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354
Chapter 5 · Extracranial Cerebral Arteries
picture emerges from scientic studies with some authors
describing high correlation between histopathologic results
and sonomorphologic appearance and others reporting poor
or no correlation (Rati etal. 1985; Droste etal. 1997; Biasi
etal. 1999; Widder etal. 1990; Schulte-Altedorneburg etal.
2000; Denzel etal. 2003; Gonçalves etal. 2004).
Despite these limitations, sonographic plaque analy-
sis
can contribute additional information for estimating
the risk of stroke
. Rapidly progressive stenosis is four
times more likely to cause TIAs and cerebral infarction
5
than less progressive stenosis of a similar degree (Widder
et al. 1992). Heterogeneous, mostly echolucent plaque is
more likely to progress. Moreover, one also has to be aware
that similar plaques may develop dierently. Plaques considered harmless on the basis of their sonomorphologic
and macroscopic appearance may rapidly turn into vulnerable, high-risk plaques, when intralesional hemorrhage
occurs, for instance.
Overall, though, caution must be exercised in predicting
the risk of embolism from the sonomorphologic appearance
of plaque.
Neovascularization of plaques has received increasing
attention as a major culprit in plaque vulnerability. Contrast-
enhanced ultrasound (CEUS)
allows semiquantitative
assessment of plaque neovascularization, which is why it has
a growing role in identifying plaques with an increased risk
of embolism. Moreover, CEUS allows very good delineation
of the plaque contour and plaque surface.
Initial CW Doppler imaging, as it used to be advocated by
some investigators, is no longer necessary since a color
duplex examination performed with adequate instrument
settings enables continuous hemodynamic evaluation. Supplementary transcranial ultrasonography, on the other hand,
provides useful additional information on intracranial arterial anomalies and stenosis.
Duplex or color duplex ultrasound is highly reliable in
evaluating the carotid bifurcation, the preferred site of carotid
stenosis. Angiography does not yield any additional information in this area. e hemodynamic assessment by duplex
ultrasound is superior in grading ICA stenosis compared
with angiography, which merely depicts the perfused lumen
in relation to the adjacent vessel segment. Only ultrasound
provides information on plaque morphology (see
5.6.1.1
and . Fig.5.27). In the NASCET study, there was poor
7 Sect.
agreement between angiography and intraoperative ndings
with regard to the evaluation of plaque surface properties
such as ulceration.
Angiography has the advantage of providing a good
overview of the target vascular anatomy and allows better
documentation of the ndings. Another advantage of
angiography is the detection of
and the base of the skull as well as intracranially
sonog raphic ndings in these carotid segments are inconclusive, angiography should be performed.
If no angiography is performed prior to CEA, the ultrasound examination must be performed with great care, especially with regard to establishing the identity of the ICA and
ECA.High gain is required to dierentiate between subtotal
and total occlusion. In particular if the examination is
impaired by calcied plaques, the examiner must attempt to
depict ow signals in the artery up to the base of the skull.
However, a control angiography should be done in such
cases and also if stenosis grading is impaired by heavy calcication.
Angiography or intra-arterial digital subtraction angiography (DSA) is indicated only in those cases where the
sonog raphic examination is inconclusive or the examination
of the extracranial cerebral arteries reveals indirect evidence
of intracranial vascular pathology. Alternatively, a transcranial duplex examination can be performed.
In addition to angiography and color duplex ultrasound,
the extracranial and intracranial cerebral arteries can be
examined by
CT angiography or MR angiography. Unlike
conventional angiography, which is a 2D projection technique, CT and MR angiography yield 3D datasets of blood
ow in a specic body region, which can then be reconstructed in multiple planes for vascular evaluation.
