Acute Coronary Syndrome
Details
Acute coronary syndromes (ACS) encompass the clinical spectrum of myocardial ischaemia caused by disruption — rupture or erosion — of an unstable coronary atherosclerotic plaque with associated partial or complete coronary thrombosis, producing reduced myocardial blood flow. The spectrum comprises unstable angina (transient ischaemia without myonecrosis), NSTEMI (subendocardial ischaemia, partially occluded artery, elevated troponin) and STEMI (transmural ischaemia, usually completely occluded artery, ST-elevation with elevated troponin). In the US approximately 805,000 AMIs occur annually — 605,000 first events and 200,000 recurrent — at an annual economic burden of approximately $84.9 billion. (sources/ACS-AHA-2025, rating: very high)
ACS is the clinical presentation; myocardial infarction is the pathological event. The two do not map one-to-one in either direction. Unstable angina is an ACS that is not an MI, and MI after non-cardiac surgery, in sepsis, or as a complication of a cardiac procedure is an MI that is not an ACS. This page therefore covers ACS proper and, because the 2026 classification spans them, the three settings in which MI arises outside it — secondary, procedure-related, and after sudden death. Management from first medical contact to discharge is on concepts/ACS-Management.
MI is diagnosed only where acute myocardial injury coexists with a clinical, ECG or imaging picture proving the cell death was ischaemic; no single criterion suffices. (sources/5thMI-AHA-2026, rating: very high)
Key Facts
5th Universal definition of MI, OMI vs Not OMI.
The Fifth Universal Definition (2026) classifies MI by pathophysiology and clinical setting — primary, secondary, procedure-related — replacing the numerical type 1–5 system that had organised diagnosis since 2007. A second framework, developed in the occlusion-MI literature, argues that MI should instead be split by whether the culprit artery is occluded (OMI) or not (NOMI), abandoning the ECG-based STEMI/NSTEMI axis entirely. The Fifth Universal Definition retains that axis and gives it distinct ICD-11 codes, so both proposals coexist with no stated resolution. The taxonomy is presented below first, then the retained ECG axis, then the rival framework.
Definition and Clinical Spectrum
- Three related conditions along a continuum of severity: unstable angina — transient ischaemia without significant myonecrosis, troponin normal; NSTEMI — subendocardial ischaemia, partially occluded artery, troponin elevated; STEMI — transmural ischaemia, usually completely occluded artery, ST-elevation with elevated troponin. (sources/ACS-AHA-2025, rating: very high)
- STEMI ECG criteria: ST-elevation ≥1 mm at the J-point in ≥2 anatomically contiguous leads; ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, and ≥1.5 mm in women in leads V2–V3. (sources/ACS-AHA-2025, rating: very high)
- These criteria are the contested object of the rest of this page. They define STEMI, gate emergent reperfusion, and — the OMI literature argues — miss a substantial fraction of occlusions. See
### The Rival Framework — OMI and NOMIbelow.
Epidemiology and Disparities
- Incidence of MI is higher in Black males than in non-Hispanic White males — multifactorial, reflecting higher CAD risk factor burden, less guideline-directed medication use and socioeconomic factors. (sources/ACS-AHA-2025, rating: very high)
- Women present with ACS approximately 10 years later than men, with a greater CVD risk factor burden; they are more likely to present without chest pain, and less likely to receive guideline-directed medical therapy and revascularisation. (sources/ACS-AHA-2025, rating: very high)
Myocardial Injury — Acute and Chronic
- Acute myocardial injury: a rise and/or fall in cardiac troponin I or T with at least one value above the sex-specific 99th percentile upper reference limit. Tachyarrhythmia, but also sepsis, pulmonary embolism, myocarditis and cardiotoxic therapy raise troponin without infarction. (sources/5thMI-AHA-2026, rating: very high)
- Non-ischaemic mechanisms are grouped as inflammation, haemodynamic stress, physiological stress, catecholamine stress, toxicity and trauma; several often coexist in one patient. Troponin elevation does not always mean necrosis — Takotsubo and myocarditis can recover fully.
