Non-astherosclerotic spontaneous coronary artery dissection (NA-SCAD)

1. NON-ATHEROSCLEROTIC SPONTANEOUS
CORONARY ARTERY DISSECTION
(NA-SCAD)
A VERY RARE CAUSE OF A VERY COMMON PRESENTATION
Kerolus Shehata, MD

2. WHAT IS NA-SCAD?
WHY IT IS SO INTERESTING TO PRESENT IT?
• Non-traumatic and non-iatrogenic separation of the coronary arterial wall creating a false
lumen.
• Rare cause of ACS representing 1:4 cases in every 1000 ACS
• Often under- or Misdiagnosed (Need advanced intra-vascular imaging for confirmation)
• Major cause of Morbidity and Mortality including Ventricular arrhythmias and SCD
• Different management than Atherosclerotic ACS

3. PATHOPHYSIOLOGY
• Intimal tear or bleeding of vasa vasorum  Intramedial
hemorrhage  false lumen filled with IMH  Pressure-
driven expansion of the false lumen  luminal
encroachment and subsequent myocardial ischemia and
infarction.
• N.B: Atherosclerotic SCAD is typically limited in extent by
medial atrophy and scarring.

4. SCAD PRESENTATION
• Interestingly, in a Japanese series, the mean
peak of CK-MB was lower in young women
with NA-SCAD versus Atherosclerotic SCAD
patients (1,689 IU/l vs. 2,874 IU/l; p = 0.025)
suggesting that the myocardium in jeopardy
with SCAD may be smaller than that with
atherosclerotic disease.
• LVEF during SCAD presentation was relatively
preserved, ranging from 51% to 56% with a
tendency to improve after the acute
presentation.

5. ASSOCIATIONS & CONTRIBUTORS
• Fibromuscular dysplasia (FMD)
• Pregnancy: history of multiple pregnancy, peri-partum
• Connective tissue disorder: Marfan’s syndrome, Ehler
Danlos syndrome, cystic medial necrosis, FMD
• Systemic inflammation: SLE, Crohn’s disease, PAN,
sarcoidosis
• Hormonal therapy
• Coronary artery spasm
• Ateriopathies
• Intense exercise (aerobic or isometric)
• Intense emotional stress
• Labor & delivery
• Intense Valsalva-type activities (e.g., severe
repetitive coughing, retching/vomiting, bowel
movement)
• Toxins: Cocaine, amphetamines, met-
amphetamines.

6. WHEN TO SUSPECT SCAD IN ACS?
• ACS in young women (especially age ≤50)
• Absence of traditional cardiovascular risk factors
• Angiographic Little or no evidence of typical atherosclerotic lesions in coronary arteries
• Peripartum state
• History of fibromuscular dysplasia
• History of relevant connective tissue disorder: Marfan’s syndrome, Ehler-Danlos syndrome, cystic
medial necrosis, fibromuscular dysplasia
• History of relevant systemic inflammation: SLE, Crohn’s disease, ulcerative colitis, PAN,
sarcoidosis
• Precipitating stress events, either emotional or physical (intensive exercise)

7. ANGIOGRAPHIC TYPES OF SCAD
• Type 1 has the classic appearance of
contrast dye staining of arterial wall
with multiple radiolucent lumen.
• Type 2 shows long diffuse (typically
>20-30 mm) and smooth narrowing
that varies in severity.
• Type 3 has focal or tubular stenosis
that mimics atherosclerosis, typically
requiring intracoronary imaging to
prove presence of intramural
hematoma or double lumen.

8. Spontaneous
dissection of the LCX
and beaded
appearance of the Rt
external iliac artery
suggesting FMD.
41 YO F who presented with NSTEMI

9. • (A) Long lesion in LAD
suggestive of SCAD. The
proximal aspect of the diseased
segment shows an intimomedial
membrane and a double lumen
appearance by OCT (B) and
IVUS (B’).
• Thrombus in the false lumen is
more clearly depicted by IVUS.
• (C) More distally, OCT detects a
severely narrowed lumen and a
side branch exit from the true
lumen (4 o’clock position).