A helical CT angiogram depicts the target vessels in relation to surrounding structures and is obtained aer injection of iodine-based X-ray contrast medium. Arterial
evaluation may be limited by adjacent structures of similar
attenuation or bones and by premature opacication of
veins. Bones may degrade the visualization of the carotid
siphon, while superimposed veins and calcied plaques may
limit adequate arterial evaluation in the area of the carotid
bifurcation. Time-consuming image postprocessing is
required to ensure adequate evaluation in these cases. Overall, CT angiography tends to underestimate the degree of
ICA stenosis (Clevert et al. 2005; Patel et al. 2002; Zhang
etal. 2005). CT angiograms have high spatial resolution and
are highly sensitive in detecting small ow volumes and slow
ow, for example, distal to subtotal occlusion, but provide
little information on blood ow direction or other hemodynamic parameters.
As with CT angiography, MRI also allows 3D reconstruction for the depiction of target vessels in relation to surrounding structures. Nearby bones do not limit evaluation
and a contrast agent is not generally required but will markedly improve image quality and depiction of vessels with
slow-owing blood.
stenosis near the aortic arch
. If the
5.9 · Diagnostic Role ofDuplex Ultrasound inEvaluating theExtracranial Cerebral Arteries
355
5
e signal intensity of blood on MR images is determined by various factors including the MR pulse sequence or
slice thickness used, the course of the vessel relative to the
imaging plane, and blood ow velocity and ow prole. e
depiction of owing blood by MRI is complex. Two basic
phenomena are time-of-ight and phase-contrast eects,
which are exploited by dierent MR techniques to highlight
arteries and/or veins. Time-of-ight MR angiography can be
manipulated to selectively image either the arteries or veins.
To selectively highlight the arteries, the venous signal is suppressed. is is accomplished by application of a saturation
band to ip longitudinal magnetization into the transverse
plane, thereby suppressing venous enhancement in the imaging volume that would result from the inow eect. e
phase-contrast technique obtains information on the vascular system from deliberately induced ow-related phase
shis. ese phase shis depend on the speed of owing protons and can be measured to calculate blood ow velocity.
In-ow and phase-contrast MR angiography only use ow
eects for vascular imaging. Contrast-agent-based MR techniques exploit the selective shortening of the T1 relaxation
time of owing blood (from 1200 to 50ms) during intravascular passage of the contrast agent to generate image contrast
between vessels and stationary tissues. e use of special
phased-array coils markedly improves the signal-to-noise
ratio while at the same time shortening image acquisition
time and increasing spatial resolution, thereby improving the
dierentiation of peripheral arteries and veins.
MR angiography diers from CT angiography in that
blood ow itself rather than the contrast-enhanced blood is
visualized in the image, and arteries and veins are dierentiated using dierent pulse sequences and imaging techniques.
Vessels are most accurately depicted on MR angiograms
when blood ow is laminar. Vortexing and turbulent ow in
a stenotic segment may impair quantitative assessment and
lead to overestimation of the degree of stenosis, especially
when the time-of-ight technique is used (Clevert etal. 2006;
Patel etal. 2002, 1995). ese ow phenomena may also lead
to misinterpretation in bifurcations and at the origins of
branches. Use of a contrast agent is necessary to visualize
very slow ow. e combination of conventional MRI with
MR angiography is an ideal imaging tool for a comprehensive evaluation of intracranial perfusion and parenchymal
changes, providing diagnostic information to supplement
color duplex ultrasound (extracranial cerebral arteries and
stenosis quantication in the carotid bifurcation) in patients
considered for CEA.
With the methodological limitations outlined above, CT
angiography is most benecial in evaluating the anterior and
posterior arteries near the base of the skull as well as the origins of arteries arising from the aortic arch. MR angiography,
on the other hand, enables good evaluation of the entire
intracranial arterial territory including the carotid siphon.
Color duplex imaging, however, performed with a high-
frequency transducer remains the most suitable imaging tool
for assessing the extracranial arteries supplying the brain,
including the detection of pathology and stenosis grading.
is is suggested by studies comparing dierent imaging
modalities with the traditional gold standard (i.e., angiography performed in two or three planes).
Several studies show that the gold standard, DSA, underestimates ICA stenosis compared with histology (Pan etal.