- Chronic myocardial injury: two or more values above the sex-specific 99th percentile while testing in a stable clinical setting, confirmed by identifying a condition associated with cardiac remodelling and excluded where analytical interference or reduced clearance explains it. It is up to five times more frequent with cTnT than with cTnI. (sources/5thMI-AHA-2026)
- A change of less than 20% between measurements suggests chronic rather than progressive injury, though the consensus concedes this threshold "is simply based on the analytical imprecision of cardiac troponin assays."
Primary Myocardial Infarction
- Likely: acute myocardial injury plus at least one of symptoms consistent with acute ischaemia, new or presumed-new ischaemic ECG changes, or development of pathological Q waves.
- Confirmed by at least one imaging feature: an acute coronary pathology — atherothrombosis, SCAD, vasospasm, embolism, or restenosis, stent thrombosis or graft failure more than 30 days from revascularisation — or a new/presumed-new regional wall motion abnormality and/or absence of viable myocardium in an ischaemic pattern. (sources/5thMI-AHA-2026, rating: very high)
- What moved in: non-atherosclerotic coronary pathology and late stent or graft failure were previously filed as type 2 or types 4/5 and are now primary MI. Reported angiographic frequencies: SCAD 0.1%–4.0%, coronary embolism 0.2%–13%, epicardial vasospasm 1%–20%, in-stent restenosis 1.0%–6.5%, stent thrombosis 0.6%–0.8%.
- SCAD should be suspected in women under 50 and in pregnancy or the post-partum period. See concepts/Coronary-Vasospasm and concepts/MINOCA.
- MINOCA is a working diagnosis rather than a diagnosis of exclusion: MI is confirmed in only 22%–27% of patients on cardiac MRI. The AHA 2019 statement framed it as an ischaemic diagnosis with atherosclerotic plaque disruption among its causes; the 2026 definition supersedes that for nomenclature by redefining MINOCA as myocardial injury with non-obstructive coronary arteries. See concepts/MINOCA. (sources/5thMI-AHA-2026, rating: very high; sources/minoca-aha-2019)
- Where angiography and imaging are unavailable, the diagnosis may rest on biomarkers plus ECG plus clinical criteria, coded as aetiology-unknown (BA41.09/BA41.19).
Secondary Myocardial Infarction
- Considered with acute myocardial injury, an alternative acute condition causing supply–demand mismatch, and at least one of symptoms, new ischaemic ECG changes or pathological Q waves; likely with known CAD or a clinical suspicion proportionate to the extent of ECG change or troponin elevation.
- Confirmed by either obstructive CAD — ≥70% stenosis in an epicardial vessel, or ≥50% stenosis that is flow-limiting on physiological assessment — WITHOUT an acute coronary pathology, or a new/presumed-new regional wall motion abnormality or absence of viable myocardium in an ischaemic pattern. (sources/5thMI-AHA-2026, rating: very high)
- The commonest trigger is tachyarrhythmia, but triggers frequently coexist, so no universal threshold can be set for any of them.
- If imaging reveals an acute coronary pathology, the event is reclassified as primary MI. In a prospective cohort of prior type-2 MI patients undergoing systematic angiography, 1 in 20 had atherothrombosis.
- Symptoms are less reliable (fewer report chest pain), ECG changes are more often global, and troponin cannot distinguish ischaemic from non-ischaemic cause.
Procedure-Related Myocardial Infarction
- Window is 30 days, explicitly "an arbitrary period," replacing the Fourth Universal Definition's 48 hours for types 4a and 5. Events beyond 30 days are primary MI.
