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304
Chapter 5 · Extracranial Cerebral Arteries
. Table 5.7 Extracranial cerebral arteries– duplex ultrasound ndings and therapeutic consequences
Diagnosis Ultrasound ndings, clinical presenta-
tion, and stenosis degree by ECST criteria
(with equivalent NASCET degrees in
brackets; see . Tables 5.8 and 5.9)
Plaques No hemodynamic stenosis, asymptomatic
or symptomatic
ICA stenosis Hemodynamically signicant stenosis
<70% (<50% NASCET), asymptomatic
5
ICA occlusion Stage IV Usually no operation, emergency operation may be contem-
Subclavian artery
stenosis/occlusion
ECA stenosis High-grade External carotid angioplasty indicated only in multiple-vessel
Carotid artery
dissection
Kinking or coiling Asymptomatic, no stenosis Medical management
Inammatory vessel
disease (Takayasu’s
arteritis, temporal
arteritis)
Carotid body tumor Well-perfused tumor in the carotid
Vertebral artery
stenosis
Stenosis >70% (>50% NASCET),
asymptomatic
Evaluation of plaque (vulnerable?) using
B-mode, CEUS
50–70% stenosis (30–50% NASCET),
symptomatic
B-mode: plaque morphology
> 70% stenosis (>50% NASCET),
symptomatic
> 70% stenosis (>50% NASCET), stage IV Surgery only after nearly complete resolution of symptoms
Steal syndrome, symptomatic PTA, extrathoracic bypass procedure or transposition
Mostly due to trauma, asymptomatic,
patent or thrombosed false lumen
Symptomatic if associated with stenosis Resection
Wall thickening (macaroni sign) with or
without hemodynamically signicant
stenosis
bifurcation (color duplex)
High-grade stenosis, asymptomatic Medical management
High-grade stenosis, symptomatic Chiey located at origin, surgical reconstruction or PTA
Therapy
Medical management
Medical management
Surgical reconstruction (CEA) acceptable but only proven if
perioperative risk is low (according to ACAS study):
Weighing of best medical treatment ←→CEA, CAS:
– If perioperative morbidity/mortality rate<3%
– Annual stroke rate of 2% in medical care group versus 1% in
surgical group
– Surgery only if life expectancy >5years
Surgical reconstruction (CEA):
– Acceptable; however, not proven in patients with
TIA<6months and plaque morphology suggesting high risk of
embolism (ulceration, hypoechogenicity, irregular surface)
Proven indication for surgery (CEA):
Risk reduction relative to natural history increases as the
perioperative morbidity and mortality rate decreases (target: < 5%)
approx. 2–6weeks after acute event
Prophylactic surgery of asymptomatic side may be indicated if
there is stenosis on this side as well
plated only immediately after the event (mortality of up to 9%);
otherwise medical management; repair may be indicated in
patients with multiple-vessel disease
disease (occlusion of ICA) with borderzone ischemias and proven
extracranial and intracranial collateralization
Medical management, anticoagulation (intimal ap becomes
attached or false lumen undergoes obliteration or thrombosis in
most cases). Fixation or resection of intimal aps only in
exceptional cases with pronounced neurologic decits and
oating aps
Cortisone therapy, no surgical reconstruction
Complete tumor resection; embolization only in patients with a
high risk of morbidity
ACAS Asymptomatic Carotid Atherosclerosis Study, CAS carotid artery stenting, CCA common carotid artery, CEA carotid endarterectomy,
CEUS contrast-enhanced ultrasound, ECA external carotid artery, ECST European Carotid Surgery Trial, ICA internal carotid artery, NASCET
North American Symptomatic Carotid Endarterectomy Trial, PTA percutaneous transluminal angioplasty, TIA transient ischemic attack
5.5 · Clinical Role ofDuplex Ultrasound
305
5
Over the last decades, carotid endarterectomy (CEA) has
evolved into a suitable method for treating high-grade ICA
stenosis– the major underlying cause of cerebral infarction.
e main drawback of CEA, and of carotid artery stenting
(CAS), is that it may cause what it is supposed to prevent,
namely TIA or stroke. is is why the surgical risk must be
weighed against the risk of untreated stenosis. Numerous
prospective randomized multicenter studies compared the
natural history and the surgical risk for symptomatic and
asymptomatic carotid stenoses of dierent degrees (see
. Table5.1). Endarterectomy in symptomatic carotid steno-
sis aims at eliminating the vascular source of emboli and/or
residual ow obstruction in individuals with a history of
cerebral infarction.