1995; Schenk et al. 1988; Alexandrov etal. 1993), while a
more recent invitro study reports signicant overestimation
for higher-grade stenosis (p=0.0007) (Smith etal. 2012). e
authors conclude that the accuracy of DSA is aected by
plaque conguration (mountain-shaped lesions, irregular
surface). Another source of error is the contrast medium
concentration, which determines plaque conspicuity. e
same study shows that CT angiography and, surprisingly, MR
angiophy also underestimate stenosis severity.
With 92% sensitivity and 74% specicity, contrastenhanced MR angiography is less accurate in identifying
stenosis requiring surgical management than duplex ultrasound, and it is also inferior in stenosis grading. e two
modalities are supplementary, with duplex ultrasound
enabling adequate evaluation of the extracranial carotid system and MR angiography providing information on the
intracranial vessels as well as on the supra-aortic origins of
arterial branches. Together, the two modalities enable comprehensive diagnostic evaluation prior to surgical repair of
ICA stenosis.
e indication for surgical management or PTA in
patients with subclavian steal syndrome due to subclavian
artery obstruction can be established if the clinical suspicion
is conrmed by duplex imaging, but only angiography will
enable exact identication of collateral pathways.
If initial management of ICA stenosis is conservative
(e.g., antiplatelet or statin treatment), follow-up ultrasonography should focus on identifying changes in plaque morphology and progression of stenosis. Rapid progression of
stenosis and changes in plaque morphology are two important criteria for switching to surgery. In patients treated by
CEA, a follow-up ultrasound examination is performed
immediately aer surgery and then at 6-month to 1-year
intervals, depending on the ndings. A focus of follow-up is
on identication of recurrent stenosis and complications
such as suture aneurysm.
356
Chapter 5 · Extracranial Cerebral Arteries
5.10 Atlas: Extracranial Cerebral Arteries
. Table5.17 lists the gures presented in the Atlas. e gures illustrate normal ndings, methodology, and vascular diseases
of the extracranial cerebral arteries.
. Table 5.17 Extracranial cerebral arteries– gures
Entity/Pathology Figure
5
Carotid bifurcation– ICA/ECA dierentiation
ECA stenosis
PSV dependence on systemic factors– blood pressure
Fig.5.49 (Atlas), page 358
.
Fig.5.49 (Atlas), page 358
.
.
Fig.5.50 (Atlas), page 358
Kinking without/with stenosis
Coiling
Measurement of intima-media thickness (IMT)
Measurement of intima-media thickness (IMT)– plaque
Stenosis with beginning hemodynamic eects
Moderate ICA origin stenosis
Distal ICA stenosis
High-grade ICA origin stenosis
Evaluation of plaque morphology
Plaque morphology– surface structure
Plaque morphology– long concentric carotid stenosis (smooth, regular surface)
Plaque morphology– high-grade stenosis with ulceration
ICA occlusion
Signs of recanalization in ICA occlusion
CCA occlusion– collaterals
Complete extracranial carotid territory occlusion
PPHA as collateral in ICA occlusion
Occlusion of the brachiocephalic trunk– collateral pathways
CCA stenosis
High-grade stenosis of the brachiocephalic trunk
ICA occlusion– compensatory ow increase in collateral pathways
Pitfall of PSV-based ICA stenosis grading in contralateral ICA occlusion
Suture aneurysm
Complications after carotid endarterectomy– suture aneurysm
True ICA aneurysm
Mycotic ICA aneurysm
Dissection of CCA
Fig.5.51 (Atlas), page 359
.
.
Fig.5.51 (Atlas), page 359
.
Fig.5.52 (Atlas), page 360
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Fig.5.52 (Atlas), page 360
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Fig.5.53 (Atlas), page 361
.
Fig.5.54 (Atlas), page 361
.
Fig.5.55 (Atlas), page 362
.
Fig.5.56 (Atlas), page 362
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Fig.5.57 (Atlas), page 363, 364
.
Fig.5.58 (Atlas), page 364
.
Fig.5.59 (Atlas), page 365
.
Fig.5.60 (Atlas), page 366
.
Fig.5.61 (Atlas), page 367
.
Fig.5.62 (Atlas), page 367
.