- Confirmed by an angiographic coronary complication (side branch occlusion, iatrogenic dissection, no/slow flow, recoil, stent thrombosis, graft failure, coronary impingement, embolism), imaging showing a new regional wall motion abnormality or loss of viability in the territory of the artery in which the complication arose, new pathological Q waves, or unexplained sudden deterioration in a sedated patient. (sources/5thMI-AHA-2026, rating: very high)
- Both features are required where the complication occurs during the index procedure or the procedure is performed in the management of acute MI; either suffices after an initially uncomplicated procedure.
- Biomarker magnitude survives only as a "likely" trigger: a continuing rise above pre-procedural levels at 6 h (>5× URL for intervention) or 24 h (>35× URL for surgery), prompting imaging rather than diagnosing MI. The Fourth Universal Definition's diagnostic 5× and 10× thresholds are abolished.
- Peak timing is 3–12 h after surgery; a later peak at 12–24 h suggests a procedure-related complication.
Myocardial Infarction After Sudden Death
- The former type 3 is removed. Where MI is the likely cause of death, the clinical classification is applied from the setting or from post-mortem findings; features favouring primary MI are age >40, prior CAD, preceding chest pain, and documented VF without known cardiomyopathy or channelopathy.
- No ECG and no autopsy → unspecified MI (BA41.Z); incomplete evaluation → MI of uncertain aetiology. Post-mortem CT-guided biopsy with CMR has >95% sensitivity and specificity for acute MI, but protocols are unstandardised.
Unstable Angina and Unrecognised Infarction
- Unstable angina is considered with new rest or minimal-exertion ischaemia (CCS class 3–4) or sudden intensification after MI has been excluded by serial troponin, and remains part of the ACS spectrum with its own code (BA40). Its diagnosis has become progressively rarer with hs-cTn.
- Unrecognised MI: Q waves alone are poorly specific; confirm with imaging, preferably CMR with late gadolinium enhancement. Prevalence is ~1 in 5 people over 70 and 3% of asymptomatic middle-aged individuals. See concepts/Late-Gadolinium-Enhancement.
The Retained ECG Axis — STEMI and NSTEMI
- Both axes coexist. The pathophysiological taxonomy (primary/secondary/procedure-related) sits alongside the ECG split, with ICD-11 assigning distinct codes to BA41.0 (STEMI) and BA41.1 (NSTEMI). (sources/5thMI-AHA-2026, rating: very high)
- This was a deliberate choice, not an oversight. The OMI literature had argued the ECG axis should be abandoned (below); the consensus retained it while noting that up to 1 in 4 patients managed as NSTEMI have an acutely occluded culprit artery.
- Consequence: the same patient is STEMI by one axis and primary MI by the other, and the two classifications gate different decisions — one drives reperfusion, the other drives coding and aetiological work-up.
The Rival Framework — OMI and NOMI
The OMI/NOMI (Occlusion Myocardial Infarction / Non-Occlusion Myocardial Infarction) paradigm is a proposed reclassification that replaces the STEMI/NSTEMI framework. Rather than stratifying by the presence of ST-elevation on ECG — a single morphological criterion — it stratifies by the underlying pathophysiology: OMI = persistent acute coronary occlusion without adequate collateral perfusion, causing imminent and ongoing infarction. NOMI = non-occlusive ischaemia without complete artery occlusion. The key argument is that ST-elevation is an imperfect surrogate for occlusion and therefore a poor gatekeeper for emergent reperfusion. (sources/failure-stemi-criteria-lad-omi-ehjacc-2025, rating: high)
Why STEMI Criteria Fail
- A meta-analysis documented only 43% sensitivity of traditional STEMI ECG quantitative criteria for acute coronary occlusion. (sources/failure-stemi-criteria-lad-omi-ehjacc-2025, rating: high)
- 38% of total LAD occlusions (TIMI-0 flow) never met STEMI criteria on any serial pre-angiography ECG; serial ECGs did not evolve to STEMI criteria in any of these 20 cases.
