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Triglycerides
Pathway / Lipid retention & oxidation

Triglycerides

lipid

Elevated triglycerides promote atherosclerotic lipid deposition and dysfunctional lipoprotein remodeling.

Pathway placement
Cascade stepLipid retention & oxidation
Confidencehigh
RationaleMI risk marker; atherogenic lipid burden; TGRL-driven atherosclerosis.
Druggability
Not assessed (no mapped human gene target).

Type I vs non-Type I discrimination

ScoresNon-Type-I-associated
R — rupture / Type-I
—
C — non-Type-I
50
A — assay feasibility
84
E — evidence strength
49
T1DI (composite)
13
Specificity differential (R−C)-35
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 inflammationmag 2
2anemia / acute blood lossmag 1
2hypovolemia / dehydrationmag 2
2tachyarrhythmiamag 1
2hypoxemia / respiratory failuremag 2
2hypertensive emergencyn/a
2high-demand / peri-operative stressmag 1
3sudden cardiac deathmag 1
4aPCI-related periproceduraln/a
4bstent thrombosisn/a
4cin-stent restenosismag 2
5CABG-relatedn/a
Coverage: 8/12 axes with evidence
Tier: deep-scored (abstract-extracted) · 14 supporting references. See the discrimination table for all markers.

Assay & specimen

Validated clinical assay
Specimen
Serum or plasma (fasting preferred)
Collection tube
Serum separator (gold/red-top, SST) · Lithium heparin (green-top)
Method / principle
Enzymatic (glycerol blanked)
Reagent / substrate
Lipase → glycerol; glycerol kinase + G3P oxidase + peroxidase Trinder
Platform
Automated analyzer
Turnaround · availability
Routine · Universal

Literature evidence(15)

Clinical trials(2)