Cortisol

metabolite

Cortisol elevation during acute MI reflects systemic stress response via HPA-axis independent of atherothrombotic cascade.

Pathway placement

Cascade stepOff-pathway / systemic markers

Confidencemedium

RationaleSystemic neuroendocrine/HPA-axis stress response; off atherothrombotic cascade.

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)-25

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationmag 2

2anemia / acute blood lossn/a

3hypovolemia / dehydrationn/a

4tachyarrhythmiamag 1

5hypoxemia / respiratory failuremag 2

6hypertensive emergencyn/a

7high-demand / peri-operative stressmag 2

Coverage: 4/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 5 supporting references. See the discrimination table for all markers.

Validated clinical assay

Specimen

Serum/plasma (timed); saliva; 24h urine (free)

Collection tube

Serum separator (gold/red-top, SST) · Sterile urine container

Method / principle

Chemiluminescent immunoassay or LC-MS/MS

Reagent / substrate

Anti-cortisol antibody; or deuterated cortisol IS for MS

Platform

Automated analyzer / LC-MS/MS

Turnaround · availability

Routine · Universal