosis and risk stratification.