Fig.5.63 (Atlas), page 368
.
Fig.5.64 (Atlas), page 369
.
Fig.5.64 (Atlas), page 369
.
Fig.5.65 (Atlas), page 370
.
Fig.5.66 (Atlas), page 370
.
Fig.5.67 (Atlas), page 371
.
Fig.5.68 (Atlas), page 371
.
Fig.5.69 (Atlas), page 371
.
Fig.5.70 (Atlas), page 372
.
Fig.5.71 (Atlas), page 372
.
Fig.5.72 (Atlas), page 373
.
Fig.5.72 (Atlas), page 373
Fig.5.73 (Atlas), page 374
.
5.10 · Atlas: Extracranial Cerebral Arteries
. Table 5.17 (continued)
Entity/Pathology Figure
357
5
Posttraumatic ICA dissection
Posttraumatic ICA dissection with patent true and false lumen
Takayasu’s arteritis
Temporal arteritis
Postoperative follow-up after carotid endarterectomy (CEA)
Carotid endarterectomy with patch closure
Recurrent stenosis after carotid endarterectomy (CEA)
Anastomotic stenosis after bypass procedure between subclavian artery and ICA for CCA occlusion
Change in pulsatility after carotid artery stenting (CAS)
ICA in-stent restenosis– neointimal proliferation
Grading of in-stent restenosis– PSV ratio
High-grade in-stent restenosis after carotid artery stenting (CAS)
Stent dislocation
Alternative ultrasound techniques: B-ow mode, 3D ultrasound
B-ow imaging for evaluation of in-stent restenosis
Vertebral artery
Hypoplastic vertebral artery
Vertebral artery hypoplasia
Vertebral artery origin stenosis
Grading of vertebral artery stenosis
Distal vertebral artery stenosis
Vertebral artery occlusion
Vertebral artery dissection
Subclavian steal syndrome with to-and-fro ow in the vertebral artery
Subclavian steal syndrome with retrograde ow in the vertebral artery
Subclavian steal syndrome with vertebrovertebral crossover
Carotid body tumor
Diagnosis of brain death
Fig.5.74 (Atlas), page 374
.
Fig.5.75 (Atlas), page 375
.
Fig.5.76 (Atlas), page 375
.
Fig.5.77 (Atlas), page 375
.
Fig.5.78 (Atlas), page 376
.
Fig.5.79 (Atlas), page 376
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Fig.5.80 (Atlas), page 377
.
Fig.5.80 (Atlas), page 377
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Fig.5.81 (Atlas), page 378
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Fig.5.82 (Atlas), page 378
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Fig.5.83 (Atlas), page 379
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Fig.5.84 (Atlas), page 379
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Fig.5.85 (Atlas), page 380
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Fig.5.86 (Atlas), page 381
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Fig.5.86 (Atlas), page 381
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Fig.5.87 (Atlas), page 382, 383
.
Fig.5.87 (Atlas), page 382, 383
.
Fig.5.87 (Atlas), page 382, 383
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Fig.5.88 (Atlas), page 383
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Fig.5.88 (Atlas), page 383
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Fig.5.89 (Atlas), page 384
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Fig.5.90 (Atlas), page 384
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Fig.5.90 (Atlas), page 384
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Fig.5.91 (Atlas), page 385
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Fig.5.92 (Atlas), page 385
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Fig.5.93 (Atlas), page 386
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Fig.5.94 (Atlas), page 387
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Fig.5.95 (Atlas), page 387
.
Chapter 5 · Extracranial Cerebral Arteries
358
5
. Fig. 5.49a, b (Atlas) Carotid bifurcation– ICA/ECA dierentiation.
a Longitudinal view of the carotid bifurcation obtained with the transducer in the posterolateral position. The internal carotid artery (ICA) is closer
to the transducer. The color change in the bulb indicates retrograde ow components due to ow separation (S) (see . Fig. 1.44b). The Doppler
waveform of the ICA is characterized by a fairly large end-diastolic ow component. The external carotid artery (ECA) is identied further away
from the transducer with ow separation at its origin (red) and the superior thyroid artery (A.T.S) arising from it. The Doppler waveform on the left
is from the ICA, the waveform on the right from the ECA.The ECA waveform is more pulsatile compared with the ICA waveform and reects the
oscillations caused by tapping of the temporal artery anterior to the ear (left portion of waveform).
