Abbreviations

• SCAD – Spontaneous Coronary Artery Dissection
• CAD – Coronary Artery disease
• MINOCA – Myocardial Injury with Non-Obstructive Coronary Artery Disease
• ACS – Acute Coronary Syndrome

• AMI – Acute Myocardial Infarction (MI)
• OCT – Optical Coherence Tomography
• IVUS – Intravascular ultrasound
• FMD – Fibromuscular Dysplasia

Spontaneous Coronary Artery Dissection (SCAD)

• Non-atherosclerotic non-traumatic cause of acute coronary syndrome and death
• 4% of all ACS
  • 35% of ACS in woman < 50yo.
• High level evidence to direct management is not available
• Pathophysiology
  • Development of hematoma within tunica media of vessel, leading to separation of intima from media (see figure).  
  • This compresses the true lumen causing ischemia and AMI.

• Two hypotheses:
  • “Inside-out” – blood enters the subintimal space from true lumen after endothelial-intimal disruption “flap”.
  • “Outside-in” – hematoma arises de novo in the media, possibly from microvessels. 
•  Three types:
  • Type 1 – Multiple radiolucent lumens with arterial wall staining
  • Type 2 – Diffuse stenosis
  • Type 3 – focal tubular stenosis mimicking atherosclerosis
•  Risk Factors
  • Multifactorial **
    • Hormones 
    • Sex
    • Genetics (connective tissue diseases)
    • Pregnancy (70% within 1st week postpartum) – termed P-SCAD, more severe
  • Emotional stressors more common triggers in women. 
  • Physical stressors more common in men (cocaine, retching, cancer)
• Presentation
  • Classically middle-aged women without significant CAD risk factors. 
  • Present as overall ACS (STEMI or NSTEMI) syndrome.
    • Chest pain, Troponin rise, ECG findings (ST elevations or depressions)
  • Ventricular arrhythmias, shock, arrest.
• Diagnosis
  • Coronary Angiography
    • Usually mid-to-distal coronary artery (typically LAD)
    • Intracoronary imaging can help confirm diagnosis (OCT and intravascular ultrasound (IVUS))
      • Usually not done unless diagnosis uncertain – instrumenting vessels can cause injury.
  • CTA may identify large-vessel SCAD, but lacks spacial resolution. 

Management

• Generally presents similar to acute MI, angiography needed to diagnose. 
  • If pregnant –> fetal shielding
• Most patients recover normal coronary architecture within 30 days (95%) 
• 10-30% lifetime recurrence
• Interventional Management
  • PCI results are unpredictable, high risk of complications, suboptimal outcomes. 
    • Can worsen dissection and cause complete occlusion. (1/3 have hematoma propagation)
    • Resorption of hematoma can cause poor stent sizing/malapposition
  • Generally treated as conservatively as possible. 
  • Stenting/CABG can be considered for large vessel high-risk dissections (left-main, shock, pain)
• Pharmacologic Management
  • Treat any LV dysfunction with standard HF therapy
  • Beta-blocker (lower rates of recurrence in some studies)
  • Lipid management – only if indication
  • ASA / DAPT – No specific recommendations.  Most clinicians recommend DAPT for 2-4 weeks then ASA for 3-12 months.  (skip if high risk of bleeding)
  • Anti-angina pain management (nitrates, analgesics)
• Non-Pharmacologic
  • Strong relationship to fibromuscular dysplasia (FMD)
    • Many consensus papers recommend FMD (arteriopathy) screen head to pelvis with CTA or MRA.
    • May identify clinically important vascular complications that may warrant treatment/follow-up (such as intracranial aneurysm)
  • Avoid high-intensity/extreme-endurance/competitive aerobic and isometric exercise (tends to trigger (SCAD))
    • Moderate intensity exercise is encouraged –  benefit likely outweighs the theoretical risk of recurrent SCAD
  • Avoid heavy lifting that require prolonged straining/valsalva

References

• JACC – State of the art Reviews

Authors

• Primary Author: Pavel Antiperovitch (MD, FRCPC Cardiologist)
• Reviewer: TBD
• Copy Editor: TBD