Creatine Kinase

protein

CK is released from infarcting myocardium upon cardiomyocyte rupture and necrosis, serving as an early marker of myocardial injury in acute MI.

Pathway placement

Cascade stepMyocardial injury (shared endpoint)

Confidencehigh

RationaleAMI myocardial-injury marker; released on cardiomyocyte necrosis.

Druggability

Not assessed (no mapped human gene target).

Type I vs Type II discrimination

ScoresShared / rises in both

R — rupture / Type-I

C — confounder / Type-II

A — assay feasibility

E — evidence strength

100

T1DI (composite)

Specificity differential (R−C)+19.3

Direct evidence: higher in Type I (D=+2)

Type 1 MI showed significantly higher mean percentage rise in CK-MB from trough to peak compared to Type 2 MI.

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationmag 2

2anemia / acute blood lossmag 3

3hypovolemia / dehydrationmag 2

4tachyarrhythmiamag 2

5hypoxemia / respiratory failuremag 2

6hypertensive emergencymag 2

7high-demand / peri-operative stressmag 2

Coverage: 7/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 24 supporting references. See the discrimination table for all markers.

Validated clinical assay

Specimen

Serum or plasma

Collection tube

Serum separator (gold/red-top, SST) · Lithium heparin (green-top)

Method / principle

Enzymatic coupled-rate (IFCC)

Reagent / substrate

Creatine phosphate + ADP → creatine + ATP; coupled hexokinase/G6PD, NADPH read at 340 nm

Platform

Automated chemistry analyzer

Turnaround · availability

Routine same-day · Universal