Spontaneous coronary artery dissection

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

SCAD compresses the true lumen from within the vessel wall. Angiographic phenotypes include visible multiple lumens or contrast staining, long diffuse smooth narrowing and focal lesions that mimic atherosclerosis.

Evidence is largely observational and expert consensus. The key acute decision is not 'Can this be stented?' but whether active ischaemia, flow, anatomy and haemodynamics make intervention safer than watchful healing.

Post-SCAD care extends beyond ejection fraction: recurrent chest pain is common, recurrence is possible, fibromuscular dysplasia or other arteriopathy may coexist, and anxiety or post-traumatic symptoms can impair recovery.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Underlying arteriopathy

Fibromuscular dysplasia and other systemic arterial abnormalities commonly coexist with SCAD and signal an associated arteriopathy, although a direct causal mechanism is not established.

Pregnancy-associated and hormonal context

SCAD disproportionately affects women and can occur during pregnancy or postpartum, when hormonal and haemodynamic changes may increase vulnerability of the arterial wall.

Physical or emotional stressors

Intense exertion, straining or severe emotional stress are reported precipitants; abrupt shear or catecholamine loading may trigger dissection in a susceptible artery.

No recognised predisposing condition

Some patients lack conventional atherosclerotic risk factors or an identifiable trigger. Absence of a recognised predisposition does not reduce the urgency of an acute coronary presentation.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Intramural bleeding develops
Blood accumulates within the arterial media, with or without an intimal disruption, creating an intramural haematoma and separating layers of the coronary wall.
2
The haematoma extends
The intramural haematoma can extend longitudinally through the vessel wall, creating a dissection plane that may propagate beyond the initially affected segment.
3
The true lumen is compressed
The intramural haematoma narrows the true coronary lumen from outside, restricting distal blood flow without the usual mechanism of ruptured atherosclerotic plaque.
4
Myocardial ischaemia follows
Reduced coronary flow may produce acute coronary syndrome, infarction, ventricular arrhythmia or shock according to the vessel involved, dissection extent and residual flow.
5
Healing or propagation occurs
In stable disease the wall haematoma often resorbs and flow recovers, whereas early extension can worsen ischaemia; instrumentation may also propagate the fragile lesion.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

SCAD-pattern ACSRed flag

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.

Angiographic type 1

Multiple lumens or contrast staining of the arterial wall is the classic but less common appearance.

Angiographic type 2

Long smooth diffuse narrowing, often in a mid-to-distal vessel, is the common pattern and may extend to the vessel tip.

Angiographic type 3

Short focal narrowing resembles atherosclerosis and may need careful expert review or selective intracoronary imaging.

High-risk SCADRed flag

Ongoing ischaemia, poor flow, proximal or left-main involvement, shock or malignant arrhythmia lowers the threshold for revascularisation.

Early extensionRed flag

Recurrent pain with new ECG change or haemodynamic deterioration during observation can indicate propagation or recurrent SCAD and needs immediate reassessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial ECG and high-sensitivity troponinFirst step
Why
Diagnose ACS, localise ischaemia and detect recurrence.
Interpretation and limitations
SCAD may present as STEMI or NSTEMI; normal conventional risk factors do not reduce urgency.
02
Invasive coronary angiography
Why
Define SCAD phenotype, flow, distribution and high-risk anatomy.
Interpretation and limitations
Review with an operator familiar with SCAD; minimise injections and catheter trauma because arteries may be fragile.
03
OCT or IVUS
Why
Confirm intramural haematoma or true and false lumen when angiography is genuinely uncertain.
Interpretation and limitations
Use selectively because wire passage and imaging can extend disease; OCT also requires forceful contrast clearance.
04
Transthoracic echocardiography
Why
Assess regional injury, LV function, thrombus and complications.
Interpretation and limitations
Repeat when clinical status changes and use the result to guide heart-failure therapy and rehabilitation.
05
Head-to-pelvis arterial imaging
Why
Look for fibromuscular dysplasia, aneurysm or dissection in other vascular beds under a specialist SCAD protocol.
Interpretation and limitations
Modality and extent depend on renal function, radiation, pregnancy status and local expertise; incidental findings need expert interpretation.
06
CMR
Why
Clarify infarction pattern or an alternative such as myocarditis or takotsubo when coronary findings are uncertain.
Interpretation and limitations
Use after stabilisation and interpret alongside angiography; a small healed dissection may not be visible on CMR.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Atherosclerotic acute coronary syndrome

Focal irregular plaque in a patient with conventional vascular risk supports atherosclerosis; long smooth narrowing or multiple lumens, particularly in a low-risk phenotype, raises suspicion of SCAD but requires expert angiographic assessment.

