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Succinate
Pathway / Myocardial injury (shared endpoint)

Succinate

metabolite

Succinate accumulates during myocardial ischemia and generates ROS upon reperfusion, marking cardiomyocyte injury and ischemia-reperfusion damage in STEMI.

Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencehigh
RationaleIschemia-reperfusion injury marker; mitochondrial ROS generation upon myocardial reperfusion.
Also acts inVascular inflammation
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
56
A — assay feasibility
42
E — evidence strength
18
T1DI (composite)
2
Specificity differential (R−C)-40.6
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
3hypovolemia / dehydrationn/a
4tachyarrhythmian/a
5hypoxemia / respiratory failuremag 2
6hypertensive emergencyn/a
7high-demand / peri-operative stressmag 1
Coverage: 3/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 2 supporting references. 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(6)