e European Carotid Surgery Trial (ECST) and the
North American Symptomatic Carotid Endarterectomy
Trial
(NASCET) compared antiplatelet therapy versus endarterectomy in patients with symptomatic carotid artery stenosis. Re-analysis of the pooled data suggests that CEA
statistically highly signicantly reduces the risk of ipsilateral
stroke by 16% aer 5years in individuals with 70–99% stenoses (by ECST criteria, which is equivalent to >50% stenosis by
NASCET criteria). In other words, six operations have to be
performed to prevent one ipsilateral stroke over a 5-year
period (number needed to treat (NNT)). In individuals with
50–69% stenosis, absolute risk reduction (ARR) drops to
4.6%. CEA has no advantage in individuals with stenoses
<50% and is harmful in those with <30% stenosis compared
to the natural history of the disease. e rate of severe perioperative complications (stroke, death) was found to be 6.2%
for patients with stenosis greater than 70% versus 8.4% for
those with 50–69% stenosis (
e wider use of validated noninvasive diagnostic modalities such as Doppler and duplex ultrasound and the known
relationship between coronary heart disease and carotid
stenosis and their associated risk of stroke make it more
and more important to establish reliable criteria for identifying patients with subclinical carotid artery stenosis who
would benet from prophylactic surgery. However, in this
population with a lower risk of spontaneous stroke (annual
rate of less than 1% in stenosis <70% versus approx. 2.5%
in those with >70% stenoses, depending on other ndings
and comorbidity), it is more dicult to demonstrate a statistical benet of therapeutic measures. While other studies
revealed no benet of operative treatment in this population,
Asymptomatic Carotid Atherosclerosis Study (ACAS)
the
demonstrated an advantage for the patients operated on for
carotid stenoses of 60–99% compared to patients undergoing
medical treatment (ACAS 1995). e 5-year stroke risk was
5.1% in the surgical group versus 11% in the medical care
group. e perioperative risk of stroke and death was 2.3%
including the rate of 1.2% of preoperative angiography. e
American Heart Association (AHA) recommends surgery
for asymptomatic carotid artery stenosis >60% if the center
performing the intervention has a perioperative risk of less
than 3%.
. Table5.6).
In clinical practice, patient management is primarily
based on the sonographic degree of stenosis (which determines the risk of embolism) and the patient’s clinical stage
. Table5.7).
(
Apart from the degree of stenosis (. Fig.5.11), plaque mor-
phology
plaques with superimposed thrombi, intraplaque hemorrhage,
and atheromatous plaques are associated with a higher risk of
stroke compared to smooth, brous plaques. However, no
imaging modality exists that enables a satisfactory estimate of
the risk of embolism on the basis of plaque morphology.
may be useful in estimating the risk of embolism. Some studies suggest that hypoechoic plaques have a two to ve times
greater tendency to embolize than hyperechoic ones.
stenosis account for 55–60% of all strokes (territorial infarction; . Fig. 5.9a). Another 30–35% are due to cardiogenic
embolism, and less than 5% are due to hemodynamically
reduced perfusion, especially in multiple-vessel disease (borderzone infarction). Other rare causes accounting for less
than 5% of cases are inammatory vessel disease, microangiopathy, and dissection.
5.5.1.1 Stenosis Grading
Despite the clinical relevance of internal carotid artery (ICA)
stenosis, there is no agreement about how it should be quantied, and various methods have been proposed. e di-
culty in grading ICA stenosis
greater width of the carotid bulb, the preferred site of ICA
stenosis. Patients with thick plaques in this slightly dilated
portion of the carotid artery may have a considerable risk of
embolism, while the degree of narrowing has little or no
hemodynamic eect (. Fig.5.10).
ICA stenosis:
e
patent residual lumen to the local vessel lumen without the
plaque and gives the best estimate of plaque thickness (which
is relevant for the ensuing risk of embolism) and the true
extent of vascular obstruction. However, angiography enables
only a rough and indirect estimate of the local degree of a
stenosis because, unlike duplex ultrasound, it does not depict
the original vessel diameter.
diameter of the residual lumen of the stenosed segment and
that of the distal ICA (which is fairly constant up to the base
of the skull). is method allows accurate assessment of the
reduction in blood supply to the brain caused by a stenosis
and classies mild to moderate stenosis of the carotid bulb as
hemodynamically nonsignicant (. Figs.5.9b and 5.10).
