spontaneous coronary artery dissection
Contents
Non-atherosclerotic, non-traumatic separation of coronary arterial wall layers causing ACS — accounts for 1–4% of all ACS but up to 35% in women <50. >90% occur in women; fibromuscular dysplasia (FMD) is present in ~50%. Conservative management preferred; spontaneous healing occurs in ~95%.
quick recognition
- young/middle-aged woman + ACS + absent traditional risk factors → think SCAD
- recent emotional/physical stressor, peripartum period, known FMD or connective tissue disorder
- troponin-positive chest pain with angiographic appearance not fitting atherosclerotic plaque
- mid-to-distal coronary involvement (especially LAD), pronounced coronary tortuosity
- multivessel involvement in ~10–15%
when to suspect
High pre-test probability:
- women 44–62 yr presenting with ACS
- peripartum (most within 1 week postpartum) — leading cause of pregnancy-associated MI
- known FMD (present in 43–56% of SCAD patients)
- connective tissue disorder (Marfan, Loeys-Dietz, vascular Ehlers-Danlos)
- preceding intense emotional (~50%) or physical (~29%) stressor
Lower pre-test probability (consider alternatives):
- multiple traditional CV risk factors
- calcified or lipid-rich plaque on angiography
- substantial luminal thrombus
diagnosis / investigations
angiographic classification (Yip-Saw)
| Type | Frequency | Appearance | Notes |
|---|---|---|---|
| 1 | <30% | contrast staining, multiple radiolucent lumens, dye hang-up | pathognomonic — intimal tear with false lumen |
| 2A | 60–75% (combined) | long (>20 mm) smooth diffuse narrowing, normal segments both ends | most common |
| 2B | long narrowing extending to distal tip, no reconstitution | ||
| 3 | <5% | focal short stenosis mimicking atherosclerosis | often requires OCT/IVUS |
intracoronary imaging
| Modality | Resolution | Strengths | Limitations |
|---|---|---|---|
| OCT | 10–20 µm | visualises intimal flaps, double lumens, IMH; best for Type 3 | requires contrast; risk of hydraulic dissection extension |
| IVUS | ~150 µm | deeper penetration; “triple-band” pattern; no contrast needed | lower resolution than OCT |
Both OCT and IVUS carry risk of hydraulic extension of dissection — use only when diagnosis remains uncertain after angiography and benefit outweighs risk.
Supporting features:
- mid-to-distal segment involvement
- coronary tortuosity (independently associated)
- absence of atherosclerotic plaque or intraluminal thrombus
- complete resolution on follow-up angiography/CCTA confirms diagnosis
vascular screening
All SCAD survivors → brain-to-pelvis CTA or MRA to screen for:
- FMD (renal, carotid, iliac arteries)
- extracoronary aneurysms/dissections (found in >47%)
- intracranial aneurysms (7–25% on screening)
genetic testing
- not routine
- consider if: peripartum SCAD, recurrent SCAD, family history of arteriopathy, clinical suspicion of connective tissue disorder
- pathogenic variants in COL3A1, SMAD3, and Loeys-Dietz genes found in ~17% of high-risk cases
management
step 1: acute — conservative vs revascularisation
~84% managed conservatively (Canadian SCAD Cohort). Spontaneous angiographic healing in ~95%. PCI success rates significantly lower than in atherosclerotic ACS due to arterial fragility.
Indications for PCI:
- ongoing ischaemia despite medical therapy
- haemodynamic instability
- left main or proximal multivessel involvement
CABG: last resort when PCI fails or is anatomically not feasible — avoid grafting directly onto dissected tissue (spontaneous healing → competitive flow)
step 2: antiplatelet therapy
| Scenario | Regimen | Duration | Rationale |
|---|---|---|---|
| conservatively managed | aspirin 81 mg (SAPT) | 1–12 months (tailored to bleeding risk) | DAPT associated with higher MACE/recurrence vs SAPT |
| post-stenting | aspirin + clopidogrel (DAPT) | ≥12 months (standard ACS protocol) | follow ACS guidelines |
Ticagrelor + aspirin → aHR 2.6 for SCAD recurrence (ANZ cohort). Pathophysiology is intramural bleeding, not plaque rupture — potent antiplatelets may worsen vessel wall haematoma. The 2026 AHA Scientific Statement on ACS in Premenopausal Women explicitly advises against ticagrelor/prasugrel in SCAD.
Discharge on OAC → aHR 3.8 for MACE (ANZ cohort). Avoid unless separate compelling indication.
step 3: long-term pharmacotherapy
| Agent | Recommendation | Evidence |
|---|---|---|
| beta-blockers | all SCAD patients | RR 0.51 for recurrence (meta-analysis, 4,206 pts); 73.5% on beta-blockers at 3 yr in Canadian cohort |
| blood pressure control | strict targets | hypertension is independent predictor of recurrence (RR 1.49); causal role inferred from GWAS |
| statins | only if concomitant dyslipidaemia | no benefit for SCAD recurrence — non-atherosclerotic pathology |
step 4: cardiac rehabilitation
- safe for SCAD survivors — no increase in MACE or arrhythmias
- moderate-intensity aerobic exercise recommended
- avoid: HIIT, competitive sports, heavy isometric exercise, Valsalva manoeuvres
- resistance training — individualise (not universally restricted)
- structured psychosocial support critical — high rates of anxiety, depression, PTSD
step 5: reproductive counselling
- pregnancy after SCAD — generally discouraged (uncertain but potentially elevated risk)
- if pursued → multidisciplinary cardio-obstetrics team
- contraception: levonorgestrel IUD preferred; avoid oestrogen-containing methods
what NOT to do
- do not default to standard ACS antiplatelet protocols — SCAD is not plaque rupture
- do not use ticagrelor or prasugrel in conservatively managed patients
- do not anticoagulate without a separate indication
- do not rush to PCI — arterial fragility → high complication rates, wire-induced extension of dissection
- do not prescribe statins solely for SCAD (non-atherosclerotic)
- do not restrict physical activity excessively — deconditioning worsens outcomes and mental health
- do not skip vascular screening — FMD and extracoronary aneurysms change management
recurrence and prognosis
Rates: 2.4% de novo recurrence at 3 yr (Canadian cohort); meta-analysis 5-yr estimate up to 27%
Predictors of recurrence:
| Factor | Effect size |
|---|---|
| FMD | aHR 3.9 (ANZ); RR 2.02 (meta-analysis) |
| history of stroke | aHR 6.2 |
| genetic disorder | HR 5.0 for MACE |
| hypertension | RR 1.49 |
| peripartum | HR 2.3 |
Protective: beta-blocker use — only pharmacological intervention consistently associated with reduced recurrence
key trials summary
| Study | Year | N | Key finding |
|---|---|---|---|
| Canadian SCAD Cohort (2022) | 2022 | 750 | 84.3% conservative; 2.4% de novo recurrence at 3 yr; FMD in 43% |
| ANZ SCAD Cohort (2025) | 2025 | 505 | ticagrelor+ASA → aHR 2.6 recurrence; OAC → aHR 3.8 MACE; FMD → aHR 3.9 |
| Chi meta-analysis (2022) | 2022 | 4,206 | beta-blockers RR 0.51; FMD RR 2.02; HTN RR 1.49 |
| Adlam GWAS (2023) | 2023 | 1,917 | 16 risk loci; F3 gene specific to SCAD; causal role for hypertension |
| Wang rare variants (2022) | 2022 | high-risk | 17% had vascular CTD gene variants; COL3A1 OR 13.4 |