Type-I MI diagnostic-utility explorer

Rank every biomarker for its usefulness in diagnosing Type-I (atherothrombotic) MI. Each marker carries nine evidence-anchored sub-scores; you decide how much each one matters using the sliders. The composite and the ranking recompute instantly. Start from a preset (rule-in, deployable-today, novel discovery) or set your own weights. Scores with no evidence show — and are never invented.

Evidence is abstract-level, and the composite is an authored heuristic. A cited study may be topically relevant to a marker without directly testing the comparison stated, and the T1DI weighting has face validity only — it is not validated against patient outcomes. This tool prioritizes hypotheses; it is not a clinical decision instrument.

Three axes are directly diagnostic — Diagnostic performance (sensitivity/specificity/AUC), Release kinetics (how early it rises), and Incremental value vs troponin — extracted from accuracy studies. Only ~11 distinct markers have any of this data (troponin T, CK-MB, myoglobin, cMyBP-C and procalcitonin for kinetics; ApoJ-Glyc, ischemia-modified albumin and cystatin C for accuracy; troponin T, CK-MB, myoglobin, cMyBP-C, GDF-15, ST2 and BNP for incremental value); for everything else these show —. That sparsity is itself the finding: very few candidates have been studied as an MI index test the way troponin has.

ⓘ Methodology — how the criteria and the ranking are built

This explorer scores each biomarker against nine criteria, each normalized to 0–100 (higher is better for a Type-I diagnostic), and combines them into a single composite using weights you set. The criteria fall into three groups. Discrimination criteria — plaque-rupture signal (R), specificity vs non-Type-I (the non-Type-I responsiveness score C, inverted), and direct T1 > non-T1 evidence (D) — come from the atlas's Type-I-vs-non-Type-I scoring and capture whether a marker reflects atherothrombosis rather than any of the other ways myocardium infarcts: the supply–demand mismatch of a Type-2 MI, periprocedural injury after PCI (4a) or CABG (5), stent thrombosis (4b), in-stent restenosis (4c), or sudden cardiac death (Type 3). Direct diagnostic criteria — diagnostic performance (sensitivity/specificity/AUC), release kinetics (how early it rises), and incremental value vs troponin — are extracted from index-test / accuracy studies in the literature; only ~11 distinct markers have any of this data, and the rest correctly show — rather than a fabricated value. Practical criteria — assay feasibility, evidence strength, and novelty — capture deployability and how under-explored a marker is (incumbents already in clinical use are capped low so they never register as novel).

Composite. The score is a weighted average of the available sub-scores. When “penalize missing data” is on, the average divides by the total weight you assigned, so a marker with unmeasured criteria is pulled down — this rewards markers that have actually been studied across the board. Turn it off to divide only by the weight of the criteria a marker does have, scoring each marker on its own evidence. Presets (rule-in, deployable-today, best diagnostic test, novel discovery) are just saved weight profiles; every weight remains adjustable.

Hover (or tab to) any criterion label or table column header for its definition. Scores are evidence-anchored inferences for hypothesis prioritization, not a validated clinical instrument — see the Methods page for the full harvest and scoring provenance.

The T1DI composite is an authored heuristic. The sub-score definitions, the 0–100 normalization, and the weighting are a reasonable, transparent design choice — but they were specified by us, not learned from data or calibrated against patient outcomes. The composite therefore has face validity only; it has not been validated for predictive accuracy against adjudicated Type-1-vs-non-Type-1 diagnoses. Use it to prioritize candidates for study, not to rank clinical performance.

Futures — how we plan to make this rigorous. To move from a heuristic map to validated evidence we intend to: (1) extract evidence from PMC full text and attach the verbatim supporting sentence to every scored claim; (2) validate against a multi-center cohort with MI type adjudicated to the Fourth Universal Definition and report real discrimination metrics (AUC, sensitivity/specificity) following STARD, and TRIPOD if a multi-marker model is built; (3) develop and prospectively test a marker panel (a rupture-axis marker plus one or more non-Type-I confounder markers), since the atlas shows no single analyte separates Type I from the non-Type-I subtypes; (4) add an expert cardiologist curation layer for the Tier-1 markers; and (5) maintain the catalog as a versioned, periodically re-harvested living resource.

Weight the criteria

Drag to set how much each dimension matters. Ranking updates live.

Plaque-rupture signal90

Specificity vs non-Type-I100

Direct T1 > non-T1 evidence90

Diagnostic performance0

Release kinetics0

Incremental vs troponin0

Assay feasibility40

Evidence strength50

Novelty10

Penalize missing data (markers with gaps rank lower)

1043 ranked

Top 15 by your weighting

1Troponin T

2Cardiac troponin I

3CK-MB

4Cardiac Myosin-Binding Protein C

5Cholesterol

6B-type natriuretic peptide

7Growth differentiation factor 15

8Neutrophil gelatinase-associated lipocalin (NGAL)

