Lucan · Conditions

Acute coronary syndrome

Australian guidance: Heart Foundation / CSANZ ACS Guidelines 2016 (updates 2025)

1. Definition and epidemiology

Acute coronary syndrome (ACS) encompasses acute myocardial infarction (AMI) and unstable angina (UA), representing conditions involving sudden reduced blood flow to the heart. In Australia in 2021 there were an estimated 57,300 acute coronary events among people aged 25 and over, equating to approximately 157 events per day, with coronary heart disease accounting for 10% of all deaths that year. First Nations peoples experience acute coronary events at twice the rate of non-Indigenous Australians, and men experience events 2.3 times more frequently than women after age adjustment, though women face longer symptom duration and lower rates of secondary prevention medication use.

2. Pathophysiology

Per Robbins Ch 11, the dominant mechanism is atherosclerotic plaque rupture, ulceration, fissure, or erosion in a major epicardial coronary artery, leading to superimposed intraluminal thrombus formation. Plaque rupture exposes the lipid-rich necrotic core and subendothelial collagen to circulating platelets; platelet adhesion and aggregation rapidly generate a platelet plug that activates the coagulation cascade, producing a fibrin-stabilised thrombus. Partial occlusion with preserved antegrade flow but impaired perfusion produces NSTEMI or UA, while complete occlusion causes transmural ischaemia and STEMI. The 2025 guideline introduces the term acute coronary occlusion myocardial infarction (ACOMI) to encompass both classical STEMI and electrocardiogram (ECG) equivalents such as posterior MI, right ventricular MI, de Winter T waves, and left bundle branch block meeting modified Sgarbossa criteria, acknowledging that significant epicardial occlusion can occur without classic ST-segment elevation. Non-atherosclerotic mechanisms including spontaneous coronary artery dissection (SCAD), coronary embolism, and vasospasm or microvascular dysfunction can produce an identical clinical and ECG picture and should be considered particularly in younger women without traditional cardiovascular risk factors.

3. Clinical presentation and diagnostic criteria

The cardinal symptom is central substernal discomfort described as squeezing, pressure, tightness, or heaviness, often radiating to the neck, arms, or jaw, exacerbated by exertion. Women, older adults, and people with diabetes more often present with angina equivalents: shortness of breath, fatigue, nausea, diaphoresis, or vomiting. Response to GTN must not be used as a diagnostic criterion. On arrival, vital signs, SpO2, and a 12-lead ECG must be obtained. Examination may reveal haemodynamic compromise, pulmonary oedema, or a new murmur. Critical differentials include aortic dissection, pulmonary embolism, and pneumothorax.

4. Investigations and AU-specific cutoffs

The initial investigation hierarchy follows: ECG first, then high-sensitivity cardiac troponin (hs-cTn), then further risk stratification.

ECG. A 12-lead ECG must be obtained and interpreted within 10 minutes of first clinical contact. If ACOMI is identified (STE, posterior changes, right ventricular leads, de Winter pattern, or Sgarbossa-positive LBBB), emergency reperfusion is indicated without waiting for troponin results. Repeat ECGs are required if symptoms persist, recur, or there is diagnostic uncertainty; right-sided and posterior leads should be added when the standard 12-lead is inconclusive.

Troponin. High-sensitivity cardiac troponin assay (hs-cTn) is the recommended biomarker. The upper reference limit is defined as the sex-specific greater than 99th percentile for the specific assay in use; sex-specific thresholds must be applied. Serial results from the same assay should be used to evaluate rise and fall (delta troponin), as a single elevated value alone may reflect chronic myocardial injury rather than acute MI. A validated clinical decision pathway (CDP) incorporating hs-cTn, including the 0 hour or 1 hour or the 0 hour or 2 hour High-STEACS algorithm, is recommended for risk stratification into low, intermediate, and high categories.

Further testing. People at intermediate risk with troponin above the 99th percentile require inpatient investigation. Those at intermediate risk with non-elevated troponin may be suitable for outpatient non-invasive testing. Low-risk people who remain symptom-free do not routinely require further cardiac testing for coronary artery disease before discharge.

5. Management

Immediate. Aspirin 300 mg orally, dissolved or chewed, is recommended for all people with suspected or confirmed ACS unless contraindicated (strong recommendation, high certainty evidence). Oxygen therapy is indicated only when oxygen saturation (SpO2) is below 90%; supplemental oxygen should be titrated to keep SpO2 at or below 96% to avoid hyperoxia. GTN sublingual tablet or spray every 5 minutes for up to three doses is appropriate for ongoing chest pain. Intravenous fentanyl or morphine boluses may be used for pain relief in the absence of contraindications.