is another major determinant of stroke risk. Ulcerated
Yet, in certain cases, the sonomorphologic appearance
Arterial emboli from atherosclerotic plaques in carotid
is chiey attributable to the
Basically, two methods exist for grading and reporting
5 e ECST (European Carotid Surgery Trial) method:
local degree of stenosis
5 e NASCET (North American Symptomatic Carotid
Endarterectomy Trial) method: distal degree of stenosis
local degree of stenosis is dened as the ratio of the
e distal degree of stenosis is calculated from the
306
Distal degree of stenosis
T)
a
Chapter 5 · Extracranial Cerebral Arteries
2
D
(degree relative to distal
vessel diameter)
R
= (1– ) x 100% (NASCE
D
L
1
3
R
5
b
. Fig. 5.9 a Types of cerebral infarction. 1 Territorial infarction: caused by arterioarterial embolism (carotid, cardiac). 2 Borderzone infarction:
hemodynamic origin, reduced perfusion in terminal vascular bed, chiey in patients with multiple-vessel disease. 3 Lacunar infarction: microangiopathy. b Methods of stenosis grading (local versus distal degree of stenosis). Due to the larger vessel diameter in the bulb, a stenosis classied as
mild to moderate using the local grading method may not be classied as a stenosis when the distal grading method is used. Since the stenosisrelated decrease in perfusion only has a minor role in the development of cerebral ischemia, whereas plaque thickness is crucial for the associated
risk of embolism, the local degree of stenosis is clinically more relevant. For instance, eccentric plaques causing only moderate stenosis of the
bulb may already carry a considerable risk of embolism based on their thickness
Local degree of stenosis
R
= (1–
) x 100% (ECST)
L
Degree of stenosis
ECST > NASCET
. Fig. 5.10 Color duplex ultrasound (longitudinal image on the left and transverse image on the right) demonstrating hypoechoic eccentric
plaque of the carotid bulb. Calculation using the local grading method yields a 65% diameter reduction (60–70% stenosis). According to the distal
stenosis grading method (NASCET) (diameter of the distal ICA in the longitudinal image: almost 5mm), this is a 20–30% stenosis and surgery
is not indicated. Conversely, the local degree of stenosis (ECST) establishes an indication for surgery, especially when additionally considering
plaque morphology (hypoechoic) and conguration (very eccentric and thickness>5mm: high shear stress). The nal decision for surgery also
depends on the patient’s age and concomitant diseases. The example illustrates how the method used for stenosis grading (local versus distal)
might lead to dierent therapeutic consequences (see . Fig.5.15)
e confusion about carotid artery stenosis grading,
both in scientic publications and in routine clinical practice, is mainly attributable to the fact that the distal grading
method is primarily used in the USA, while determination
of the local degree, which is also favored in Germany, is
more common in Europe. Hence the NASCET used the former and the ECST the latter. To overcome this confusion, a
consensus conference in 2010 issued the recommendation
that the distal degree of ICA stenosis (NASCET criteria)
should be used in reports. In other words, authors using the
local degree of stenosis, which is a better predictor of the risk
of embolism, should explicitly say so. Before this consensus
was reached, the local grading method was favored by the
German Society of Ultrasound in Medicine (Deutsche
Gesellscha für Ultraschall in der Medizin, DEGUM) (Widder etal. 1986).
5-year stroke risk (%)
30
25
20
15
10
0>
Local stenosis degree (%)
5.5 · Clinical Role ofDuplex Ultrasound
5
0
. Fig. 5.11 Risk of ipsilateral cerebral infarction by degree of internal
carotid artery (ICA) stenosis in symptomatic and asymptomatic individuals (According to Widder 2004)
and that of the distant internal carotid is fairly constant, the
degrees of ICA stenosis by NASCET and ECST criteria can
be easily converted into each other using the following
equations:
5 Local (ECST) degree of stenosis (%)=0.6×distal
5 Distal (NASCET) degree of stenosis (%)=local (ECST)
e resulting correspondences between the distal and local
degrees of ICA stenosis are presented in
carotid bulb is classied as a nonstenotic lesion using the distal quantication method because stenosis with a local degree
of up to 30% reduces the bulbous lumen only to the diameter
of the distal carotid artery (. Fig.5.11). Note, however, that
hemodynamic alterations are less relevant for the risk of cerebral infarction than the risk of embolism, which increases
with plaque thickness
bulb may already pose a considerable risk of embolism before
it causes hemodynamic eects.
artery assessment, has methodological limitations as it grades
a stenosis on the basis of purely morphologic criteria. It is an
invasive procedure that involves radiation exposure and
contrast-medium-related side eects as well as the risk of
minor stroke in 1.3–4.5% of cases and major stroke in 0.6–
1.3% (Davies and Humphrey 1993; Dion etal. 1987; Hankey
307
. Table 5.8 Correspondences between distal (NASCET) and local (ECST) degrees of internal carotid artery (ICA) stenosis
Grading method Degree of stenosis Study
Distal (%) 0 50 60 67 70 75 85 90 NASCET
Local (%) 40 70 75 80 82 85 90 95 ECST
etal. 1990; Moore 2003). e risk of angiography is higher in
symptomatic stenoses than in asymptomatic ones, and the
risk of inducing stroke may be as high as 12.5% in patients
with bilateral high-grade carotid stenosis (eodotou etal.
