Ceramide(d18:1/18:0)
lipidCeramide(d18:1/18:0) accumulation reflects lipid dysmetabolism and vascular inflammation in acute myocardial injury.
Pathway placement
Cascade stepLipid retention & oxidation
Confidencemedium
RationaleLipid species elevated in AMI; dysregulated lipid metabolism and vitamin D status.
Also acts inVascular inflammation
Druggability
Not assessed (no mapped human gene target).
Type I vs Type II discrimination
ScoresLow-confidence (proxy)
R — rupture / Type-I57
C — confounder / Type-II87
A — assay feasibility40
E — evidence strength32
T1DI (composite)5
Specificity differential (R−C)-29.7
Confounder panel (Type-II drivers)
No confounder evidence retrieved.
Tier: light (literature co-occurrence proxy — lower confidence). 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)
- Vitamin D and Ceramide Metabolomic Profile in Acute Myocardial Infarction.Metabolites · 2024 · PMID 38668361 · doi