ISCHEMIC STROKE / ETIOLOGY

Assessment and classification of atherosclerotic plaques

David Goldemund M.D.
Updated on 18/11/2023, published on 18/04/2023

Atherosclerosis

  • atherosclerosis (AS) is a chronic, progressive systemic disease affecting the arterial wall that is a leading cause of death and disability in developed countries
    • the disease involves the accumulation of lipids, calcium, and other blood components within the arterial wall
    • these lesions, called plaques, can result in arterial stenosis and may be complicated (thrombosis, rupture, etc.)
    • plaques are predominantly found in specific segments of large and medium-sized arteries (carotid and coronary arteries, thoracic and abdominal aorta, arteries of the circle of Willis, etc.). Segments with arterial branches have the highest affinity for atherosclerotic changes
    • while the exact cause is unknown, numerous vascular risk factors contribute to the disease
  • plaques may either be asymptomatic or may cause cardiovascular events (such as coronary artery disease, stroke, peripheral artery disease, etc.) due to:
    • progressive narrowing to complete arterial occlusion (symptoms vary depending on the quality of the collateral circulation)
    • artery to artery embolisms
    • combination of both mechanisms (embolism occurring at the time of ICA occlusion)
Progression of atherosclerosis
  • atherosclerosis generally begins in young adulthood and progresses with age; the rate of progression is individual, but nearly everyone is affected to some degree by the age of 65
  • modern imaging techniques allow a qualitative assessment of atherosclerotic plaque beyond mere measurement of the stenosis grade
  • the first stage of atherosclerosis in the carotid arteries, detectable by sonography or MRI, is an increase in the intima-media thickness (IMT) (classified as a type 3 lesion according to AHA)   Carotid intima-media thickness (CIMT)

Atherosclerotic plaques classification

Basic classification of AS lesions

Endothelial dysfunction

  • microscopic changes

Fatty streaks

  • yellow streaks that do not extend into the lumen of the artery
  • formed by foam cells

Fibroatheroma

  • well-defined, stiff, pale grey or yellow deposits in the vessel wall (the color depends on the fat content)
  • fibroatheroma protrudes into the lumen and causes its narrowing
  • it may lack the lipid core and exhibit heavy calcifications

Complicated lesions

  • complex plaques with lipid core with either surface defect, hemorrhage, or thrombus
AHA clasification 1995
Type I 
  • an initial lesion characterized by foam cells
  • a manifestation of endothelial dysfunction caused by various factors (mechanical damage, chemical, degenerative, immune, metabolic, immunological, infectious, etc.)
  • only microscopic and chemically detectable intimal lipid deposits
Type II
  • fatty streaks with multiple foam cell layers
  • most lipids are stored intracellularly
  • streaks contain macrophages and foam cells, T-lymphocytes, and mast cells
Type III
  • preatheroma with extracellular lipid pools (a precursor of advanced lesions)
  • contains larger extracellular fat deposits that may deform the intima and, in the advanced stages, affect the media and adventitia
Type IV
  • atheroma with a confluent extracellular lipid core
Type V
  
Va
  • fibroatheroma, the dominant content is connective tissue still containing a lipid core
Vb
  • plaque with extensive calcifications (sometimes called type VII)
Vc
  • plaque with extensive fibrotic tissue without lipid core (also type VIII)
Type VI
  • complex plaques with either surface defect, hemorrhage, or thrombus
    • VIa – rupture
    • VIb – hematoma
    • VIc – thrombosis

(Stary, 1995)

Ultrasound classification of AS plaques
Ultrasound evaluation of atherosclerotic plaques
Atherosclerotic (AS) plaque is defined as a lesion ≥ 1.5 mm on cross-section; lesions < 1.5 mm are classified as enlarged intima-media thickness (IMT)
Echogenicity

  • hypoechogenic (lipid-rich)
  • isoechogenic (fibrous)
  • hyperechogenic (calcified)
 Hypoechoic, isoechoic and hyperechogenic plaque
Homogeneity