1987). e ACAS provides the most detailed analysis.
According to this study, angiography performed at radiologic
centers is associated with a combined neurologic morbidity
and mortality of 1.2% in asymptomatic patients, which is
only slightly lower than the 1.52% risk associated with carotid
asymptomatic
symptomatic
<7070809
90
endarterectomy (CEA) in the same patient population. In
light of these ndings, it was recommended to perform CEA
without prior diagnostic angiography (Chervu et al. 1994)
(
. Fig.5.12). is is made possible in part by the use of high-
resolution ultrasound, which has been shown in comparative
studies with histologic workup to be superior to angiography
in assessing plaque morphology and the ensuing risk of
embolism (Ten Kate etal. 2010; Honda etal. 2004).
5.5.1.2 Plaque Morphology
As the relation between the diameter of the carotid bulb
Ultrasound measurement of carotid intima-media thickness
(IMT) has become an established technique for estimating the
risk of cardiovascular morbidity and mortality. IMT is used
as a surrogate marker for pre- or subclinical atherosclerosis
and for monitoring the outcome of treatment (e.g., statins) in
interventional studies.
(NASCET) degree (%)+40%
Risk factors such as long-standing hypertension or hyper-
lipoproteinemia damage the intima, rst becoming manifest
degree of stenosis (%)– 40%/0.6
as thickening of the intima-media complex. ickening
above 1mm is considered abnormal and a thickness of 2mm
or more is dened as plaque (Li etal. 1996).
. Table5.8.
Plaque causing luminal narrowing of up to 40% in the
However, thickening of the intima–media complex is also
an age-related phenomenon. While IMT is below 0.6mm in
young healthy individuals (Rubbia etal. 1994), an average
increase of 0.1mm per decade of life is regarded as normal
aer the age of 40 (Homma etal. 2000). Serious arterial wall
changes
exceeds 1.5mm
should be expected when the increase in thickness
. Individuals with an IMT>1.5mm or small
focal plaques oen have aortic plaques, which have been
. erefore, eccentric plaque in the
implicated as a cause of embolic cerebral infarction. Measurement of IMT therefore provides a general estimate of the
total atherosclerotic burden, and patients with marked thick-
Angiography, the traditional gold standard for carotid
ening of the intima-media complex have an increased
embolic risk arising from atherosclerotic plaques in the aortic arch.
Intimal lipid accumulation is a crucial mechanism in
plaque development. Macrophages inltrate the atheroscle-
rotic lesions and phagocytose cholesterol, giving rise to foam
cells. Following recruitment of muscle cells and broblasts, a
5
308
Chapter 5 · Extracranial Cerebral Arteries
Patient contact
High-risk patient
No history of
cerebral disease
Pulses/auscultation
Doppler as needed
5
Normal Abnormal
CW Doppler/
duplex ultrasound
Normal Abnormal
<80% stenosis
No further
examination
. Fig. 5.12 Diagnostic algorithm in patients with suspected internal carotid artery (ICA) stenosis. Degrees of stenosis in the algorithm are ECST
degrees (with 70% stenosis by ECST criteria being equivalent to 50% stenosis by NASCET criteria). If >70% ECST stenosis (>50% NASCET) has
beendiagnosed by duplex ultrasound, the patient can proceed to surgery without further preoperative imaging of the carotid arteries. In patients
with 60–70% ECST stenosis (40–50% NASCET), plaque morphology on B-mode imaging is considered as an additional criterion in identifying
thosefor whom carotid endarterectomy (CEA) is recommended (see . Figs.5.9b and 5.10 and . Table5.9)
Follow-up
cardiac source of embolism
>80% stenosis
(plaque morphology?)
Normal
<60% stenosis
Echocardiography
TIA
(Color) duplex ultrasound
>70% stenosis
if 60-70% stenosis:
plus plaque
morphology
CEA & CAS
Preop cranial
MRI
Occlusion
Contralateral
ICA
(stenosis->CEA)
Stroke
CT/MRI
Ischemia
Hemorrhage
Treatment
collagen matrix is formed, and advanced lesions may develop
a brous cap. Inammatory processes appear to play an
important role in the further development and also in rendering a plaque vulnerable. Mechanisms such as intimal stress
and damage in conjunction with slow ow but high wall pressure contribute to plaque development opposite a ow divider
in vessel bifurcations (
7 Sect. 1.2.1 and . Fig. 1.44).
Once a plaque has reached a certain thickness, it disturbs
the nutrition of the intima, which is not supplied by vessels of
its own but through diusion from the vessel lumen. e initial plaque continues to grow through the accumulation of
lipids, lipoproteins, and cholesterol. e interruption of the
nutrient supply can lead to central necrosis (. Fig.5.13) with
formation of an atheroma, which may become organized
through broblast invasion and thus develop into a stable
lesion. Alternatively, there may be rupture of the covering
intimal layer with discharge of degenerative atheromatous
debris into the bloodstream and embolization to the brain.