Coronary vasospasm

Dynamic narrowing that resolves with intracoronary vasodilator supports spasm, whereas persistent long narrowing from intramural haematoma favours SCAD; unnecessary instrumentation can be hazardous.

Takotsubo syndrome

Transient ventricular dysfunction extending beyond one coronary territory with no culprit lesion suggests takotsubo, though emotional stress and the demographic profile can overlap with SCAD.

Myocarditis

A non-ischaemic injury pattern on cardiac magnetic resonance and unobstructed coronary anatomy favour myocarditis; infarction from SCAD follows the territory of the affected artery.

Aortic dissection

Abrupt tearing pain, pulse or blood-pressure asymmetry and aortic imaging abnormalities suggest aortic dissection, which can secondarily compromise a coronary ostium.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Preferred routeAcute diagnosisFirst stepPreferredACS where SCAD is plausible

1Treat as an emergency ACS, obtain serial ECG and troponin and involve interventional cardiology early.
2Perform coronary angiography with SCAD-aware technique; avoid assuming a focal lesion is atherosclerotic in a low-risk phenotype.
3Use intracoronary imaging only if uncertainty will change treatment and the procedural risk is acceptable.
4Assess LV function and monitor for recurrent pain, ECG change, arrhythmia and haemodynamic deterioration.

02Preferred routeConservative managementPreferredStable patient, preserved coronary flow and no ongoing ischaemia or high-risk anatomy

1Avoid routine PCI and observe in hospital because early extension or recurrent ischaemia can occur; expert practice commonly uses several days, often 3–5, individualised to presentation.
2Stop therapeutic anticoagulation once SCAD is confirmed unless there is another compelling indication, after senior review.
3Individualise antiplatelet therapy, blood-pressure control and LV-dysfunction treatment; do not automatically copy atherosclerotic ACS regimens.
4Repeat angiography only for clinical deterioration or a management-changing question, not simply to document healing.

03EscalationRevascularisationEscalationOngoing ischaemia, poor flow, shock, left-main or critical proximal anatomy

1Discuss immediately with a SCAD-experienced interventionalist and cardiothoracic surgeon where feasible.
2If PCI is necessary, minimise instrumentation and recognise the risk of entering the false lumen or extending intramural haematoma.
3Consider CABG for left-main or extensive proximal disease not safely treatable by PCI, recognising graft failure can follow native-vessel healing.
4Use standard post-stent DAPT unless bleeding risk demands specialist modification.

04Ongoing careSCAD-specific follow-upAfter acute stabilisation

1Refer to SCAD-informed cardiac rehabilitation with gradual aerobic progression and avoidance of extreme straining rather than blanket inactivity.
2Arrange specialist assessment for extracoronary arteriopathy and manage blood pressure.
3Review recurrent chest pain, migraine or vasoactive medicines, mental health and emergency return advice.
4Provide pre-conception and contraception counselling through a multidisciplinary pregnancy-heart team before any future pregnancy.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Single antiplatelet therapy may be considered after conservatively managed SCAD; aspirin remains part of standard post-PCI DAPT.

Aspirin

After 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.

Evidence for routine long-term therapy in non-stented SCAD is observational; consider bleeding and heavy menstrual bleeding and do not imply a universal duration.

P2Y12 component of DAPT after PCI; routine DAPT after conservatively managed SCAD is uncertain and not automatic.

Clopidogrel

When 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.

Bleeding, planned surgery and concomitant anticoagulation; the antiplatelet choice and duration should reflect stent and ACS guidance plus SCAD-specific risk.

Treat hypertension, LV dysfunction or arrhythmia and may reduce recurrent arterial shear; recurrence evidence is observational.

