SCAD - Spontaneous Coronary Artery Dissection

Spontaneous coronary artery dissection is an underrecognized cause of acute coronary syndrome, especially in younger women and during pregnancy or the postpartum period. SCAD often presents like routine ACS despite a normal first troponin or nonspecific ECG, and its management diverges sharply from thrombotic MI once the diagnosis is made.

Recognizing SCAD in Acute Coronary Syndrome

• Young women with ACS: SCAD accounts for up to 25% of acute coronary syndrome in women 50 and younger, making it a crucial diagnosis when chest pain seems out of proportion to the usual risk profile.
• Normal first troponin: About 20% of patients have an initially negative troponin and a low HEART score, so serial biomarkers matter when the story still sounds ischemic. We get into that diagnostic tension in the episode.
• Subtle ECG findings: ECGs may be normal or show only nonspecific ST-T changes, although roughly half of SCAD patients present with STEMI and pregnancy-associated cases tend to involve more proximal LAD lesions.
• Stress and recurrence pattern: Female sex, pregnancy or postpartum state, and intense emotional or physical stress are classic clues, and prior SCAD meaningfully raises the risk of recurrence.
• Intramural hematoma phenotype: Most SCAD cases are not a visible intimal flap but an intramural hematoma, which is why intracoronary imaging with OCT or IVUS may be needed to confirm the diagnosis.

Management Differences From Thrombotic MI

• Conservative healing trajectory: Eighty to ninety percent of affected coronary arteries heal completely with conservative management, so stable patients with preserved flow are often observed rather than stented.
• Fragile vessel intervention: PCI is harder in SCAD because the vessels are fragile and dissections can extend; early propagation occurs in about 10%, which is part of why inpatient observation matters.
• Avoid routine thrombolysis: Thrombolytics can worsen an intramural hematoma, making lytics a poor fit when SCAD is the true mechanism of infarction.
• Stop heparin after diagnosis: Once SCAD is confirmed, heparin can usually be discontinued because intracoronary thrombus is uncommon and ongoing anticoagulation may add harm.
• Selective secondary prevention: Beta-blockers are associated with fewer recurrences, whereas statins are not routine unless there is a separate indication like severe hyperlipidemia. We walk through the practical medication distinctions in the chapter.
• Persistent post infarct pain: Recurrent chest pain after SCAD is often vasospastic rather than a new infarction, and long-acting nitrates or calcium channel blockers can help even when repeat ED workups are negative.

Associated Arteriopathy and Follow Up

• Systemic vascular disease signal: Sixty to eighty percent of SCAD patients have an underlying arteriopathy, most commonly fibromuscular dysplasia, with potential aneurysm or dissection elsewhere in the body.
• Brain to pelvis imaging: After recovery, screening CT angiography from brain to pelvis is recommended to look for extracoronary vascular abnormalities that change counseling and follow-up.
• Cardiac rehab role: Cardiac rehab is especially valuable because many patients are young, previously healthy, and psychologically shaken after being initially dismissed or misread in the ED.
• Pregnancy associated severity: Pregnancy-related SCAD more often involves proximal coronary segments, larger infarcts, and worse outcomes than nonpregnancy SCAD.

References:

• Hayes, Sharonne N. "Spontaneous coronary artery dissection (SCAD): new insights into this not-so-rare condition." Texas Heart Institute Journal 41.3 (2014): 295-298.
• Saw, Jacqueline, et al. "Nonatherosclerotic coronary artery disease in young women." Canadian journal of cardiology 30.7 (2014): 814-819.