Neovascularization and inammatory processes appear to
contribute to plaque vulnerability (. Fig.5.14). As a result of
lipid inclusion and central necrosis, a plaque can increase in
size to such an extent that it represents a considerable obstacle to pulsatile blood ow. Sonographically, such a plaque is
identied by pulsatile longitudinal movement with the
blood ow
. Fibroblast invasion leads to sclerosis, ultimately
resulting in calcication of the plaque.
A rapid increase in plaque size may also be due to internal hemorrhage, which is attributed to very minute, vulnerable vessels growing in from the adventitia. Exposure to
owing blood can lead to rupture of the thin plaque cap
(intima) with embolization to the brain of necrotic or thrombotic plaque components (
. Fig.5.13). Plaque rupture trig-
gers repair processes with re-endothelization of the former
plaque area, resulting in a rather smoothly covered niche that
poses no risk of embolization. Unfortunately, this fairly
harmless state may be dicult to dierentiate from ulceration by angiography and ultrasound alike.
Less harmless sequelae are ulcerative defects with incomplete re-endothelialization that may still release thrombotic
material into the bloodstream.
e turbulent ow occurring in stenotic segments can
induce the deposition of thrombotic material, especially at
the distal end of a plaque, with ultimate progression to occlusion of the ICA.
e risk of embolism is determined not only by the degree
of stenosis but also by plaque morphology as such. e following types of plaques can be distinguished in the carotid
system on the basis of their macroscopic appearance:
a bcdef
5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
309
. Fig. 5.13a–f Stages of plaque development. a Initial atherosclerotic wall thickening (intima-media complex thickening). b Further increase
in wall thickness. c Plaque increases in size through lipid accumulation and may undergo central necrosis (atheroma); disturbed nutrition of the
plaque. d Intramural hemorrhage through rupture of ingrowing vessels. e Rupture of the plaque cap induced by pulsatile blood ow (longitudinal
pulsation) with ulceration mainly of proximal portions. f Re-endothelialization of the ulcer with formation of a washed-out niche as a fairly stable
residue (bottom); re-endothelialization of the vulnerable plaque (middle); or persisting ulcerative plaque with recurrent embolism and only partial
repair of the vulnerable surface (top)
5
5 Flat, brous plaque
5 Atheromatous or so plaque
5 Calcied or hard plaque
5 Ulcerative plaque
5 Hemorrhagic plaque
In a large series of 1252 consecutive patients, Park et al.
(1998) correlated plaque morphology in carotid endarterectomy specimens with clinical symptoms. e incidence of
plaque ulceration was 77% in patients with transient ischemic attacks (TIAs) and 79% in those with prior stroke,
which was signicantly higher than in asymptomatic patients
(60%). e incidence of intraplaque hemorrhage did not differ signicantly between symptomatic and asymptomatic
patients but was signicantly higher in patients with greater
than 90% carotid stenosis.
For estimation of the risk of embolism, it would be desirable to have an imaging modality (like ultrasound or contrastenhanced ultrasound (CEUS)) that provides reliable
information on plaque morphology. is is dicult, however, since most atherosclerotic lesions are chiey composed
of variable amounts of atheromatous material with high lipid
content and brous material rich in collagen. e inhomogeneous composition of plaques is reected in their ultrasound
appearance, but it is not possible to identify individual plaque
components on the basis of their echogenicity and to exploit
this information for predicting the risk of embolism. Specically, ulcerated plaques are dicult to dierentiate from
washed-out cavities that have become re-endothelialized.
origin of the vertebral artery rarely requires surgical or interventional treatment, in particular because the risk of embolism is lower. In patients with multiple-vessel disease and a
global reduction in cerebral perfusion, repair is mainly done
in the carotid territory.
While lesions in the carotid system present with highly
specic hemispheric symptoms, the clinical manifestation is
much less specic when the vertebrobasilar system is
involved. Dizziness is the chief symptom, but may also be
caused by numerous nonvascular conditions. Apart from
atherosclerotic lesions, acute symptoms of vertebrobasilar
insuciency may be due to dissection, typically occurring
aer trauma.
In patients with subclavian artery occlusion, the vertebral
artery is scanned to evaluate its collateral function in subclavian steal syndrome (complete vs. incomplete).
