Spontaneous coronary artery dissection classification

Spontaneous Coronary Artery Dissection Microchapters
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Type 1 Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Case 7 Type 2A Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Type 2B Case 1 Case 2 Case 3 Case 4 Type 3 Case 1 Case 2 Case 3 Case 4 Case 5 Case 6

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nate Michalak, B.A.

Synonyms and keywords: SCAD

Overview

Spontaneous coronary artery dissection can be classified based on angiographic appearance into type 1 (evident arterial wall stain with multiple radiolucent lumens), type 2 (diffuse smooth stenosis of varying severity), and type 3 lesions (focal or tubular stenosis mimicking atherosclerosis).

Classification

The National Heart, Lung, and Blood Institute (NHLBI) classification scheme for coronary dissection was devised in the pre-stent era for classifying the dissection following balloon angioplasty (i.e., iatrogenic dissection). In light of the distinctive angiographic features of spontaneous coronary artery dissection (SCAD), Saw et al. proposed a classification system to better characterize the lesions:

Type	Feature
Type 1	Pathognomonic multiple radiolucent lumen Contrast dye staining of arterial wall Presence or absence of dye hang-up or slow contrast clearing from the lumen
Type 2	Diffuse (typically >20–30 mm) Smooth narrowing varying in severity (ranging from 40 to 100% stenosis) No response to intracoronary nitroglycerin No atherosclerotic lesions in other coronary arteries Repeat coronary angiogram showing spontaneous resolution of the dissected segment or previous angiogram showing normal artery Intracoronary imaging with OCT or IVUS proving the presence of intramural hematoma and double-lumen
2A variant	Normal arterial caliber proximal and distal to dissection
2B variant	Dissection extends to the distal tip of the artery without discernible normal segment distally
Type 3	Mimics atherosclerosis with focal or tubular stenosis Lack of atherosclerotic changes in other coronary arteries Long lesions (11–20 mm) Hazy stenosis Linear stenosis Note: requires OCT or IVUS to prove the presence of intramural hematoma or double-lumen

Spontaneous Coronary Artery Dissection Type 1

Type 1 SCAD lesion is characterized by the pathognomonic appearance of contrast dye staining of arterial wall with multiple radiolucent lumens, with or without the presence of dye hang-up or slow contrast clearing from the lumen.

Projection angle: 14 RAO, 35 CRA. Type 1 SCAD is seen in OM2.

Spontaneous Coronary Artery Dissection Type 2

Type 2 SCAD lesion is characterized diffuse (typically >20–30 mm) and usually smooth narrowing that can vary in severity from an inconspicuous mild stenosis to complete occlusion, plus:

a. no response to intracoronary nitroglycerin and no atherosclerotic lesions in other coronary arteries

OR

b. repeat coronary angiogram showing angiographic resolution of the dissected segment or previous angiogram showing normal artery

OR

c. intracoronary imaging with optical coherence tomography or intravascular ultrasound proving the presence of intramural hematoma (IMH) and double-lumen

Type 2 SCAD lesion commonly involves the mid to distal segments of coronary arteries, and can be so extensive that it affects the distal tip. Accordingly, type 2 lesions can be further divided into two variants (type 2 variant A and variant B).

Type 2 Variant A

In type 2 variant A lesion, the coronary segments proximal and distal to dissection are normal.

Projection angle: 25 LAO, 20 CRA. Type 2A SCAD is seen in R3, R4.

Type 2 Variant B

In type 2 variant B lesion, the dissection extends to the apical tip of the artery without discernible normal segment distally.

Projection angle: 41 RAO, 19 CRA. Type 2B SCAD is seen starting in L2 resulting in a total occlusion.