- Sensitivity of STEMI criteria by TIMI flow (all arteries, n=808): TIMI-0 → 49%; TIMI-1 → 35%; TIMI-2 → 29%; TIMI-3 → 27%.
- Among patients with NSTEMI, 25–34% have TIMI-0/1 flow at angiography — a subgroup with nearly twice the mortality of NSTEMI with TIMI ≥2, despite younger age and fewer comorbidities.
- Only 64% of definite STEMI have TIMI-0 flow at angiography; 16–20% have TIMI-3 flow — spontaneous reperfusion during transfer is common.
- The LAD territory is the highest-risk occlusion site because of its larger myocardial territory: LAD OMI produces larger infarcts with higher mortality than occlusion of other epicardial arteries.
- Meyers et al. 2025 confirm STEMI criteria sensitivity of 41% (97% specificity) in an independent 1,395-patient validation cohort — consistent with all prior studies. The HATW score matched this specificity (97%) with 45% sensitivity; combining both yielded 96% specificity and 53% sensitivity. (sources/hatw-jacc-advances-2025, rating: very high)
OMI Features Beyond ST-Elevation
The following ECG findings, assessed by expert or AI, reliably identify OMI even in the absence of diagnostic STE criteria. Prevalence in 20 subtle LAD OMI cases (TIMI-0, no STEMI criteria): (sources/failure-stemi-criteria-lad-omi-ehjacc-2025, rating: high)
| ECG Finding | Prevalence in Subtle LAD OMI |
|---|---|
| Subtle STE (<1 mm, not meeting criteria) | 85% |
| Hyperacute T-waves (incl. de Winter pattern) | 85% |
| Pathologic Q-waves (with subtle STE) | 70% |
| Reciprocal STD and/or T-wave inversion | 50% |
| Terminal QRS distortion | 20% |
| Inferior STE + aVL STD/T-inversion | 20% |
| Posterior OMI pattern (STD maximal V2–V4) | 0% |
| Modified Sgarbossa criteria (LBBB/VPR) | 0% |
- Hyperacute T-waves are not defined by amplitude alone; the T/R amplitude ratio is a key feature — anterior OMI T-waves are not taller than normal-variant early repolarisation, but R-waves are smaller, giving an elevated ratio. See concepts/Hyperacute-T-waves.
- Terminal QRS distortion: absence of both J-wave and S-wave in a lead where an S-wave would be expected, preceding any subtle STE.
- Posterior OMI: STD maximal in V1–V4 (formerly "posterior MI") — not seen in the LAD subgroup but an important OMI pattern for circumflex occlusion.
- Modified Sgarbossa criteria: concordant STE ≥1 mm, concordant STD ≥1 mm in V1–V3, or discordant STE:S ratio ≥0.25 — applies where LBBB or ventricular paced rhythm is present. See concepts/Sgarbossa-Criteria.
Expert, AI and STEMI-Criteria Performance
- Expert OMI interpretation: 100% sensitivity for all 53 LAD TIMI-0 cases on the first ECG; roughly double the sensitivity of STEMI criteria overall at near-equal specificity. (sources/failure-stemi-criteria-lad-omi-ehjacc-2025, rating: high)
- PMCardio Queen of Hearts AI model: 100% sensitivity for all 53 LAD TIMI-0 cases on the first ECG (P<0.0001 vs STEMI criteria).
- In the validation cohort the AI model demonstrated double the sensitivity (67% vs 33%) of STEMI millimetre criteria for OMI (TIMI-0/1, or TIMI-2/3 with culprit plus intervention) at fixed specificity.
- See entities/PMCardio-Queen-of-Hearts for AI model details.
Clinical Consequences of the STEMI-Only Model
- Patients with LAD occlusion not meeting STEMI criteria had median door-to-balloon time 97 min vs 40 min (P<0.001); DBT >90 min in 55% vs 21% (P=0.012). (sources/failure-stemi-criteria-lad-omi-ehjacc-2025, rating: high)
- Despite the longer delays, infarct size was equivalent: peak troponin (P=0.52–0.53) and post-angiography ejection fraction (P=0.94) did not differ.
