Decision support only — not a substitute for the full NHFA/CSANZ 2025 guideline, Fifth Universal Definition of MI 2026, eTG, or your cardiology team. Confirm every dose, contraindication and local cath-lab pathway. Timing anchors are labelled: FMC = first medical contact.
1 STEMI / ACOMI reperfusion clock — time from first medical contact
12-lead ECGevery suspected ACS
Primary PCI · on-sitePCI-capable centre
Primary PCI · transfernon-PCI centre
≤90 min; total PCI ≤120≤90m · total≤120m
Fibrinolysisif PCI >120 min
ACOMI = STEMI plus occlusion equivalents (high-lateral, posterior, RV MI, De Winter pattern, LBBB/paced rhythm meeting modified Sgarbossa) → urgent reperfusion; do not wait for troponin or etiologic MI classification. If primary PCI cannot be delivered within 120 min of FMC, give fibrinolysis: Australian target ≤30 min from FMC; ESC target ≤10 min from diagnosis. Transfer immediately. Failed lysis → rescue PCI; successful lysis → angiography 2–24 h. Cardiogenic shock → culprit-vessel PCI only. NHFA/CSANZ 2025; ESC ACS 2023
2 NSTEACS — invasive strategy timing
| Risk tier | Defined by | Angiography |
|---|
| Very high |
Haemodynamic instability / cardiogenic shock, refractory or recurrent chest pain, life-threatening arrhythmia, acute heart failure, mechanical complication, recurrent dynamic ST changes |
Immediate <2hNHFA/CSANZ 2025: consensus |
| High |
Confirmed NSTEMI (rise/fall hs-troponin), GRACE >140, dynamic ST/T-wave changes |
Consider early <24hNHFA/CSANZ 2025: weak/high · TIMACS, VERDICT |
| Intermediate / low |
No high-risk features; diagnosis uncertain. Intermediate without known CAD → angiography or CTCA to clarify prognosis beyond 30 days |
Risk-guided / selectiveCTCA is useful when anatomy will change the plan |
3 Diagnosis, 2026 MI definition & antithrombotic doses
Diagnose fast
- ECG≤10 min of FMC. Read for ACOMI patterns, not just classic STE.
- hs-TropRise/fall with ≥1 value above the assay- and sex-specific 99th percentile = acute myocardial injury. MI additionally requires evidence of ischaemia. Use validated 0/1 h, 0/2 h or High-STEACS pathways.
- ACOMIPosterior (V7–9), high-lateral/RV MI, De Winter pattern, or modified Sgarbossa-positive LBBB/pacing can signal occlusion. Diffuse ST depression with aVR elevation signals high-risk global subendocardial ischaemia; it is not automatically an occluded left main.
Antiplatelet & anticoagulation
- Aspirin300 mg load → 100 mg/day. Everyone, unless true contraindication.
- P2Y12 (PCI)Potent agent preferred: ticagrelor 180 mg → 90 mg BD, or prasugrel 60 mg → 10 mg daily. Prasugrel: contraindicated after stroke/TIA; generally avoid ≥75 y; use 5 mg daily if <60 kg. PLATO; TRITON–TIMI 38
- P2Y12 (lysis)Clopidogrel — pair with fibrinolysis, not a potent P2Y12.
- AnticoagEnoxaparin / UFH / fondaparinux / bivalirudin per pathway. With lysis: weight- & age-adjusted enoxaparin.
Fifth Universal Definition of MI (2026) — classify after the urgent reperfusion decision
- Primary MIAcute myocardial ischaemia from an acute coronary process: atherothrombosis, SCAD, coronary embolism, spasm, or late restenosis/stent thrombosis/graft failure >30 days after revascularisation.
- Secondary MIAcute injury with ischaemia from supply–demand imbalance caused by another acute illness, after considering acute coronary pathology. Troponin elevation during sepsis, hypoxia, anaemia or tachyarrhythmia alone is not enough. Use echo/CMR and coronary imaging when the mechanism remains uncertain.
- Procedure-related MIA complication of PCI or cardiac surgery within 30 days. A fixed troponin multiple alone no longer establishes the diagnosis; demonstrate the procedural complication and new ischaemic injury.
- MINOCA“Myocardial injury with non-obstructive coronary arteries” (<50% stenosis) is a working diagnosis. Pursue the mechanism with CMR, intravascular imaging and/or coronary functional testing as appropriate.
ESC/ACC/AHA/WHF Fifth Universal Definition of MI 2026, Boxes 1 and 3–5. Previous numeric MI types 1–5 are retired; STEMI/NSTEMI labels remain useful for initial reperfusion triage.
