Acute coronary syndromes

At a glance

• ACS covers STEMI, NSTEMI and unstable angina. NSTEMI and unstable angina together are NSTEACS.
• The first ECG, done within 10 minutes of first clinical contact, splits the pathway: ACOMI (STEMI or an equivalent) means reperfusion now; NSTEACS means risk stratification and timed angiography.
• High-sensitivity troponin, with sex-specific 99th centile limits, separates NSTEMI (myocardial injury) from unstable angina (none).
• Long-term outcome depends on secondary prevention: antiplatelets, high-intensity statin to an LDL target, beta-blocker and ACE inhibitor where indicated, and cardiac rehabilitation.

Definitions

The Fifth Universal Definition of MI (ESC, ACC, AHA and WHF, 2026) replaced the numbered types 1 to 5. Exam questions and older guidelines, including parts of the Australian 2025 guideline, still use the type 1 and type 2 labels, so know both.

Term	Meaning
Myocardial injury	Troponin above the sex-specific 99th centile upper reference limit
Primary MI (formerly type 1)	Acute coronary pathology: plaque rupture or erosion with thrombus, and also SCAD, coronary embolism and spasm
Secondary MI (formerly type 2)	Supply and demand mismatch from another acute illness without acute coronary pathology: tachyarrhythmia, anaemia, hypotension, hypoxia
Procedure-related MI (formerly types 4 and 5)	Coronary complication within 30 days of PCI or cardiac surgery, defined the same way for both. Troponin over 5× URL after PCI or over 35× after surgery is only suggestive and prompts further tests
MINOCA	Now myocardial injury with non-obstructive coronary arteries (no stenosis ≥50%). A working diagnosis: look for SCAD, spasm, embolism, myocarditis and takotsubo, with cardiac MRI
ACOMI	Acute coronary occlusion MI (Australian 2025 guideline): STEMI plus the ECG equivalents that need emergency reperfusion

Terminology: the 4th UDMI called SCAD, embolism and spasm type 2 (supply and demand). The Australian 2025 guideline reclassifies them as occlusive MI, and the 5th UDMI calls them primary MI.

Pitfall: a raised troponin isn't automatically an MI. Sepsis, PE, myocarditis, renal failure and heart failure all raise it. MI needs a rise or fall plus ischaemic symptoms, ECG changes, imaging or thrombus.

Recognition

• Typical pain: central pressure or heaviness, radiating to the arm, jaw or neck, lasting over 10 to 20 minutes, with sweating or nausea.
• Atypical presentations are common in older people, women and people with diabetes: breathlessness, fatigue, epigastric pain or syncope.
• Examine for heart failure, shock, new murmurs (mechanical complication) and differentials: aortic dissection (pulse or BP difference between arms, tearing pain to the back), PE, pericarditis, pneumothorax, oesophageal rupture.

ECG patterns

Territory	Leads	Usual artery
Anterior	V1 to V4	Left anterior descending
Lateral	I, aVL, V5 to V6	Circumflex or diagonal
Inferior	II, III, aVF	Right coronary (about 80%) or circumflex
Posterior	ST depression V1 to V3, elevation V7 to V9	Circumflex or RCA
Right ventricle	V4R	Proximal RCA

• ACOMI patterns that need the reperfusion pathway even without classic ST elevation: posterior MI, de Winter T waves (upsloping ST depression with tall T waves in the precordial leads), high lateral MI, RV MI, and LBBB or paced rhythm meeting modified Sgarbossa criteria (a discordant ST elevation more than 25% of the preceding S wave depth counts).
• High-risk patterns that can progress to occlusion: Wellens T waves, hyperacute T waves, and widespread ST depression with ST elevation in aVR. Monitor continuously and discuss urgent angiography.
• Pitfall: a normal first ECG doesn't exclude ACS. Repeat it with each episode of pain and at 15 to 30 minute intervals if suspicion is high, adding right-sided and posterior leads if the 12-lead is inconclusive.