- 55% of the 20 missed cases had EF <50% post-angiography; there was 1 death during index hospitalisation.
- The majority of electrocardiographically subtle LAD OMI cases did not undergo timely reperfusion because they lacked diagnostic ST-elevation.
- Diagnostic label paradox: among the 20 STEMI(−) OMI cases, those with DBT <120 min received a "STEMI" discharge diagnosis in 75% of cases, while those with DBT >120 min received "NSTEMI" in 88% — suggesting the label was sometimes shaped retrospectively by how quickly the patient was treated rather than by the ECG.
Guideline Recognition and the HATW Score
- The 2022 ACC chest pain guideline acknowledged limited STE sensitivity and proposed additional criteria — hyperacute T-waves including de Winter T-waves, posterior MI findings, and LBBB/paced rhythm meeting modified Sgarbossa criteria — but provides no quantitative definition for hyperacute T-waves or posterior MI patterns. (sources/failure-stemi-criteria-lad-omi-ehjacc-2025, rating: high)
- The 2024 SCAI expert consensus on managing STEMI patients similarly acknowledged limited STE sensitivity for occlusion.
- Neither document provides actionable criteria for the most common subtle OMI finding — hyperacute T-waves — leaving most physicians unable to act on the updated guidance.
- The HATW score (Meyers et al. 2025) is the first objective, validated definition: T-wave magnitude (amplitude/QRS amplitude) plus T-wave symmetry, ≥0.7 in 2 contiguous leads → 98.4% specificity, 20.7% sensitivity in non-STEMI patients; 99.6% specificity, 30.3% sensitivity using expert chart review as the OMI reference. (sources/hatw-jacc-advances-2025, rating: very high)
Classification and Coding
- ICD-11 assigns the taxonomy. Sixth digits for primary MI run _.1 atherothrombosis, _.2 SCAD, _.3 coronary embolism, _.4 coronary vasospasm, _.5 restenosis >30 days, _.6 stent thrombosis >30 days, _.7 graft failure >30 days, _.8 undetermined after angiography, _.9 unknown without coronary imaging; _.A is secondary MI, _.B procedure-related percutaneous and _.C procedure-related surgical. (sources/5thMI-AHA-2026, rating: very high)
- The prior taxonomy never reached the data. The Fourth Universal Definition plus hs-cTn increased diagnoses of type 1 and type 2 MI by 11% and 22%, yet in two European countries fewer than 20% of patients meeting type-2 criteria received an ICD-10 MI code.
Contradictions / Open Questions
- Sensitivity and specificity are deliberately traded against each other, with no arbitration rule. Primary criteria prioritise sensitivity to avoid missing an acute coronary pathology; secondary and procedure-related criteria prioritise specificity so the label carries treatment implications. The same patient can therefore be classified differently depending on which setting the clinician assigns, and there is no guidance for the acutely ill patient with both a supply–demand trigger and an incidental non-obstructive plaque. (sources/5thMI-AHA-2026, rating: very high)
- Biomarker multiples are condemned and then partly retained — and the two pathways they serve were harmonised without validation. The 5× and 10× thresholds are called arbitrary, yet 5× (intervention) and 35× (surgery) reappear as "likely" triggers with unknown sensitivity and negative predictive value; the document itself states that further research is required to confirm the prognostic implications are genuinely similar for the percutaneous and surgical criteria.
- Procedure-related criteria presuppose troponin measurement many centres do not perform. EACTS and some guidelines oppose routine pre- and post-procedural troponin while EAPCI supports it, so the apparent incidence of procedure-related MI will vary by centre and by trial.