Ultrasound is the method of choice for morphologic
assessment as well as demonstration of atherosclerotic lesions
and dissection. Published data suggest that the vertebral
artery is amenable to sonographic assessment in over 80–90%
of cases, depending on the segments included in the analysis.
5.6 Ultrasound Criteria, Measurement
Parameters, andDiagnostic Role
5.6.1 Carotid Arteries
5.6.1.1 Plaque Evaluation andMorphology
5.6.1.1.1 Intima-Media Thickness
5.5.2 Vertebral Arteries
ere has been a long controversy regarding the role of
B-mode plaque evaluation in estimating the risk of embo-
Transient ischemic attacks (TIAs) or strokes due to pathology of the vertebrobasilar system are much less common
than those arising from the carotid territory. Stenosis at the
lism, and even more recent studies have not claried this
issue. What is undisputed is that B-mode sonomorphologic
criteria allow a detailed description and classication of
Posterolateral
Chapter 5 · Extracranial Cerebral Arteries
310
Anterolateral
Plaque
5
Posterolateral
a
Anterolateral
Plaque
Posterolateral
b
Anterolateral
Plaque
c
d e
. Fig. 5.14a–e Scanning in at least two planes (as in angiography) is required for sonographic plaque characterization (thickness, morphology)
(anterior and posterolateral transducer positions). If, for instance, a small bowl-shaped plaque is imaged in only one plane, the degree of stenois can be
overestimated or underestimated (see . Fig.5.27). Diagrams a–e illustrate dierent sonomorphologic plaque shapes (transverse plane on the left and
anterolateral and posterolateral longitudinal sections on the right). The drawings show eccentric concave (a, d) and convex (b, e) plaques and ulceration (c) and illustrate how eccentric plaques convexly protruding into the lumen can be overestimated in certain scan planes, while concave eccentric
plaques may be underestimated. The plaques in a and b (diagrams and corresponding ultrasound images) cause roughly the same cross-sectional area
reduction (approx. 50%) but dier in thickness and in the amount of diameter reduction they cause (how these parameters are evaluated depends on
the scan plane). With the transducer in the posterolateral position, the degree of stenosis caused by a large eccentric plaque (examples b and e) may be
overestimated; with an anterior approach, it may be slightly underestimated. c Ulcer in a large eccentric plaque. In this example, only the posterolateral
transducer position allows adequate evaluation (as illustrated by the diagrams)
Plaque
Posterolateral
Anterolateral
Posterolateral
Anterolateral
Plaque
5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
311
5
plaques with good interobserver and intraobserver agreement. Technical developments and the use of high-resolution
transducers (>10 MHz) have improved the detection and
evaluation of small plaques as well as the measurement of
intima-media thickness (IMT). e latter is therefore increasingly being used to identify individuals with an increased
cardiovascular risk.
e thickness of the intimal and medial layers can be
most reliably measured in longitudinal orientation using the
leading- edge method (see . Figs.5.52 and 5.53 (both Atlas)
and 7 Sect. 5.2.1). is method allows measurement of the
intima-media complex with good interobserver agreement
and was used to determine age-related IMT reference values.
e normal IMT is <0.7mm, with a thickness>1mm being
abnormal and >2 mm representing plaque. Homma et al.
(1997, 1999, 2000) found a linear increase in IMT from a
mean of 0.49mm before age 40 to 1.02mm in subjects older
than 100 and proposed the following formula for calculating
age-related normal IMT: (0.009×age)+0.116.
e intima and media cannot be dierentiated sonographically, and this is why the intima-media complex is
measured to identify atherosclerotic thickening of the intima.
e media is thickened in patients with inammatory vascular conditions.
Interventional studies (e.g., of statin treatment; Hedblad
et al. 2001; Kang et al. 2004) used serial sonographic IMT
measurement to monitor treatment outcome, assuming a
measurement accuracy with an error of less than 0.1 mm
(Reley et al. 1992; Meyer and Strobel 2008). is accuracy
requires an axial resolution that only a transducer with a very
high frequency of >15MHz can oer. Such transducers in
turn may not provide the penetration necessary for imaging
the CCA in all patients. Transducers with a frequency of
10MHz or less have a maximum axial resolution of approx.
0.2mm and are unlikely to detect changes of less than 0.1mm
in serial measurements. In addition, deviations of 0.1–
0.2mm result from interobserver variability and the use of
dierent ultrasound systems (Baldassarre etal. 2000; Kanters
etal. 1997). Despite these limitations, high-resolution transducers provide a good option for monitoring IMT.
