Glutamate
metaboliteExcitatory amino-acid dysregulation impairs cardiovascular homoeostasis and contributes to ischemic myocardial injury.
Pathway placement
Cascade stepMyocardial injury (shared endpoint)
Confidencelow
RationaleExcitatory amino acid dysregulation associated with ischemic cardiomyocyte injury.
Druggability
Not assessed (no mapped human gene target).
Type I vs non-Type I discrimination
ScoresIndeterminate
R — rupture / Type-I0
C — non-Type-I46
A — assay feasibility42
E — evidence strength42
T1DI (composite)5
Specificity differential (R−C)-45.8
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 lossn/a
2hypovolemia / dehydrationmag 1
2tachyarrhythmiamag 1
2hypoxemia / respiratory failuremag 2
2hypertensive emergencyn/a
2high-demand / peri-operative stressmag 1
3sudden cardiac deathmag 2
4aPCI-related periproceduraln/a
4bstent thrombosisn/a
4cin-stent restenosismag 1
5CABG-relatedmag 1
Coverage: 8/12 axes with evidence
Tier: deep-scored (abstract-extracted) · 22 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, plasma or urine
Collection tube
Serum separator (gold/red-top, SST) · Lithium heparin (green-top) · Sterile urine container
Method / principle
LC-MS/MS (targeted metabolomics) or enzymatic colorimetric where available
Reagent / substrate
Stable-isotope-labeled internal standard (MS); or enzyme-coupled Trinder reagent
Platform
LC-MS/MS; some automated chemistry
Turnaround · availability
Send-out / research · Specialized / research
Literature evidence(2)
- Relationship between amino acid metabolism and inflammation in coronary heart disease (Review).International journal of molecular medicine · 2025 · PMID 40476584 · doi
- A Metabolomics-Based Study on NMDAR-Mediated Mitochondrial Damage through Calcium Overload and ROS Accumulation in Myocardial Infarction.Frontiers in bioscience (Landmark edition) · 2023 · PMID 37525913 · doi