ECA stenosis.
b Stenosis of the ECA reduces pulsatility in the stenotic segment, which may make it dicult to correctly assign the stenosis to the ICA or
ECA.When the ECA waveform is altered by stenosis and becomes internalized, the temporal tap sign enables reliable dierentiation of the two
arteries. (Inverted color encoding of ow direction compared to a)
. Fig. 5.50a–c (Atlas) PSV dependence on systemic factors– blood pressure.
Peak systolic velocity (PSV) is higher in hypertension. This patient with a blood pressure of 205/100mmHg during the ultrasound examination
had a PSV of 145cm/s in the ICA (a), a PSV of 157cm/s in the CCA (b), and a PSV of 230cm/s in the axillary artery (c) without signs of stenosis in
gray-scale or color duplex images. These PSVs were present in long segments of the arteries and also in the contralateral arteries. In a patient with
normal blood pressure, these PSVs would suggest 50–60% stenosis
5.10 · Atlas: Extracranial Cerebral Arteries
359
5
. Fig. 5.51a–d (Atlas) Kinking without/with stenosis.
a Elongation of the internal carotid artery (ICA) may lead to kinks or coils (see . Fig.5.1). The resulting tortuosity of the ICA can lead to dierent
angles of insonation with localized increases in the Doppler shift frequency, which must not be misinterpreted as evidence of stenosis. The corresponding color duplex image will show color aliasing in vessel segments insonated at a small angle. Depending on the insonation angle used,
kinks or coils in the course of the ICA may be depicted as ow reversal (change in color coding). The color ow image (left) depicts the junction of
the common carotid artery (CCA) with the ICA on the right and the distal ICA on the left. The Doppler waveform obtained after angle correction
shows laminar ow with a PSV of 95cm/s, conrming that aliasing in the color mode is due to a small insonation angle. The color change from red
to blue is caused by the change in ow direction relative to the transducer.
b Stenosis due to ICA kinking is rare. Such a stenosis may be caused by sclerotic wall changes with plaque (P) at the site of the kink. Here, a PSV of
145cm/s indicates a stenosis of approximately 60% (by ECST criteria; see . Fig.5.9b and . Table5.9).
Coiling.
c Coiling of the tortuous ICA is seen on color duplex images as a change in color coding, which indicates a change in ow direction relative to
the transducer. The right section shows the proximal, straight segment of the ICA (rst 2.5cm) with the arrowhead indicating the transition to
the coiled segment. The left section depicts the coiled segment and the transition from the straight portion (change from blue, ow away from
transducer, to red, ow toward transducer). A coiled ICA segment is often not visualized in a single plane, but in most cases exible transducer
positioning will allow full evaluation. In the example, one segment is imaged at a 90° Doppler angle, resulting in the artifactual absence of ow.
Color aliasing is due to use of a low pulse repetition frequency.
d Angiogram showing the loop (arrow) in the distal extracranial ICA
Chapter 5 · Extracranial Cerebral Arteries
360
5
a
b
c
. Fig. 5.52a–c (Atlas) Measurement of intima-media thickness (IMT).
a 38-year-old man with a history of hyperlipidemia, in whom an intima-media thickness (IMT) of 0.8mm was measured in the far wall 2cm proximal to the bifurcation (indicated by calipers). An IMT of 0.8mm is abnormal for the patient’s age but would be normal for an individual over 60
(see. Fig.5.5).
b In another patient, measurement in the far wall of the common carotid artery (CCA) just before the bifurcation shows thickening of the intimamedia complex to 0.9mm and a plaque with a maximum thickness of 3.2mm and an irregular surface to the right of it.
