SAH

metabolite

Elevated SAH/SAM ratio post-MI reflects impaired methylation capacity and mitochondrial CoQ deficiency.

Pathway placement

Cascade stepOff-pathway / systemic markers

Confidencelow

RationaleS-adenosylhomocysteine; decreased SAM/SAH ratio marks methyl-transfer dysfunction post-MI.

Also acts inMyocardial injury

Druggability

Not assessed (no mapped human gene target).

Type I vs Type II discrimination

ScoresType-II-associated

R — rupture / Type-I

—

C — confounder / Type-II

A — assay feasibility

E — evidence strength

T1DI (composite)

Specificity differential (R−C)-51.7

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationmag 2

2anemia / acute blood lossn/a

3hypovolemia / dehydrationn/a

4tachyarrhythmian/a

5hypoxemia / respiratory failuren/a

6hypertensive emergencymag 2

7high-demand / peri-operative stressn/a

Coverage: 2/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 29 supporting references. See the discrimination table for all markers.

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