Various sites in the CCA and ICA have been explored to
measure IMT, and the distal CCA 2–3 cm proximal to the
bifurcation has emerged as the best site for IMT measure-
ment
. Areas of plaque should be excluded, but once plaque
has been demonstrated, IMT measurement is no longer
required to estimate the cardiovascular risk (Poli etal. 1988;
Bond etal. 1989; Ebrahim etal. 1999; Sun etal. 2002; Homma
etal. 2001; Sakaguchi etal. 2003; Sutton-Tyrrell etal. 1992;
Meyer and Strobel 2008).
Long circumferential thickening of the arterial wall, especially when homogeneous and hypoechoic, could point to
early vasculitis. Suspected vasculitis should be ruled out or
conrmed by additional clinical and laboratory examinations and sonographic evaluation of the vascular territories
most susceptible to this condition (subclavian artery).
Small plaques in the ICA become more frequent in the
normal population aer age 50 with a prevalence of up to
80% in those over 80. Because they are so common and their
natural history is unclear, the signicance of small ICA
plaques and their therapeutic relevance remain unclear.
5.6.1.1.2 Plaque Features
Carotid plaque and stenosis mainly occur in the bifurcation
and the rst 2cm of the ICA and ECA.is is because the
local reduction in blood ow velocity occurring in zones of
separation (with local eddy currents) (see . Fig. 1.44b)
increases pressure on the arterial wall, which can cause local
intimal damage. Carotid bulb plaque therefore tends to arise
in the separation zone of the bifurcation and hence opposite
the ECA origin (. Figs.5.18 and 5.16). e natural dilatation
of the bulb additionally contributes to the higher pressure
(Bernoulli equation). e supercial location of these carotid
segments enables imaging with a high-resolution, highfrequency transducer that also allows evaluation of plaque
morphology. e morphologic description of a plaque comprises the following
5 Localization:
5 Anterior/posterior wall
5 Proximal/distal
5 Extent:
5 Circular/semicircular
5 Plaque diameter
5 Plaque conguration:
5 Concentric
5 Eccentric
5 Plaque surface:
5 Clearly delineated/poorly delineated/not delineated
5 Smooth/irregular (0.4–2.0mm ssures);
ulcer (> 2.0mm deep)
5 Plaque composition:
5 Homogeneous/inhomogeneous
5 Echogenicity:
5 Echogenic (with or without acoustic shadowing)/
echolucent/cannot be visualized
e great exibility in positioning the transducer facilitates
plaque evaluation in dierent planes in a way not aorded by
other cross-sectional imaging modalities. Nevertheless, the
individual ultrasound scan reduces the three- dimensional
(3D) plaque to a two-dimensional (2D) representation
. Fig. 5.14). Serial measurement of plaque thickness over
(
time– an important predictor of the risk of embolism– thus
becomes unreliable using B-mode ultrasound alone. erefore, it is recommended to insonate the plaque from dierent
directions and measure its greatest thickness instead of using
standardized planes for measurement. Plaque conguration
also contributes to the risk of embolism and must not be
neglected. e risk is higher for an eccentric plaque because
it is thicker on one side and the shear forces acting on this
thicker plaque portion protruding into the lumen are greater
than those acting on a concentric plaque– even when the
two are causing the same degree of stenosis (. Fig.5.15).
Using a high-resolution transducer, the examiner should
rst obtain an unbiased impression of plaque morphology
features:
312
Chapter 5 · Extracranial Cerebral Arteries
ICA
D2
D2b
D1
ICA
D1
D2a
5
CCA
III III IV
b
. Fig. 5.15 a Diagrams illustrating internal carotid artery (ICA) stenosis caused by concentric (left drawing) versus eccentric plaque (right draw-
ing). Although the degree of stenosis is the same (approx. 65% based on the local grading method/ECST ceriteria), an eccentric plaque is thicker
(twice as thick in the example) and therefore poses a higher risk of embolism: the shear forces acting on it (red arrow) are greater, and the plaque
is therefore more likely to rupture. b Sonomorphologic types of carotid artery plaque (based on the Gray-Weale classication; see . Figs.5.57,
5.58, and 5.59 (Atlas)): Type I– predominantly echolucent lesions with a low gray-scale value, similar to that of the lumen; the surface is inter-
rupted and not consistently visible. Type II– mixed, substantially echolucent lesions with small areas of echogenicity and interrupted, irregular
surfaces. Type III– mixed, substantially echogenic lesions with mostly regular and clearly delineated surfaces. Type IV– predominantly echogenic
lesions of uniform density with mostly smooth and clearly delineated surfaces
CCAa
without any gross pathologic criteria or prognostic factors in
mind. Plaque appearance on gray-scale images provides no
direct information whatsoever about plaque composition–
whether brous, atheromatous, stable, unstable, or ulcerated.