Spontaneous Coronary Artery Dissection Type 3

Type 3 SCAD lesion is characterized by focal or tubular (typically <20 mm) stenosis that mimics atherosclerosis, which requires intracoronary imaging (e.g. optical coherence tomography or intravascular ultrasound) to prove the presence of intramural hematoma or double-lumen. Angiographic features that may be useful in differentiating type 3 SCAD lesion from atherosclerosis include:

a. lack of atherosclerotic changes in other coronary arteries

b. long lesions (11–20 mm)

c. hazy stenosis

d. linear stenosis

Projection angle: 1 LAO, 35 CRA. Type 3 SCAD is seen in D1.

Algorithm for Diagnosing Non-Atherosclerotic Spontaneous Coronary Artery Dissection

A stepwise algorithm for diagnosing non-atherosclerotic SCAD has been proposed by Saw et al. Clinicians should maintain a high index of suspicion for SCAD and consider early coronary angiography to ensure timely diagnosis and management. If the pathognomonic appearance of arterial wall stain with multiple radiolucent lumens is evident, then the diagnosis of type 1 SCAD can be established without additional intracoronary imaging. If type 1 SCAD appearance is not evident, angiographers should then assess for the presence of atherosclerotic changes in other coronary arteries, and consider intracoronary imaging if there is uncertainty as to non-atherosclerotic SCAD. For diffuse (>20 mm) and smooth stenosis of varying severity suggestive of type 2 SCAD, intracoronary nitroglycerin may be administered to rule out coronary spasm. If the stenosis remains unchanged after nitroglycerin administration, then optical coherence tomography (OCT) or intravascular ultrasound (IVUS) should be pursued. If there are concerns of compromising coronary flow with intracoronary imaging, then the stenosis could be reassessed in 4 to 6 weeks for hemodynamically stable patients, as SCAD typically resolves spontaneously.

Algorithm for the Angiographic Diagnosis and Confirmation of Spontaneous Coronary Artery Dissection

Presence of features that raise suspicion for SCAD? (click for details) ❑  Myocardial infarction in young women (age ≤50) ❑  Absence of traditional cardiovascular risk factors ❑  Little or no evidence of coronary atherosclerosis ❑  Peripartum state ❑  History of fibromuscular dysplasia ❑  History of connective tissue disorder or systemic inflammation     ❑  Marfan's syndrome     ❑  Type 4 Ehlers-Danlos syndrome     ❑  Loeys-Dietz syndrome     ❑  Cystic medial necrosis     ❑  Systemic lupus erythematosus     ❑  Crohn's disease     ❑  Ulcerative colitis     ❑  Polyarteritis nodosa     ❑  Sarcoidosis     ❑  Churg-Strauss syndrome     ❑  Wegener's granulomatosis     ❑  Rheumatoid arthritis     ❑  Giant cell arteritis

Perform early coronary angiography

Presence of type 1 SCAD lesion characteristics? (click for details) ❑  Contrast staining of arterial wall ❑  Multiple radiolucent lumens ❑  Contrast hang-up or slow clearing from the lumen

YES

NO

Type 1 SCAD most likely

Presence of type 2 SCAD lesion characteristics? (click for details) ❑  Diffuse lesion (typically >20–30 mm) ❑  Smooth luminal narrowing with varying severity ❑  Involvement of mid to distal segments

YES

NO

Stenosis relieved by intracoronary nitroglycerin?

Look for type 3 SCAD lesion characteristics (click for details) ❑  Focal or tubular stenosis (typically <20 mm) ❑  Mimics atherosclerosis ❑  Additional features     ❑  No atherosclerosis in other arteries     ❑  Long lesions (11–20 mm)     ❑  Hazy stenosis     ❑  Linear stenosis

YES

NO

Type 3 SCAD most likely ❑  Consider OCT or IVUS for definitive diagnosis ❑  Reassess with angiography in 4 to 6 weeks

R/O coronary spasm or other conditions

Type 2 SCAD most likely ❑  Consider OCT or IVUS for definitive diagnosis ❑  Reassess with angiography in 4 to 6 weeks