Investigations

• Serial ECGs and continuous monitoring.
• High-sensitivity troponin in a clinical decision pathway (0 and 1 hour, 0 and 2 hours, or High-STEACS). Use one assay for serial deltas. Don't use a pathway when the ECG already shows ACOMI.
• FBC, electrolytes, renal function, glucose, lipids, HbA1c.
• Chest X-ray for differentials and heart failure.
• Echocardiogram for LV function, regional wall motion and mechanical complications.
• CT coronary angiography or other non-invasive testing for intermediate-risk patients with normal troponin, often as outpatients.

Management of STEMI and ACOMI

1. Aspirin 300 mg orally, chewed or dissolved, unless contraindicated.
2. Reperfusion if symptoms began within 12 hours (or later with ongoing ischaemia, haemodynamic compromise or life-threatening arrhythmia, by primary PCI):
   • Primary PCI is preferred if it can be performed within 120 minutes of first medical contact. Wire-crossing targets: under 60 minutes at a PCI-capable centre, under 90 minutes for transfers.
   • Fibrinolysis within 30 minutes of first medical contact (consider pre-hospital) if PCI can't happen within 120 minutes and there's no contraindication. Then transfer: urgently if reperfusion fails (less than 50% ST resolution at 60 to 90 minutes), otherwise angiography within 2 to 24 hours (pharmaco-invasive strategy).
3. P2Y12 inhibitor: ticagrelor or prasugrel for primary PCI. The Australian 2025 guideline noted prasugrel wasn't available, leaving ticagrelor as the potent option, but a generic was PBS-listed from May 2025. Pre-treatment can be considered once the diagnosis is certain; deferring until the anatomy is known is reasonable if the diagnosis is uncertain or surgery is possible. Clopidogrel with fibrinolysis, with an oral anticoagulant, or when the others are contraindicated.
4. Anticoagulation: unfractionated heparin or bivalirudin during primary PCI; enoxaparin (preferred) or heparin with lysis.
5. Symptom relief: sublingual GTN every 5 minutes for up to three doses (not with RV infarction, hypotension or recent PDE-5 inhibitor use), and IV fentanyl or morphine for pain.
6. Oxygen: none if SpO2 is 90% or more. If oxygen is needed, don't let SpO2 exceed 96%.

Fibrinolysis details (Australian 2025 guideline)

• Tenecteplase is the practical choice (single weight-adjusted bolus). Give half the standard dose at age 70 or over as part of a pharmaco-invasive strategy (STREAM-2).
• Enoxaparin: omit the IV bolus over age 75.
• Clopidogrel: 300 mg loading dose, but no loading dose over age 75 (75 mg only).

Contraindications to fibrinolysis (absolute)

• Any previous intracranial haemorrhage
• Known structural cerebral vascular lesion (such as an AVM)
• Known malignant intracranial neoplasm, primary or metastatic
• Ischaemic stroke within 3 months, except acute ischaemic stroke within 4.5 hours
• Suspected aortic dissection
• Active bleeding or bleeding diathesis (not menses)
• Significant closed-head or facial trauma within 3 months
• Intracranial or intraspinal surgery within 2 months

Management of NSTEACS

• Aspirin plus a P2Y12 inhibitor and parenteral anticoagulation (heparin, enoxaparin or fondaparinux).
• P2Y12 choice: ticagrelor or prasugrel for a routine invasive strategy; ticagrelor or clopidogrel for a selective invasive strategy. Prasugrel isn't used without PCI. The P2Y12 inhibitor can be withheld until the anatomy is known if angiography happens within the target times.
• Risk-guided timing of angiography:

Risk	Features	Timing
Very high	Shock or instability, refractory pain, life-threatening arrhythmia, mechanical complication, acute heart failure	Immediate (under 2 hours)
High	Confirmed NSTEMI, dynamic ST or T changes, GRACE score over 140	Early (within 24 hours)
Not high	Unstable angina with negative troponin and no high-risk features	Selective invasive, guided by testing for inducible ischaemia

• Pitfall: fibrinolysis has no role in NSTEACS; it causes harm.

