LPC (20:3)
lipidDecreased LPC (20:3) content post-MI reflects phospholipid catabolism and myocardial dysfunction progression.
Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencemedium
RationaleDecreased lysophosphatidylcholine predicts heart-failure after MI; myocardial injury and lipid remodeling 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-II67
A — assay feasibility40
E — evidence strength67
T1DI (composite)7
Specificity differential (R−C)-51.7
Confounder panel (Type-II drivers)
1sepsis / systemic inflammationmag 2
2anemia / acute blood lossn/a
3hypovolemia / dehydrationn/a
4tachyarrhythmian/a
5hypoxemia / respiratory failuremag 2
6hypertensive emergencyn/a
7high-demand / peri-operative stressn/a
Coverage: 2/7 confounders with evidence
Tier: deep-scored (abstract-extracted) · 16 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 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
Literature evidence(1)
- Lipidomic analyses reveal potential biomarkers for predicting death and heart failure after acute myocardial infarction.Clinica chimica acta; international journal of clinical chemistry · 2024 · PMID 39068962 · doi