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.
- Thrombolysis is contraindicated once SCAD is diagnosed because it can extend the dissection or cause coronary rupture and tamponade.
- Stable patients with preserved flow and no ongoing ischaemia are usually managed conservatively because spontaneous healing is common and PCI has higher failure and propagation risk.
- Use intracoronary OCT or IVUS only when diagnostic uncertainty will change management; instrumentation can extend the dissection.
- Antiplatelet therapy after conservatively managed SCAD is not evidence-equivalent to plaque-rupture ACS and should be individualised; standard DAPT is required after stenting unless bleeding forces modification.
- Assess ventricular function, offer SCAD-informed cardiac rehabilitation and screen for associated extracoronary arteriopathy through a specialist pathway.
- Future pregnancy, contraception, migraine vasoactive drugs, recurrence fears and psychological recovery require planned multidisciplinary review.