Spontaneous coronary artery dissection classification

Spontaneous Coronary Artery Dissection Microchapters
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Overview
Historical Perspective
Classification
Pathophysiology
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Differentiating Spontaneous coronary artery dissection from other Diseases
Epidemiology and Demographics
Risk Factors
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Natural History, Complications and Prognosis
Diagnosis
Diagnostic Approach
History and Symptoms
Physical Examination
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Electrocardiogram
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Treatment
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Medical Therapy
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Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
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		Example
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	The unnamed parameter 2= is no longer supported. Please see the documentation for {{columns-list}}. 2
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	The unnamed parameter 2= is no longer supported. Please see the documentation for {{columns-list}}. 2
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	The unnamed parameter 2= is no longer supported. Please see the documentation for {{columns-list}}. 2

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.