Synopsis
Recognise SCAD as a non-atherosclerotic cause of ACS, avoid harmful reflex intervention and provide conservative, multidisciplinary follow-up when the patient is stable.
- SCAD is separation within the coronary arterial wall caused by intramural haematoma or an intimal disruption, not plaque rupture, trauma or an iatrogenic tear.
- Consider it in ACS at any age or sex, particularly in younger or middle-aged women, pregnancy or postpartum presentations and patients without conventional atherosclerotic risk factors.
- Coronary angiography is the usual diagnostic test; long smooth narrowing is common and can be mistaken for spasm or atherosclerosis.
Key red flags
Acute chest pain with ECG change or troponin rise in a person without the expected atherosclerotic profile; pregnancy or postpartum status and emotional or physical stressors can be clues but are not required.
Investigation priorities
Diagnose ACS, localise ischaemia and detect recurrence.
Management branches
ACS where SCAD is plausible
- Treat as an emergency ACS, obtain serial ECG and troponin and involve interventional cardiology early.
- Perform coronary angiography with SCAD-aware technique; avoid assuming a focal lesion is atherosclerotic in a low-risk phenotype.
Stable patient, preserved coronary flow and no ongoing ischaemia or high-risk anatomy
Key medicines
AspirinAfter the acute 300 mg load, a common conservative regimen is 75 mg once daily, but duration after non-stented SCAD must be individualised by a SCAD specialist.
ClopidogrelWhen a stent is placed, use the PCI protocol loading dose, commonly 600 mg orally, then 75 mg once daily with aspirin for the specialist-defined duration.