CoronaryAtlas logo
CoronaryAtlas
LPC (18:2)
Pathway / Myocardial injury (shared endpoint)

LPC (18:2)

lipid

Decreased LPC (18:2) content post-MI reflects myocardial injury, phospholipase-A2 activation, and inflammatory lipid mediator generation.

Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencehigh
RationaleMI biomarker; decreased content predicts HF post-MI; links myocardial injury and systemic inflammation.
Also acts inVascular inflammation
Druggability
Not assessed (no mapped human gene target).

Type I vs non-Type I discrimination

ScoresIndeterminate
R — rupture / Type-I
—
C — non-Type-I
0
A — assay feasibility
40
E — evidence strength
95
T1DI (composite)
22
Specificity differential (R−C)+15
Non-Type-I axis panel
Does this marker also move in each non-Type-I setting? mag 0–3; higher means less Type-I-specific. n/a = no evidence retrieved, which is not the same as no change.
2sepsis / systemic inflammationn/a
2anemia / acute blood lossn/a
2hypovolemia / dehydrationn/a
2tachyarrhythmian/a
2hypoxemia / respiratory failuremag 0
2hypertensive emergencyn/a
2high-demand / peri-operative stressn/a
3sudden cardiac deathn/a
4aPCI-related periproceduraln/a
4bstent thrombosisn/a
4cin-stent restenosisn/a
5CABG-relatedn/a
Coverage: 1/12 axes with evidence
Tier: deep-scored (abstract-extracted) · 1 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(2)