9Lactate

10Chymase

11SRC tyrosine kinase

12PCSK9

13HDL

14Methylglyoxal

15Transforming Growth Factor-Beta

#	Marker	Score	Cov	Rupt	nT1.spec	T1>nT1	Perf	Kin	Incr	Feas	Evid	Novel	Class
1	Troponin TTNNT2	75	100%	100	38	83	—	60	20	96	85	12	Shared / rises in both
2	Cardiac troponin ITNNI3	74	100%	100	38	83	—	—	—	96	78	12	Shared / rises in both
3	CK-MBCKM	69	100%	67	39	83	—	85	40	96	100	12	Shared / rises in both
4	Cardiac Myosin-Binding Protein CMYBPC3	62	100%	67	33	83	—	100	75	68	67	82	Shared / rises in both
5	Cholesterol	57	76%	—	67	67	—	—	—	84	95	71	Indeterminate
6	B-type natriuretic peptideNPPB	55	100%	67	47	33	—	—	40	96	67	12	Shared / rises in both
7	Growth differentiation factor 15GDF15	54	100%	100	27	17	—	—	40	84	73	51	Shared / rises in both
8	Neutrophil gelatinase-associated lipocalin (NGAL)LCN2	53	76%	100	41	—	—	—	—	68	73	60	Shared / rises in both
9	Lactate	52	76%	67	47	—	—	—	—	96	86	82	Shared / rises in both
10	ChymaseCMA1	52	76%	100	43	—	—	—	—	72	53	76	Shared / rises in both
11	SRC tyrosine kinaseSRC	51	76%	100	40	—	—	—	—	72	54	68	Shared / rises in both
12	PCSK9PCSK9	51	76%	67	50	—	—	—	—	72	95	56	Shared / rises in both
13	HDL	50	76%	67	67	—	—	—	—	84	55	38	Indeterminate
14	Methylglyoxal	50	76%	100	33	—	—	—	—	42	84	90	Shared / rises in both
15	Transforming Growth Factor-BetaTGFB1	50	76%	67	57	—	—	—	—	72	75	66	Indeterminate
16	LDL cholesterol	50	76%	67	52	—	—	—	—	84	82	23	Indeterminate
17	FOXP3FOXP3	50	76%	67	57	—	—	—	—	52	86	76	Indeterminate
18	C-X-C Chemokine Receptor Type 4CXCR4	49	76%	67	54	—	—	—	—	52	86	70	Indeterminate
19	Apolipoprotein A-IAPOA1	49	76%	67	56	—	—	—	—	84	62	44	Indeterminate
20	ADAMTS13ADAMTS13	48	76%	67	52	—	—	—	—	72	69	78	Indeterminate
21	Hexokinase 2HK2	48	76%	67	67	—	—	—	—	52	51	92	Indeterminate
22	Ischemia-modified albuminALB	48	76%	67	50	—	63	—	—	84	65	53	Shared / rises in both
23	Matrix Metalloproteinase-2MMP2	47	76%	67	48	—	—	—	—	72	75	57	Shared / rises in both
24	Albumin	47	76%	67	52	—	—	—	—	84	52	71	Indeterminate
25	Oxidized LDL	47	76%	67	39	—	—	—	—	82	86	30	Shared / rises in both
26	Methionine	47	76%	67	62	—	—	—	—	42	60	90	Indeterminate
27	Integrin alphaIIbbeta3	47	76%	86	51	—	—	—	—	68	26	84	Low-confidence (proxy)
28	triglyceride	46	76%	67	56	—	—	—	—	42	72	77	Indeterminate
29	Glycoprotein VIGP6	46	76%	90	47	—	—	—	—	72	28	53	Low-confidence (proxy)
30	Integrin αIIbβ3	46	76%	86	53	—	—	—	—	68	25	60	Low-confidence (proxy)
31	Anti-β2-glycoprotein I antibodies	46	76%	79	57	—	—	—	—	68	22	92	Low-confidence (proxy)
32	Cytochrome b-245 Alpha SubunitCYBA	46	76%	67	67	—	—	—	—	52	39	82	Indeterminate
33	Immunoglobulin G	46	76%	67	40	—	—	—	—	68	86	51	Shared / rises in both
34	Interleukin-2IL2	46	76%	67	52	—	—	—	—	68	58	68	Indeterminate
35	von Willebrand factorVWF	46	76%	67	36	—	—	—	—	72	95	22	Shared / rises in both
36	Hemoglobin	46	76%	67	39	—	—	—	—	84	67	88	Shared / rises in both
37	Peroxisome proliferator-activated receptor	46	76%	67	37	—	—	—	—	68	80	88	Shared / rises in both
38	Endothelin-1EDN1	45	76%	67	33	—	—	—	—	66	95	56	Shared / rises in both
39	Glutathione peroxidaseGPX1	45	76%	67	39	—	—	—	—	68	75	86	Shared / rises in both
40	LPC (18:2)	45	53%	—	100	—	—	—	—	40	95	86	Indeterminate

How the composite works: each sub-score is 0–100 (higher = better for a Type-I diagnostic). The composite is a weighted average of the sub-scores using your slider weights. “Penalize missing data” divides by the total weight rather than only the covered weight, so markers with gaps rank lower — turn it off to score markers on the evidence they do have. This is a hypothesis-prioritization tool, not a validated clinical instrument.