ISCHEMIC STROKE / ETIOLOGY

Assessment and classification of atherosclerotic plaques

Created 18/04/2023, last revision 02/05/2023

Atherosclerosis

  • atherosclerosis (AS) is a chronic, progressive systemic disease affecting the arterial wall and a leading cause of death and disability in the developed world
    • it involves the accumulation of lipids, calcium, and other blood components in the arterial wall
    • these lesions (plaques) can lead to arterial stenosis and may be complicated by thrombosis, rupture, etc.
    • plaques occur at 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 branches have the highest affinity for atherosclerotic changes
    • the exact cause is unknown, numerous vascular risk factors are involved
  • plaques may be asymptomatic or may cause cardiovascular events (coronary artery disease, stroke, peripheral artery disease, etc.)
Progression of atherosclerosis
  • atherosclerosis generally begins in young adulthood and progresses with age; the rate of progression is individual, but almost all people are affected to some degree by the age of 65
  • modern imaging techniques allow a qualitative assessment of atherosclerotic plaque beyond simple measurement of the stenosis grade
  • the first subclinical stage of atherosclerosis in the carotid arteries, detectable by sonography or MRI, is an increase in the intima-media thickness (IMT) (type 3 lesion according to AHA)

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 (color depends on the fat content)
  • fibroatheroma protrudes into the lumen and causes its narrowing
  • it may lack the lipid core and be heavily calcified

Complicated lesions

  • complex plaques with lipid core with either surface defect, hemorrhage, or thrombus
AHA clasification 1995
Type I 
  • an initial lesion with foam cells
  • a manifestation of endothelial dysfunction caused by a variety of 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)
  • contain larger extracellular fat deposits that can deform the intima and, in the highest stages, 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 large calcifications (also type VII)
Vc
  • plaque with large fibrotic tissue, no 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
AS plaque is defined as a lesion ≥ 1.5 mm on cross-section; lesions < 1.5 mm  are classified as increased 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)
  • presence of intraluminal thrombi (ILT) or ulcers increases the likelihood of symptomatic stenosis
  • smooth or heavily calcified plaques are associated with a low risk of CV event [Eesa, 2010]
  • in the presence of extensive calcifications, CTA outperforms the ultrasound, which must rely on the 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 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
  • plaques with intraplaque hemorrhage (IPH) Intraplaque hemorrhage on T1
  • plaques 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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