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External validation · cardiovascular ICU snapshot

External validation in a cardiovascular ICU snapshot

The atlas is built from literature-mined, molecule-level evidence. This page tests one of its central predictions — that a demand / hypoperfusion axis separates Type 2 (demand-related) MI from Type 1 (atherothrombotic) MI — against real patients in an independent, de-identified single-center medical cardiovascular ICU snapshot spanning 7 years. It is an out-of-sample reality check on the feature prior, not a deployable classifier.

1,265
CICU admissions
over 7 years
224
MI admissions
pooled primary + secondary dx
162
Type 1 / ACS
62
Type 2 (demand)
17
with numeric troponin
the coverage ceiling
What the snapshot confirms

Type 2 MI carries a multiorgan demand-stress fingerprint — higher lactate (AUC 0.80) and creatinine (AUC 0.69) — consistent with supply–demand mismatch from sepsis, hypoxia, or shock. This echoes the atlas's two-axis design. It does not mean Type 1 is separable by plaque-rupture markers here: troponin and CK-MB — the atlas's top two markers — are the exact analytes this ICU snapshot barely captures (troponin, 8%) or never measures (CK-MB).

1 · How MI is coded

MI coded via Primary/Secondary presenting cardiac problem. 'Acute coronary syndrome' is the Type-1/plaque-rupture umbrella (not sub-split into STEMI/NSTEMI, not adjudicated); 'Type 2 (Demand-related) MI' is an explicit separate category.

2 · What is actually measured

This is a critical-care ICU snapshot, not a chest-pain workup: labs are recorded for ICU severity scoring, not to work up the index MI. Cardiac-specific markers are the sparsest. Not collected at all: CK-MB, CRP, procalcitonin, D-dimer, myoglobin, hs-CRP, copeptin.

Numeric coverage of MI-relevant analytes across the 224 MI patients

3 · Which markers separate Type 2 from Type 1

Mann–Whitney tests on every analyte with usable coverage. AUC is on the measured subset (n varies). Rows in red are the two markers that meaningfully discriminate.

MarkerType 1 medianType 2 medianHigher inpAUCn
Lactate1.8 mmol/L4.2 mmol/LType 20.0300.8045
Creatinine1.46 mg/dL2.81 mg/dLType 20.0030.69129
Bilirubin1.2 mg/dL1.2 mg/dLType 1 (weak)0.0010.62207
ALT200 U/L200 U/LType 10.0020.57165
Platelets150 K/uL150 K/uL0.0960.54211
Glucose156 mg/dL160 mg/dL0.5380.53224
Age65 yrs65.5 yrs0.5500.53224
Single-marker AUC for Type 2 vs Type 1 MI

4 · Relation to the atlas catalog

Registry analytes map onto atlas catalog entries: troponin (cTnI/T), natriuretic peptides (BNP/NT-proBNP), LDH, creatinine, bilirubin. The atlas's #1/#2 markers (troponin, CK-MB) are exactly the ones this registry barely captures (troponin, 8%) or omits (CK-MB).

5 · What this can and cannot support

In this cohort Type 2 MI is separated by the demand/hypoperfusion axis — higher lactate and creatinine — consistent with supply-demand mismatch. Troponin is numeric in only 17/224 patients, so it cannot anchor a panel here. The registry validates the demand-axis feature prior but cannot serve as a training set for a deployable Type-1-vs-Type-2 classifier; that needs an ED chest-pain / rule-out cohort with universal serial hs-troponin and adjudicated labels.

Provenance & limits. Source dataset de-identified; site and dataset name withheld. “ACS” is an initial clinical impression, not adjudicated Type 1. The lactate/creatinine signal is partly confounded with the shock / mechanical-support subgroup, so it may track illness severity as well as Type 2 biology. These results support hypothesis prioritization, not a validated clinical instrument. See the Methods page for atlas provenance.