LPE (18:2)

lipid

Decreased LPE (18:2) content post-MI reflects phospholipid catabolism and severity of myocardial ischemic injury.

Pathway placement

Cascade stepMyocardial injury (shared endpoint)

Confidencemedium

RationaleDecreased lysophosphatidylethanolamine predicts post-MI mortality; myocardial lipid remodeling and injury marker.

Also acts inSystemic / off-pathway

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)-52

Confounder panel (Type-II drivers)

1sepsis / systemic inflammationn/a

2anemia / acute blood lossn/a

3hypovolemia / dehydrationmag 2

4tachyarrhythmian/a

5hypoxemia / respiratory failuren/a

6hypertensive emergencyn/a

7high-demand / peri-operative stressn/a

Coverage: 1/7 confounders with evidence

Tier: deep-scored (abstract-extracted) · 2 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 or plasma (EDTA to limit oxidation)

Collection tube

K2/K3-EDTA (lavender-top) · Serum separator (gold/red-top, SST)

Method / principle

LC-MS/MS lipidomics (targeted or shotgun)

Reagent / substrate

Deuterated lipid-class internal standards; MS/MS transitions

Platform

LC-MS/MS

Turnaround · availability

Research · Research-only