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Corticosterone
Pathway / Off-pathway / systemic markers

Corticosterone

metabolite

Corticosterone elevation reflects acute stress and inflammatory regulation during myocardial injury and recovery.

Pathway placement
Cascade stepOff-pathway / systemic markers
Confidencemedium
RationaleGlucocorticoid stress response; systemic inflammatory modulation post-MI.
Also acts inVascular inflammation
Druggability
Not assessed (no mapped human gene target).

Type I vs non-Type I discrimination

ScoresNon-Type-I-associated
R — rupture / Type-I
33
C — non-Type-I
57
A — assay feasibility
42
E — evidence strength
12
T1DI (composite)
2
Specificity differential (R−C)-23.8
Non-Type-I axis panel
Does this marker also move in each non-Type-I setting? mag 0–3; higher means less Type-I-specific. n/a = no evidence retrieved, which is not the same as no change.
2sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
2hypovolemia / dehydrationmag 2
2tachyarrhythmiamag 1
2hypoxemia / respiratory failuremag 1
2hypertensive emergencymag 2
2high-demand / peri-operative stressmag 2
3sudden cardiac deathn/a
4aPCI-related periproceduraln/a
4bstent thrombosisn/a
4cin-stent restenosisn/a
5CABG-relatedmag 2
Coverage: 7/12 axes with evidence
Tier: deep-scored (abstract-extracted) · 13 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(2)