Bisoprolol

A pragmatic anti-adrenergic start is 2.5–5 mg orally once daily, titrated to heart rate, blood pressure, LV function and tolerance; stable-angina dosing commonly increases to 10 mg once daily.

Bradycardia, AV block, hypotension, bronchospasm and acute decompensated heart failure; do not present recurrence prevention as proven by randomised trials.

Symptom relief for post-SCAD chest pain or coexisting vasospasm, not treatment of the arterial-wall haematoma.

Glyceryl trinitrate sublingual spray

400–800 micrograms under the tongue for recurrent chest pain when safe; repeat at 5-minute intervals to a maximum total of 3 sprays while seeking urgent assessment if pain persists.

Avoid with hypotension or riociguat and within at least 24 hours of sildenafil or vardenafil or 48 hours of tadalafil; recurrent or prolonged pain still requires ECG and troponin assessment.

Risk reduction for coexisting atherosclerotic disease, not routine healing or recurrence prevention for isolated SCAD.

Atorvastatin

Use 80 mg orally once daily for coexisting established atherosclerotic CVD when high-intensity treatment is indicated; for another lipid-lowering indication, use the NICE-recommended intensity and dose rather than assuming 80 mg.

Do not prescribe solely because SCAD caused MI; assess lipids, liver disease, myopathy, pregnancy and drug interactions.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Myocardial infarction and ventricular dysfunction

Prolonged severe true-lumen compression can cause myocardial necrosis and regional dysfunction, which may leave persistent left-ventricular impairment, ventricular thrombus or symptomatic heart failure.

Ventricular arrhythmia or cardiac arrest

Acute ischaemia destabilises myocardial electrical activity, allowing ventricular tachycardia or fibrillation and explaining sudden collapse in severe presentations during the acute phase.

Propagation and recurrent ischaemia

The intramural haematoma can extend during early observation or after coronary instrumentation, further narrowing the true lumen and causing renewed pain, ECG change or shock.

Cardiogenic shock

Left-main, proximal or extensive involvement can compromise a large myocardial territory, sharply reduce cardiac output and require high-risk emergency revascularisation or circulatory support.

Recurrent SCAD and psychological morbidity

A later dissection may affect another segment, while recurrent chest pain and fear of recurrence can drive anxiety, hypervigilance and impaired rehabilitation even without new ischaemia.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During admission monitor ECG, pain, haemodynamics and arrhythmia closely for early extension or recurrent ischaemia.
Assess LV function before discharge and repeat according to the degree of dysfunction and recovery.
Track blood pressure and beta-blocker tolerance without inducing symptomatic hypotension or bradycardia.
Document bleeding, menstrual impact and exact indication and stop date for each antithrombotic.
Ensure completion and expert review of extracoronary vascular imaging where offered.
At follow-up ask about recurrent chest pain, exercise confidence, migraine treatment, pregnancy intentions, anxiety and trauma symptoms.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Conservative is active care

Observation, rhythm monitoring, repeat clinical assessment and a deterioration plan are essential while the artery heals.

PCI can worsen the wall haematoma

A wire may enter the false lumen and stenting can propagate intramural blood beyond the treated segment.

Atherosclerotic reflexes mislead

Routine high-intensity statin or prolonged DAPT is not automatically justified for isolated non-stented SCAD.

Recurrent pain is common but must be assessed

Post-SCAD chest pain can be non-ischaemic or vasomotor, yet a changed, prolonged or severe episode still needs ACS evaluation.

Screen beyond the coronaries

Fibromuscular dysplasia and aneurysm or dissection elsewhere can alter counselling and surveillance.

Recovery includes psychological care

An abrupt MI in a previously healthy person can produce anxiety, hypervigilance and post-traumatic symptoms that cardiac rehabilitation should address.

11Common pitfallsFrequent interpretation and management errors.

01
Dismissing ACS in a younger woman because conventional coronary risk is low.
02
Giving thrombolysis after SCAD has been diagnosed.
03
Stenting a stable, flowing SCAD segment simply because narrowing looks severe.
04
Continuing full anticoagulation or potent DAPT automatically after non-stented SCAD without another indication.
05
Prescribing a statin solely because SCAD caused MI despite no atherosclerotic indication.
06
Discharging without SCAD-specific rehabilitation, extracoronary arteriopathy review and pregnancy or psychological counselling.