- "Absence of viable myocardium" is physiologically loose as an acute criterion. Viability loss is an evolving concept framed elsewhere around hibernation and revascularisation benefit, yet here it confirms an acute MI within the same episode; how soon it can be asserted is not specified. See concepts/Myocardial-Viability.
- Secondary MI may shrink the diagnosis rather than grow it — the opposite direction from the Fourth Universal Definition, which expanded MI diagnoses. One supporting study suggests the new criteria reduce the frequency of MI in acute illness while identifying higher-risk patients; no trial has tested outcomes under the new criteria.
- The Fifth Universal Definition keeps STEMI/NSTEMI rather than replacing it with OMI/NOMI. Where the OMI literature argues the ECG split should be abandoned in favour of occlusion status, the 2026 consensus retains it as a legitimate axis, assigns distinct ICD-11 codes (BA41.0 and BA41.1), and makes no mention of OMI as an alternative — while itself noting that up to 1 in 4 patients managed as NSTEMI have an occluded culprit. The wiki holds both proposals with no stated resolution.
- No prospective randomised evidence that OMI-based activation beats STEMI-based activation exists. The published literature documents door-to-balloon delay and equivalent infarct size, but no trial has tested whether switching activation strategy improves mortality or LV function.
- Expert and AI specificity is uncharacterised in the key subgroup. The LAD TIMI-0 sub-study had no non-OMI control group and could not calculate specificity; the full DOMI-ARIGATO cohort showed near-equal specificity for experts and double sensitivity for AI at fixed specificity, but the trade-off remains to be characterised prospectively in real-world data.
- Hyperacute T-waves lacked any clinical definition until 2025. Smith et al. proposed the T/R amplitude ratio; the AI model recognises them via saliency mapping without an explicit computational mechanism; clinicians find this the hardest OMI criterion to apply. The HATW score partially resolves this, but external validation in independent cohorts and diverse populations is still needed. (sources/hatw-jacc-advances-2025, rating: very high)
- Discharge diagnosis correlates with door-to-balloon time, not with the ECG. In patients with confirmed LAD occlusion not meeting STEMI criteria, those treated quickly were labelled STEMI and those treated late NSTEMI — consistent with labels being assigned to satisfy quality metrics rather than to describe pathophysiology.
- Conflict of interest in the OMI literature. Key authors (Meyers, Herman, Smith) hold equity in Powerful Medical, the manufacturer of the Queen of Hearts model. This does not invalidate the finding that expert interpretation alone achieved 100% sensitivity, but the AI performance data should be read in that context.
- ICD-11 coding was provisional at publication, with the codes still under WHO review — yet registries and electronic records are urged to adopt them.
- Aging the 99th percentile remains unresolved. No assay has regulatory approval for age-adjusted thresholds, though 1 in 3 patients over 75 with possible MI have elevated troponin versus 1 in 20 under 50.
Connections
- Management: concepts/ACS-Management — first medical contact, reperfusion, antithrombotic therapy, secondary prevention
- Chronic phase: entities/Chronic-Coronary-Disease — ACS stabilises into CCD
- Mechanisms and MINOCA: concepts/MINOCA · concepts/Coronary-Vasospasm
- ECG: concepts/ST-T-Changes · concepts/Hyperacute-T-waves · concepts/Sgarbossa-Criteria · concepts/Wellens-Syndrome
- AI ECG interpretation: entities/PMCardio-Queen-of-Hearts
- Imaging: concepts/Late-Gadolinium-Enhancement · concepts/Myocardial-Viability
- Comorbidity and mimics: entities/Heart-Failure · concepts/Chronic-Kidney-Disease · entities/Takotsubo · concepts/Pericarditis
- Perioperative context: concepts/Perioperative-Cardiovascular-Assessment — MINS and post-operative MI
- Special settings: concepts/Cancer-Therapy-Related-CV-Toxicity · concepts/Aortic-Stenosis (procedure-related MI after TAVI) · concepts/Cardiopulmonary-Resuscitation