Introduction
Spontaneous Coronary Artery Dissection is a non-atherosclerotic, non-traumatic separation of the coronary arterial wall leading to formation of a false lumen or intramural hematoma, resulting in impaired coronary blood flow and acute coronary syndrome (ACS). It is an important cause of myocardial infarction in young and middle-aged women without traditional cardiovascular risk factors.
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Epidemiology
Predominantly affects women (≈85–90%)
Common in age 44–53 years
Important cause of MI in women <50 years
Pregnancy-associated SCAD is well recognized
May account for up to 4% of all ACS cases overall and a much higher proportion in younger women
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Pathophysiology
Two proposed mechanisms:
1. Inside-out mechanism
An intimal tear allows blood to enter the arterial wall creating a false lumen.
2. Outside-in mechanism
Bleeding from vasa vasorum causes intramural hematoma without an intimal tear.
The expanding hematoma compresses the true lumen causing myocardial ischemia or infarction.
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Predisposing Factors
1. Female sex hormones
2. Pregnancy and postpartum state
3. Fibromuscular dysplasia (FMD)
4. Connective tissue disorders
5. Extreme emotional stress
6. Intense physical exertion
7. Multiparity
8. Systemic inflammatory diseases
9. Hormonal therapy
10. Sympathomimetic drug use
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Commonly Involved Arteries
Left anterior descending artery (most common)
Circumflex artery
Right coronary artery
Multivessel involvement may occur
Distal vessels are more commonly involved.
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Clinical Presentation
Patients usually present as ACS:
1. Chest pain
2. STEMI or NSTEMI
3. Dyspnea
4. Diaphoresis
5. Ventricular arrhythmias
6. Cardiogenic shock
7. Sudden cardiac death
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ECG Findings
ST elevation
ST depression
T-wave inversion
Arrhythmias
Sometimes normal ECG initially
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Diagnosis
Coronary Angiography — Gold Standard
Coronary Angiography is the primary diagnostic modality.
Angiographic Types
Type 1
Classic multiple radiolucent lumens or dye staining.
Type 2
Long diffuse smooth narrowing (most common).
Type 3
Focal stenosis mimicking atherosclerosis.
Adjunctive Imaging
OCT (Optical Coherence Tomography)
IVUS (Intravascular Ultrasound)
Useful when angiography is inconclusive.
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Echocardiography Findings
Regional wall motion abnormalities
Reduced LV systolic function
Complications such as MR or LV thrombus
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Management
Conservative Therapy (Preferred)
Most stable SCAD lesions heal spontaneously.
Medical Treatment
1. Aspirin
2. Beta blockers
3. Control hypertension
4. Nitrates/calcium channel blockers for chest pain
5. Cardiac rehabilitation
Conservative therapy is preferred because PCI has higher complication and failure rates in SCAD.
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When Revascularization is Needed
PCI or CABG may be required in:
Left main involvement
Ongoing ischemia
Hemodynamic instability
Refractory ventricular arrhythmias
Persistent TIMI 0–1 flow
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PCI Challenges in SCAD
Propagation of dissection
Difficulty wiring true lumen
Extension of intramural hematoma
Stent malapposition after healing
Therefore PCI is avoided unless necessary.
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Prognosis
Most lesions heal within weeks to months
Recurrence occurs in a significant proportion
Long-term follow-up is essential
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Recurrence Risk Factors
1. Hypertension
2. Fibromuscular dysplasia
3. Persistent stressors
4. Pregnancy after SCAD
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Important Clinical Pearls
Think SCAD in young women with MI but few risk factors
SCAD management differs from atherosclerotic ACS
Conservative management is usually preferred
FMD screening should be considered
Avoid extreme physical exertion after recovery
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Conclusion
Spontaneous Coronary Artery Dissection is an increasingly recognized cause of ACS, particularly in younger women without significant atherosclerotic risk factors. Early recognition is crucial because treatment strategies differ markedly from traditional coronary artery disease. Conservative management remains the cornerstone in stable patients, while invasive therapy is reserved for high-risk situations.
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