4 Fibrinolysis, oxygen & adjuncts
Tenecteplase (weight-based)
- <60kg30 mg
- 60–6935 mg
- 70–7940 mg
- 80–8945 mg
- ≥90kg50 mg
- ≥70yHalve the dose in a pharmacoinvasive strategy. This is the Australian 2025 threshold; check the local lysis protocol. STREAM / STREAM-2
- After TNKTransfer immediately. Rescue PCI if ongoing pain, instability, or ≤50% ST recovery at 60–90 min; otherwise angiography at 2–24 h.
Adjuncts
- StatinHigh-intensity, early. Target LDL <1.4 mmol/L + ≥50% drop; add ezetimibe → PCSK9i.
- ACEi/ARBIf LV dysfunction, HF, diabetes, hypertension.
- MRAIf EF ≤40% with HF or diabetes.
- MorphineSparingly — delays oral P2Y12 absorption.
Watch — changed / contested
- OxygenDo not give if SpO₂ ≥90%; if required, target 90–96%. No benefit in normoxaemia. DETO2X-AMI; AVOID
- β-blockerNo early IV treatment in possible shock (COMMIT). Without another indication, routine long-term treatment after MI with EF ≥50% has not reduced death, recurrent MI or HF. REDUCE-AMI; REBOOT; 2025 IPD meta-analysis
- ShockCulprit-only PCI (CULPRIT-SHOCK). Routine IABP or early VA-ECMO is unsupported (IABP-SHOCK II; ECLS-SHOCK). A microaxial flow pump may help carefully selected STEMI shock patients, but complications are substantial (DanGer-Shock).
5 Revascularisation strategy & discharge
Beyond the culprit
- STEMI MVDStable: complete revascularisation, same-setting or staged according to anatomy, renal function and procedural burden. Do not routinely treat non-culprit vessels during shock. COMPLETE; BIOVASC; CULPRIT-SHOCK
- PCI qualityRadial access is preferred. Use intravascular imaging for complex lesions; physiology can guide non-culprit decisions. NHFA/CSANZ 2025; ACC/AHA 2025
- DAPTAustralian pathway: 6–12 months if ischaemic risk is high and bleeding risk low; stop at 1–3 months if bleeding risk dominates, then single antiplatelet therapy. After DAPT, long-term P2Y12 monotherapy is preferred to aspirin. ESC/ACC default remains 12 months when bleeding risk is acceptable.
Before they leave
- RehabRefer to cardiac rehabilitation — every patient.
- LipidsRecheck, escalate to LDL <1.4. PCSK9i for very-high-risk not at target.
- ColchicineAustralia: consider 0.5 mg daily after stabilisation (weak recommendation). ESC 2026 consensus is more selective after neutral CLEAR-SYNERGY despite positive COLCOT; check renal/hepatic function and interactions.
- Whole-personMental-health screen, respiratory vaccination, adherence support, structured follow-up.
Primary sources.
Brieger D, Cullen L, Briffa T, et al. NHFA & CSANZ Comprehensive Australian Clinical Guideline for Diagnosing and Managing ACS 2025. Heart Lung Circ 2025;34:309–397. doi:10.1016/j.hlc.2025.02.102. Fifth Universal Definition of Myocardial Infarction (ESC/ACC/AHA/WHF 2026). Eur Heart J. doi:10.1093/eurheartj/ehag101. ESC ACS guideline 2023. doi:10.1093/eurheartj/ehad191. ACC/AHA ACS guideline 2025. doi:10.1161/CIR.0000000000001309.
Consensus updates.
ESC DAPT personalisation consensus 2026. doi:10.1093/ehjacc/zuag021. ESC inflammation in ACS consensus 2026. doi:10.1093/ehjacc/zuag086.
Key trials.
STREAM/STREAM-2 (pharmacoinvasive TNK); TIMACS and VERDICT (NSTEACS timing); PLATO and TRITON–TIMI 38 (P2Y12); COMPLETE and BIOVASC (complete revascularisation); CULPRIT-SHOCK, ECLS-SHOCK and DanGer-Shock (shock); DETO2X-AMI and AVOID (oxygen); COMMIT, REDUCE-AMI and REBOOT (β-blockers); COLCOT and CLEAR-SYNERGY (colchicine).
Caveats.
The 2026 paper is a diagnostic and classification consensus, not a replacement ACS treatment guideline; the 2025 Australian guideline remains the local management anchor. ACOMI is the Australian term for STEMI plus under-recognised occlusion patterns needing emergency reperfusion. DAPT duration, antithrombotic selection and shock-device use require individual bleeding, anatomy and haemodynamic assessment.