Table 1

What Should Interventional Cardiologists Know About SCAD

Clinical attributes:
  • Prevalence ∼1%

  • Affects predominantly younger women (men in ∼5% to 10% of cases)

  • Associated or predisposing etiologies include: pregnancy, fibromuscular dysplasia, chronic systemic inflammatory diseases, hormonal therapy, connective tissues disorders (e.g., Marfan and Ehler-Danlos type 4 syndromes), familial inheritance (∼1% of cases), and so on.

  • Possible precipitating factors: extreme emotional stress or physical activity, sympathomimetic drugs, high-dose hormonal therapy exposure, activities with intense Valsalva-like maneuvers (e.g., vomiting, coughing, childbirth)

  • Clinical presentation: usually AMI (less commonly: ventricular arrhythmias, cardiogenic shock, sudden cardiac death)

  • SCAD patients have usually preserved LV ejection fraction and/or near full-recovery after their initial presentation

  • Inpatient monitoring for at least 5 days is recommended among conservatively managed SCAD patients (given risk of early progression of the dissection)

  • Recurrence: SCAD can recur in the same or different artery (∼27% at 4 to 5 yrs after the initial event); future pregnancy should likely be avoided; CTA utility is uncertain (likely not helpful for diagnosis, but possibly helpful to document coronary healing)

Angiographic characteristics:
  • Angiographic types of SCAD:

    • Type I: extraluminal contrast staining, multiple radiolucent lumen, spiral dissection (∼29% of cases)

    • Type II: diffuse stenosis of varying severity/length—usually >20 mm in length—with abrupt changes in arterial caliber, from normal caliber to diffuse narrowing (∼68% of cases)

    • Type III: focal/tubular stenosis mimicking atherosclerosis—usually < 20 mm in length (∼3% of cases)

  • Usually (>90%) affects the middle and distal coronary segments

  • Coronary artery involvement:

    • LAD and branches: ∼45% to 60% of cases (most affected)

    • Left circumflex and branches: ∼15% to 45% of cases

    • RCA and branches: ∼10% to 40% of cases

    • LM: ∼0% to 4% of cases

    • Multiple arteries dissected: ∼9% to 19% of cases

  • TIMI flow grade 3: ∼19% to 55% of cases on presentation

Medical therapies:
  • Dual-antiplatelet therapy (aspirin + P2Y12 receptor inhibitor): likely useful, theoretically may reduce false lumen thrombosis and consequent true lumen compression

  • Beta-blocker: reduces arterial shear stress, and possibly useful in the short-term and in the long-term to prevent recurrence

  • Anticoagulation: controversial, risk of extending the dissection vs. helping resolve the lumen thrombus and improve true lumen patency

  • Fibrinolytic therapy: likely harmful and should be avoided (possible extension of the dissection and intramural hematoma)

  • Angiotensin-converting enzyme or angiotensin receptor inhibitor: beneficial in SCAD patients with LV dysfunction; no proven benefits otherwise

  • HMG CoA-reductase inhibitor (statin): no proven benefit in the absence of concomitant atherosclerotic disease

  • Cardiac rehabilitation program: evidence shows that a dedicated program is beneficial in SCAD patients

Revascularization vs. conservative management:
  • SCAD arteries usually heal spontaneously (100% healing ≥26 days post-dissection)

  • PCI is associated with low success rates (range 47% to 73%)

  • The optimal therapeutic strategy (revascularization versus conservative) should be tailored to patient’s clinical scenario. Conservative management may be reasonable in many instances. However, revascularization, preferably with PCI (or CABG if needed), should be undertaken in patients with ongoing ischemia and/or electrical and hemodynamic instability.

PCI technical challenges and tips:
  • The femoral artery approach is preferred (more iatrogenic dissections observed with radial artery catheterization)

  • Long stents are preferred to adequately cover both edges of the intramural hematoma

  • For very long lesions, multistep and multistenting approach is reasonable (i.e., stenting the distal then the proximal edge, to prevent propagation of the intramural hematoma, followed by stenting of the middle coronary segment)

  • The distal coronary segments—usually affected by SCAD—may be too small and not amenable to PCI with stenting

  • Intravascular imaging—OCT or IVUS—should be used cautiously. Intravascular imaging is possibly helpful (e.g., helps visualize intimal tears, false lumen, and intramural hematoma and thrombi; also ascertains the extent of dissection and adequate stent coverage and apposition), but carries potential hazards (see the following text)

  • Operators should beware of the:

    • Risk of iatrogenic catheter-induced dissection

    • Potential difficulty to enter the true lumen with the wire or balloon/stent

    • Risk of propagation of the dissection (by the wire/imaging catheter/balloon/stent or through contrast-induced hydraulic extension)

    • Risk of coronary rupture

    • Risk of stent malapposition following the resorption of the intramural hematoma

Table compiled from multiple studies and reviews (1–3,6,8–10).

AMI = acute myocardial infarction; CABG = coronary artery bypass graft; CTA = computed tomography angiography; IVUS = intravascular ultrasound; LAD = left anterior descending coronary artery; LM = left main coronary artery; LV = left ventricular; OCT = optical coherence tomography; PCI = percutaneous coronary intervention; RCA = right coronary artery; SCAD = spontaneous coronary artery dissection; TIMI = Thrombolysis In Myocardial Infarction.

  • Likely an underestimate.

  • Only SCAD-specific benefits are summarized in this section. Evidence-based recommendations for medical therapies are lacking, and the summarized therapies herein are theoretical and extrapolated from the known benefits of these treatments in AMI patients.

  • The SAFER-SCAD (Statin and Angiotensin-Converting Enzyme Inhibitors on Symptoms in Patients With SCAD) trial is ongoing, and should shed light on the utility of statins and angiotensin-converting enzyme inhibitors in SCAD patients.