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Triglyceride-rich lipoprotein
Pathway / Lipid retention & oxidation

Triglyceride-rich lipoprotein

lipoprotein

Triglyceride-rich lipoprotein accumulation in subendothelium initiates lipid oxidation and atherogenic inflammation driving atherothrombotic MI.

Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleCausal atherogenic remnant particles; promote atherosclerosis and vascular toxicity via subendothelial retention.
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
32
C — confounder / Type-II
37
A — assay feasibility
82
E — evidence strength
18
T1DI (composite)
7
Specificity differential (R−C)-5.3
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

Specialized reference method
Specimen
Serum or plasma (EDTA)
Collection tube
K2/K3-EDTA (lavender-top) · Serum separator (gold/red-top, SST)
Method / principle
NMR lipoprotein particle analysis or density-gradient ultracentrifugation
Reagent / substrate
No chemical reagent — NMR spectral deconvolution of lipid methyl signals (or ultracentrifugal separation by density)
Platform
NMR (LabCorp NMR LipoProfile) / analytical ultracentrifuge
Turnaround · availability
Send-out · Specialized reference lab

Literature evidence(3)