10. MANAGEMENT OF SCAD
• ASA: Recommended acutely and long term
• P2Y12 antagonists and GPIIb/IIIa inhibitors: Not
recommended unless stent(s) was deployed
• AC: Contraindicated (IMH expansion)
• Thrombolytics: Contraindicated, however should
NOT be withheld for STEMI patients because the
overall frequency of thrombotic occlusion is much
higher than SCAD.
• Beta Blockers: Recommended acutely and long
term.
• Statins: Not recommended unless there is
concomitant dyslipidemia

11. REVASCULARIZATION IN SCAD
• Conservative treatment is preferred for most stable patients without ongoing
CP.
• Indications: patients with ongoing CP, uptrending troponins, ST elevation, or
HD instability.
• OCT or IVUS are always recommended to ensure adequate stent coverage
and wall apposition.
• If the lesion is relatively focal, recommend longer stents that would provide
adequate coverage for both edges of the lesion (at least 5-10 mm longer
proximally and distally) to accommodate extension of the IMH proximally and
distally when compressed by the stent.
• For longer lesions, a multistep approach of stenting the distal edge, followed
by the proximal edge, and then stenting the middle of the dissection, may be
useful in preventing IMH propagation.
• The use of bioresorbable stents has theoretical benefits of avoiding late stent
mal-apposition following IMH resorption.
Challenges in SCAD Revascularization:
• PCI is not feasible if the dissected artery segment is distal,
of small caliber, or with extensive dissection
• Accurate advancement of the guidewire to the TRUE
lumen.
• Stent deployment can cause IMH extension antegradely or
retrogradely with further impedance of arterial blood flow
and extending the dissection.
• IST: in very small distal lesions or very long lesions.
• Very lately, IMH resorb may result in late strut
malapposition, increasing the risk of stent thrombosis
especially after cessation of DAPT.

12. REVASCULARIZATION IN SCAD, CONTINUED
Indications for CABG in SCAD
• >2 proximal vessels SCAD
• Ostial LAD SCAD
• SCAD length >100 mm
• Proximal Lt main dissection
Role of follow up Angiogram:
Significant proportion of patients have recurrent chest pains after their initial event, it may be
useful to repeat coronary angiography several weeks later to investigate potential ischemic
causes of pain, and to assess arterial healing.

13. PROGNOSIS OF SCAD
• Early mortality is low regardless of initial treatment modality
• PCI is associated with high rates of complication and procedural failure
• Risk of recurrent SCAD is higher in women (Up to 20%)
• Prognosis is generally better than atherosclerotic SCAD
*** More Research need to be done to fill all the persistent knowledge gaps regarding the triggers,
associations, management and outcome of SCAD.

14. REFERENCES
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10.3978/j.issn.2223-3652.2015.01.08
• Nishiguchi T., et al Prevalence of spontaneous coronary artery dissection in patients with acute coronary syndrome.
Eur Heart J Acute Cardiovasc Care. doi: 10.1177/2048872613504310.
• Tweet MS, Hayes SN, Pitta SR, Simari RD, Lerman A, Lennon RJ, Gersh BJ, Khambatta S, Best PJ, Rihal CS, Gulati R.
Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation. 2012;126:579–
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• Alfonso F, Paulo M, Lennie V, Dutary J, Bernardo E, Jiménez-Quevedo P, Gonzalo N, Escaned J, Bañuelos C, Pérez-
Vizcayno MJ, Hernández R, Macaya C. Spontaneous coronary artery dissection: long-term follow-up of a large series
of patients prospectively managed with a “conservative” therapeutic strategy. JACC Cardiovasc Interv. 2012;5:1062–
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• Buja P, Coccato M, Fraccaro C, Tarantini G, Isabella G, Almamary A, Dariol G, Panfili M, Iliceto S, Napodano M.
Management and outcome of spontaneous coronary artery dissection: conservative therapy versus
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