  • homogeneous
  • heterogeneous
 Plaque homogeneity
Surface

  • smooth
  • uneven
  • exulcerated (≥ 0,2mm)
 Exulcerated plaque at the ICA origin   Exulcerated plaque at the ICA origin
Gray-Weale classification of plaque echogenicity
Type I – hypoechogenic plaque
Type II – predominantly hypoechogenic plaque with hyperechogenic areas
Type III – predominantly hyperechogenic plaque with small hypoechogenic foci
Type IV – homogeneous hyperechogenic plaques
CTA assessment of AS plaques
  • each plaque can be characterized by:
    • size (length and width)
    • shape (circular, semicircular, eccentric)
    • surface (smooth, rough, exulcerated)
    • density (hypodense, isodense, hyperdense)
    • homogeneity (homogeneous x heterogeneous)
    • presence of calcifications and intraluminal thrombi (ILT)
  • the presence of ILT or ulcers increases the likelihood of symptomatic stenosis
  • smooth or heavily calcified plaques are associated with a relatively low risk of cardiovascular events [Eesa, 2010]
  • in the case of extensive calcifications, CTA (with an adjusted window) outperforms ultrasound, which must rely on Doppler examination (B-mode and color mode are usually inconclusive due to acoustic shadows) A significant left ICA stenosis, caused by heterogeneous plaque with significant calcifications, that limit the ultrasound evaluation Hemodynamically significant stenosis (Doppler examination)
Smooth, irregular and exulcerated plaque on CTA
Homogenous and heterogenous plaque
Hypodense, isodense and hyperdense plaque on CTA

→ Carotid stenosis evaluation on CTA

MR classification of AS plaques
AHA classification MRI classification
Type I: initial lesion with foam cells (endothelial dysfunction) Type I-II: near-normal wall thickness, no calcification
Type II: fatty streak
Type III: preatheroma with extracellular lipid pools  Type III: diffuse intimal thickening or small eccentric plaque with a small lipid core, no calcification
Type IV: atheroma with a confluent extracellular lipid core Type IV-Va:  plaque with lipid or necrotic core surrounded by fibrous tissue with calcium
Type Va: fibroatheroma
Type Vb: plaque with lipid core or fibrotic tissue, large calcifications (also type VII)
 Type Vb: plaque with a lipid core or fibrous tissue, large calcifications
Type Vc: plaque with large fibrotic tissue, no lipid core (also type VIII)
 Type Vc: plaque with fibrous tissue, no lipid core
Type VI: complex plaque (with hemorrhage and/or thrombus)
  Type VI: complex plaque with hemorrhage or thrombus

(Koops, 2006)

MRI findings of the plaque components
TOF T1 T2 T1-enhanced
Fibrous tissue iso/hypo iso hyper +
Lipid-rich iso iso/hyper hypo –
Calcification hypo hypo hypo –
Hemorrhage hyper hyper variable –
Intraplaque hemorrhage (IPH) on T1W
Stable x unstable plaque

Stable plaque

  • low lipid content
  • minima tendency to rupture or thrombosis (usually Vb and Vc lesions according to AHA classification)

Unstable (high-risk) plaque

  • mostly type Va and VI lesions (according to AHA classification)
  • associated with a high risk of CV events

 

  • exulcerated plaque [Kuk, 2014][Kanber, 2013]
  • plaque with high lipid content
  • plaque with necrotic core and fibrous cap
  • plaque with a mobile component   AS plaque with a mobile component on the ultrasound
  • plaque with intraplaque hemorrhage (IPH) Intraplaque hemorrhage on T1
  • plaque with ↑angiogenesis    [Vicenzini, 2012]   [Saito, 2014]   [Hiyama, 2010]
    • dynamic contrast-enhanced MRI   Contrast-enhanced MRI showing intraplaque angiogenesis
    • contrast-enhanced carotid ultrasound  Neovascularization of atherosclerotic plaque on ultrasound after contrast agent administration (Vicenzini, 2012)

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Assessment and classification of atherosclerotic plaques
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