STEMI and ACOMI. Primary PCI is the preferred reperfusion strategy within 12 hours of symptom onset when it can be delivered within 120 minutes of first medical contact (strong, high). At a PCI-capable centre, balloon inflation must occur within 60 minutes of arrival; at a non-PCI centre, within 90 minutes of arrival. When primary PCI cannot be achieved in time, fibrinolysis must be given within 30 minutes of first medical contact (strong, moderate); half-dose tenecteplase applies in those aged 70 years or older. Radial access is preferred (strong, high). Post-fibrinolysis transfer to a PCI-capable centre for angiography within 2 to 24 hours is recommended.

NSTEACS. The GRACE risk score guides short-term and long-term cardiovascular prognosis. People with NSTEACS at high or very high risk require routine invasive coronary angiography with revascularisation where appropriate (strong, high). Those at very high risk require an immediate invasive strategy within 2 hours of diagnosis; those at high risk require an early invasive strategy within 24 hours.

Antiplatelet therapy. DAPT with aspirin plus a potent P2Y12 inhibitor (ticagrelor or prasugrel) is standard for primary PCI and NSTEACS with a routine invasive strategy (strong, high). Clopidogrel replaces potent P2Y12 inhibitors when these are contraindicated or when the patient is on oral anticoagulation. Fibrinolysis-treated STEMI receives aspirin plus clopidogrel. Routine glycoprotein IIa/IIIb inhibitor use is not recommended.

Anticoagulation. Fibrinolysis patients receive unfractionated heparin or enoxaparin. Primary PCI patients receive unfractionated heparin or bivalirudin. NSTEACS patients receive unfractionated heparin, enoxaparin, or fondaparinux.

Secondary prevention and post-discharge. Multidisciplinary exercise-based cardiac rehabilitation is recommended prior to discharge (strong, moderate). DAPT with aspirin and a P2Y12 inhibitor for 6 to 12 months is standard for people at high ischaemic and low bleeding risk; cessation of DAPT at 1 to 3 months with continuation of single antiplatelet therapy is recommended for those at low ischaemic or high bleeding risk. High-intensity statin therapy is initiated before hospital discharge and continued indefinitely (strong, high). ACE inhibitors (angiotensin converting enzyme inhibitors) or angiotensin receptor blockers are indicated when LVEF is 40% or less, or when heart failure symptoms, diabetes, hypertension, or chronic kidney disease are present (strong, high). Beta blockers are recommended for people with left ventricular impairment. Colchicine 0.5 mg daily may be considered long-term for secondary prevention.

6. Pharmacology and AU PBS notes

Antiplatelet agents. Aspirin 300 mg loading then 100 mg daily. Ticagrelor (Brilinta) 180 mg loading then 90 mg twice daily (PBS listed for ACS). Prasugrel (Effient) 60 mg loading then 10 mg daily (PBS listed for PCI-ACS). Clopidogrel (Plavix, generic) 300 to 600 mg loading then 75 mg daily.

Lipid-lowering. LDL-C target post-ACS is less than 1.4 mmol/L with at least 50% reduction from baseline. High-intensity statins are first-line: rosuvastatin (Crestor) 20 to 40 mg daily or atorvastatin (Lipitor) 40 to 80 mg daily. Add ezetimibe (Ezetrol) if target not reached on statin. PCSK9 inhibitors (evolocumab, alirocumab) when statin plus ezetimibe fails (strong, high); PBS requires specialist initiation and prior failure criteria.

Cardioprotective agents. ACE inhibitors (ramipril, perindopril) first-line when indicated. Mineralocorticoid receptor antagonists (eplerenone or spironolactone) for LVEF 40% or less with heart failure (strong, high). Tenecteplase (Metalyse) weight-adjusted; half-dose for age 70 or older. Colchicine 0.5 mg daily for secondary prevention (authority may be required on PBS).

7. Complications and monitoring

Early complications include ventricular fibrillation, cardiogenic shock, mechanical complications (ventricular septal defect, free wall rupture, papillary muscle rupture with acute mitral regurgitation), right ventricular infarction, and complete heart block. In cardiogenic shock, PCI targets the infarct-related artery only; routine intra-aortic balloon pump and routine venoarterial extracorporeal membrane oxygenation are not recommended. Continuous cardiac monitoring with defibrillator availability is required while ACOMI assessment continues or haemodynamic compromise is present.

Late complications include reinfarction, heart failure with reduced ejection fraction, Dressler syndrome, left ventricular aneurysm, and sudden cardiac death.

Post-discharge: echocardiography to assess left ventricular function, lipid monitoring toward the LDL-C target, blood pressure, and renal function monitoring when ACE inhibitors or mineralocorticoid receptor antagonists are prescribed. Cardiac rehabilitation prior to discharge and influenza vaccination are both recommended.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.