Instead, the examiner must always bear in mind that the
ultrasound image is a display of dierences in acoustic
impedance between tissues and does not reect tissue properties directly.
e
plaque surface, which is the boundary between
owing blood and the plaque components, is described in
terms of visibility and irregularity or disruption. Note, however, that the visibility of a reecting structure such as the
plaque boundary is primarily determined by the angle of
incidence of the ultrasound beam (i.e., the intensity with
which the boundary is depicted depends on whether the
returning echoes have been reected or scattered by the
interface; see . Figs. 1.2 and 1.3).
5.6.1.1.3 Plaque Dierentiation
e way in which a gray-scale ultrasound image is formed
also plays a role when evaluating plaque makeup and
echotexture. Echodensity is described in shades of gray
ranging from very dark to very bright (echolucent to echogenic). e reference values used are those of the hypoechoic
owing blood (lowest gray-scale value) and the hyperechoic
boundary (high gray-scale value) between the adventitia and
surrounding connective tissue in the far wall. e echotexture can be described as homogeneous (uniform appearance) or inhomogeneous (irregular distribution of bright
pixels or absence of echoes). In a heterogeneous plaque,
echolucent areas near the surface are most relevant for estimating the risk of embolism. Acoustic shadowing is the only
ultrasound phenomenon that provides direct information
on a histopathologic tissue feature, as it indicates total reection of the incident ultrasound beam by a calcied structure.
It is a sign of a calcied plaque, which is more stable. e
Gray-Weale classication was proposed to provide a unied
description on the basis of the many criteria of plaque morphology used in the literature and distinguishes four types of
plaques based on echogenicity (Gray-Weale et al. 1988;
. Fig.5.15b).
Supplementing this classication with other important
criteria including plaque surface characteristics (Geroulakos
etal. 1994; Langsfeld etal. 1989; Lusby 1993; Widder 1995),
one can distinguish the following types of plaques on
ultrasound (. Figs.5.16, 5.57 (Atlas), and 5.58 (Atlas)):
5 Type IV: echogenic and homogeneous plaque with a
clearly delineated, smooth surface
5 Type III: plaque of mixed echogenicity with predomi-
nantly echogenic portions and an irregular surface
5.6 · Ultrasound Criteria, Measurement Parameters, andDiagnostic Role
. Fig. 5.16a–c Evaluation of
plaque morphology. a Relatively
hyperechoic, partially inhomogeneous, noncalcied plaque
(type III) with a smooth surface
(indicated by P in the left image)
causing higher-grade stenosis
with a peak systolic velocity
(PSV) of 230cm/s (>70% ECST
stenosis/>50% NASCET stenosis).
Overall, the morphologic features
suggest a stable lesion, except
that it is eccentric and thus
exposed to greater shear stress
(compared with a concentric
plaque). b Echogenic, calcied
(acoustic shadowing), and very
eccentric plaque with a rather
regular surface (longitudinal
image on the left and transverse
image on the right). The small
indentation in the center of the
lesion suggests an irregularity
rather than ulceration. The longitudinal image (dierent perspective) suggests a higher-grade
stenosis compared with the
transverse image (70% diameter
reduction). c Very hypoechoic,
concentric plaque, almost
indistinct from owing blood,
with hemodynamically moderate stenosis (PSV of 130cm/s;
50–60% ECST stenosis/40%
NASCET stenosis). . Figure5.19
shows the same plaque 6months
later (CEUS; dierent plane, with
the transducer in a slightly more
posterolateral position). While
there is only a slight increase in
the degree of stenosis (PSV of
150cm/s), the plaque is ulcerated
and the patient has clinical stage
II disease
a
b
313
5
c
5 Type II: predominantly echolucent or heterogeneous
plaque with a poorly delineated surface
5 Type I: plaque not visualized or suggested only by
isolated echogenic spots in an otherwise echolucent
lesion; the color ow mode is required to estimate
plaque size based on the extent of the color lling defect
Assigning a plaque to one of these four categories faces two
fundamental problems. First, most plaques are very heterogeneous, with components belonging to dierent categories,
while other portions are not visualized at all and simply cannot be categorized. And one must also bear in mind that the
echoes used to form the image are aected by the interaction
of ultrasound with structures in the body and are not a direct
representation of the target tissue (see 7 Sect. 1.1.1.4). Second, an intraoperative analysis has shown that echolucent
plaques are brous or atheromatous with surprisingly similar
frequency (Widder etal. 1990).
Despite these discouraging remarks, the following
assumptions are valid regarding the modied Gray-Weale
classication of plaques.
Some studies suggest that predominantly echolucent
plaque with isolated bright spots (type I) corresponds to atheroma with lipid inclusions and intraplaque hemorrhage,
which make the plaque unstable and have been shown to be
associated with a signicantly increased risk of stroke.