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Trimethylamine N-oxide
Pathway / Lipid retention & oxidation

Trimethylamine N-oxide

metabolite

TMAO promotes lipid oxidation, plaque inflammation and destabilization, increasing atherothrombotic rupture and thrombotic risk.

Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleAtherosclerotic-burden predictor; plaque rupture and instability biomarker; MACE predictor in STEMI.
Also acts inVascular inflammation, Systemic / off-pathway, Cap degradation / rupture
Druggability
Not assessed (no mapped human gene target).

Type I vs Type II discrimination

ScoresLow-confidence (proxy)
R — rupture / Type-I
69
C — confounder / Type-II
60
A — assay feasibility
42
E — evidence strength
27
T1DI (composite)
6
Specificity differential (R−C)+8.8
Confounder panel (Type-II drivers)
No confounder evidence retrieved.
Tier: light (literature co-occurrence proxy — lower confidence). See the discrimination table for all markers.

Assay & specimen

Class-level default (no specific cleared assay)— generic method inferred from analyte class; confirm against a specific product insert before use.
Specimen
Serum, plasma or urine
Collection tube
Serum separator (gold/red-top, SST) · Lithium heparin (green-top) · Sterile urine container
Method / principle
LC-MS/MS (targeted metabolomics) or enzymatic colorimetric where available
Reagent / substrate
Stable-isotope-labeled internal standard (MS); or enzyme-coupled Trinder reagent
Platform
LC-MS/MS; some automated chemistry
Turnaround · availability
Send-out / research · Specialized / research

Literature evidence(13)