LPC (18:0)

lipid

Decreased LPC (18:0) content post-MI reflects phospholipid catabolism linked to myocardial injury and inflammatory response.

Pathway placement

Cascade stepMyocardial injury (shared endpoint)

Confidencemedium

RationaleDecreased lysophosphatidylcholine predicts post-MI mortality; myocardial injury and inflammation marker.

Also acts inVascular inflammation

Druggability

Not assessed (no mapped human gene target).

Type I vs Type II discrimination

ScoresLow-confidence (proxy)

R — rupture / Type-I

C — confounder / Type-II

A — assay feasibility

E — evidence strength

T1DI (composite)

Specificity differential (R−C)-17.9

Confounder panel (Type-II drivers)

No confounder evidence retrieved.

Tier: light (literature co-occurrence proxy — lower confidence). 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