Spontaneous Coronary Artery Dissection (SCAD)

Epicardial coronary artery dissection that is not associated with atherosclerosis, trauma, or medical intervention. Intramural haematoma formation within the coronary artery wall compresses the true lumen causing myocardial infarction (MI)

Overview
  • Cause of 1-4% of cases of acute coronary syndrome (ACS)
  • Most commonly occurs in women 45-55 with few or no traditional cardiac risk factors — the “low risk” group
  • Most common cause of pregnancy-associated MI, and the cause of ACS in 1/3 pre-menopausal women
  • Conservative management is generally preferred in clinically stable patients without ongoing ischaemia

Pathophysiology

Two theories:

  • Intimal tear –> blood from true lumen enters and generates a false lumen
  • Spontaneous haemorrhage from vasa vasorum within the vessel wall

Both theories have the same end point of intramural haematoma formation with the coronary artery wall, which compresses the true lumen causing coronary insufficiency and MI.

An intimal tear cannot always be identified. This may support the second theory more so. Even when a tear is found, it may be due to increasing pressure in the false lumen, or as a result of subsequent coronary instrumentation/intervention.


History

Almost all presentations experience classical symptoms of atherosclerotic ACS, with chest pain the most prevalent feature:

  • Chest pain (96%)
  • Radiation to arm (50%)
  • Nausea/vomiting (25%)
  • Diaphoresis (25%)
  • Shortness of breath (25%)
  • Back pain (15%)
  • Fatigue (5%)

Syncope is rare and is seen in less than 0.5% of cases.


Risk factors

Associated conditions:

  • Fibromuscular dysplasia (50%)
  • Pregnancy (5%) — majority in third trimester or early postpartum period
  • Exogenous hormones (10%)
  • Systemic inflammatory disease (5%)
  • Inherited connective tissue disorder (2%)

Around half of patients report some form of preceding extreme physical or emotional stress:

  • Intense exercise
  • Retching, vomiting, bowel movement ,coughing
  • Intense emotional stress
  • Labour and delivery
  • Recreational drugs (cocaine, amphetamines)

Investigations
Bedside
  • ECG
    • Around half of patients will present with STEMI, with infarct territory corresponding to affected vessel
    • Left anterior descending artery (LAD) is most common (50%), left circumflex (20%), right coronary artery (30%), multi-vessel (10%)
  • Echocardiography
    • Left ventricular (LV) wall motion abnormalities corresponding to infarct territory
Laboratory
  • Hs-cTnT — almost invariably increased, although may be normal on presentation
Imaging
  • Coronary angiography
    • First-line investigation, as initial presentation is often indistinguishable from atherosclerotic ACS
    • 2D imaging limits specific assessment of arterial lumen
    • Note higher risk of iatrogenic coronary artery dissection (see complications)
  • Dedicated intracoronary imaging
    • Intravascular USS
    • Not available in all centers
    • Only pursued if angiographic diagnosis uncertain
  • Cardiac computed tomography angiography (CCTA)
    • May be reasonable first-line investigation for low risk patients presenting with ACS
    • Interpret with caution — normal CCTA does not exclude SCAD

Management

The decision for conservative versus invasive therapy depends on haemodynamic stability, pattern of dissection, and presence of any ongoing ischaemia.

Conservative therapy
  • Observational studies suggest that the majority of SCAD lesions will undergo spontaneous angiographic healing after conservative management. Such healing usually occurs by one month
  • Recurrent MI may occur in 5-10%, usually due to extension of dissection in the first week after onset
  • Patients require an extended period of inpatient monitoring
  • Not appropriate for high-risk patients (see below)
Invasive therapy
  • Associated with high rates of complications, and should be reserved for patients with ongoing ischaemia, LMCA dissection, or haemodynamic instability
  • Percutaneous coronary intervention (PCI) demonstrates technical failure in up to 50%, due to iatrogenic dissection, stent displacement, and stent thrombosis
  • Coronary artery bypass grafting (CABG) is an alternative option although evidence base is limited, with delayed graft failure common
  • Stent and graft failure in PCI and CABG is likely due to concurrent spontaneous healing of SCAD. Spontaneous resolution of intramural haematoma can predispose to stent displacement, and in CABG patients native revascularisation promotes graft occlusion
Medical management
  • Anticoagulation
    • No clear evidence
    • Given presentation consistent with ACS, most patients with SCAD are commenced on heparin prior to diagnosis
    • Theoretical risk of accentuating bleeding into intramural haematoma or extending dissection. As such, cessation should be considered following diagnosis of SCAD
  • Beta-blockers
    • Reduces recurrence (HR 0.36)
    • Use may be limited by side effects
  • Statins
    • Not recommended, may increase risk of recurrence
  • Antianginal therapy
    • May relieve symptoms in patients with post-SCAD chest pain syndromes — in particular due to coronary vasospasm or microvascular dysfunction

Complications
Immediate
  • Ventricular arrhythmias (10%)
  • Cardiogenic shock
  • Sudden cardiac death
Early
  • Iatrogenic coronary artery dissection
    • 3-4% of patients with SCAD, compared to < 0.2% for standard angiography
    • Likely due to underlying arterial frailty that predisposed to initial dissection
  • Recurrent MI
    • Occurs in 5-10% of conservatively managed patients, due to extension of initial dissection
Late
  • Post-SCAD chest pain syndrome (50%) — recurrent chest pain, without inducible ischaemia on stress testing
  • Stent occlusion, stent displacement, and graft failure are common in patients managed with PCI or CABG
  • Other complications are similar to those of atherosclerotic MI — LV systolic dysfunction, LV aneurysm formation

  • SCAD is an underrecognised cause of ACS, especially in the “low risk” young female population. An initial normal troponin does not exclude the diagnosis
  • Initial emergency department management is identical to atherosclerotic ACS, with angiography the main diagnostic modality
  • Following diagnosis, conservative therapy is the current preferred management option
  • Invasive therapies including PCI/CABG may be indicated in patients with haemodynamic instability, ongoing ischaemia, or large proximal vessel dissections

Journal articles and textbooks

FOAM and web resources


Critical Care

Compendium

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library. Twitter: @rob_buttner

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