Secondary prevention

Therapy	Who
DAPT	Aspirin plus a P2Y12 inhibitor for 6 to 12 months if high ischaemic or low bleeding risk; 1 to 3 months if high bleeding risk. Then a long-term P2Y12 inhibitor is preferred over aspirin (PBS doesn't fund ticagrelor alone, so usually clopidogrel). De-escalation from ticagrelor or prasugrel to clopidogrel can be considered, but not in the first 30 days
With an oral anticoagulant	Triple therapy (DOAC, aspirin, clopidogrel) for 1 to 4 weeks, then DOAC plus clopidogrel, then DOAC alone from 6 to 12 months
High-intensity statin	Everyone, started before discharge. LDL under 1.4 mmol/L and at least a 50% reduction (Australian 2025 and ESC 2023); add ezetimibe, then a PCSK9 inhibitor if needed
Beta-blocker	Recommended with LV impairment. With preserved LVEF (≥50%, as in REDUCE-AMI) after revascularisation on optimal therapy, consider not using one: REDUCE-AMI and REBOOT found no benefit. Evidence conflicts at 40 to 49%: BETAMI-DANBLOCK (NEJM 2025) found fewer events with LVEF ≥40%
ACE inhibitor (ARB if not tolerated)	Heart failure symptoms, LVEF 40% or less, diabetes, hypertension or CKD
MRA (eplerenone, spironolactone)	LVEF 40% or less and heart failure, with or without diabetes
ARNI	Not recommended in ACS (PARADISE-MI showed no advantage over ramipril)
Colchicine	Consider 0.5 mg daily long term (weak recommendation)
Cardiac rehabilitation	Everyone, referred before discharge. It reduces mortality and readmission but is underused

• Stop smoking (behavioural support plus nicotine replacement, varenicline or bupropion), treat blood pressure and diabetes (an SGLT2 inhibitor or GLP-1 receptor agonist has cardiovascular benefit), vaccinate against influenza and other respiratory pathogens, and screen for depression.
• Driving: private licence holders usually stop driving for 2 weeks after MI, with a shorter period after PCI alone and longer periods for commercial licences. Check the current Austroads standards.
• Aboriginal and Torres Strait Islander people have higher ACS rates at younger ages and lower access to angiography and rehabilitation. Arrange culturally safe follow-up and Aboriginal health worker involvement.

Complications

When	Complication	Clues
Hours	VF or VT	Most deaths before hospital. Defibrillate
Hours to days	AV block	Inferior MI (AV nodal artery from RCA): often transient. Anterior MI block is infranodal and needs pacing
Days	Cardiogenic shock	Hypotension, hypoperfusion. Urgent PCI of the culprit artery only; routine balloon pump isn't recommended
2 to 7 days	Papillary muscle rupture	Sudden pulmonary oedema with new MR, usually posteromedial muscle (inferior MI)
3 to 5 days	Ventricular septal rupture	New harsh pansystolic murmur, oxygen step-up in the RV
Up to 2 weeks	Free wall rupture	Sudden tamponade and PEA arrest
Weeks	LV thrombus	Large anterior MI with apical akinesia. Anticoagulate for 3 to 6 months if present
Weeks to months	LV aneurysm	Persistent ST elevation, heart failure, VT, thrombus
1 to 6 weeks	Dressler syndrome	Pericarditis with fever and effusion. Treat with aspirin

Pitfalls

• Aortic dissection can involve the right coronary ostium and mimic inferior STEMI. Antiplatelets and lysis can be fatal.
• Cocaine-associated chest pain: benzodiazepines and nitrates first; avoid beta-blockers acutely.
• Takotsubo looks like an anterior STEMI. Angiography shows no culprit lesion, with apical ballooning on ventriculography or echo.
• Don't forget secondary MI (old type 2) in the anaemic, septic or tachycardic patient: treat the cause, not with DAPT.
• A posterior MI or LBBB with Sgarbossa changes and no ST elevation in the standard leads is still ACOMI. Don't let it wait in an NSTEACS pathway.