Measurement of intima-media thickness (IMT)– plaque.
c The thickness of the intima-media complex is measured in the wall away from the transducer, where the interface between the perfused lumen
and the intima produces a sharp reection due to the intervening owing blood. The intima and media are indistinct with the second bright reection occurring at the boundary between the adventitia and the surrounding connective tissue. The layer between these two reections, which is
measured, is the intima-media complex. The IMT of 0.9mm measured in this case is abnormal in a 50-year-old individual. A plaque is dened as an
IMT >2mm. In the example, an eccentric plaque measuring 3.3mm in thickness is seen in the center of the image
5.10 · Atlas: Extracranial Cerebral Arteries
. Fig. 5.53a, b (Atlas) Stenosis with beginning hemodynamic eects.
a A circular plaque in the internal carotid artery (ICA) reduces the cross-sectional area by 75% (left image). To achieve complete color lling of the
perfused lumen in the transverse plane, a low pulse repetition frequency (PRF) is employed, which produces aliasing. In the right image, faster
blood ow in the center of the artery is indicated by brighter blue and yellow and eddy currents as a change in color coding (red) (see 7 Sect. 1.2.3).
The hemodynamic stenosis severity with a peak systolic velocity (PSV) of 128cm/s and spectral broadening correlates with the cross-sectional
area reduction. A 65–83% cross-sectional area reduction corresponds to a 40–60% diameter reduction (by ECST criteria;
. Table5.9), suggesting a stenosis which is just becoming hemodynamically signicant. This is shown here for illustration only, and measurement
of the cross-sectional area reduction from a transverse image should not be used for stenosis grading (perpendicular angle of insonation results
in lower Doppler shift frequencies, and turning up the gain for color imaging can result in blooming artifacts). All relevant stenoses are graded
hemodynamically from angle-corrected spectral Doppler measurement in longitudinal orientation.
b Angiogram: Moderate stenosis of the ICA origin
see . Fig.5.9b and
361
5
. Fig. 5.54a–c (Atlas) Moderate ICA origin stenosis.
a The severity of luminal narrowing caused by plaque at the internal carotid artery (ICA) origin cannot be evaluated in the gray-scale mode due to
calcication with posterior acoustic shadowing (SS). Color ow imaging is also impaired. Distal to the acoustic shadow, there is an eccentric jet with
aliasing (yellow) and turbulent ow. Peak systolic velocity (PSV) is increased to 200cm/s and end-diastolic velocity (EDV) to 70cm/s, consistent
with approx. 70% stenosis by ECST criteria (equivalent to 50% NASCET stenosis; see . Fig.5.9b and . Table5.9). In this case, it was not possible to
depict ow by moving the transducer and thus avoiding the calcication. Instead, a high gain was used to obtain a Doppler waveform from the area
of acoustic shadowing for hemodynamic quantication of the stenosis by measuring PSV at the site of the plaque.
b Angiogram: 60–80% diameter reduction.
c Example of a plaque causing a similar degree of stenosis as in a but with better visualization of the stenosis because the plaque is not calcied. Echolu-
cency suggests a vulnerable plaque, but the surface is smooth. The plaque causes moderate to severe stenosis of the carotid bulb (aliasing, PSV of 225cm/s
and EDV of 80cm/s). The B-mode image (left) depicts the common carotid artery (CCA) on the right and the ICA on the left, both with ow coded in blue
362
Chapter 5 · Extracranial Cerebral Arteries
5
. Fig. 5.55a, b (Atlas) Distal ICA stenosis.
a From a posterolateral transducer position, stenosis is depicted in the internal carotid artery (ICA) approx. 2.5cm upstream of the origin of the
external carotid artery (ECA). In the color duplex image, stenosis is suggested by aliasing; the plaque is echolucent. A peak systolic velocity (PSV)
of 380cm/s suggests a diameter reduction of >80%. More distal evaluation of the ICA is precluded by acoustic shadowing and scattering produced by connective tissue structures at the base of the skull. In the postoperative evaluation after carotid endarterectomy (CEA), it is important
to exclude stenosis at the distal patch end.
b Angiogram: Filling defect (arrowhead) just below the skull base and normal origin of the ICA
. Fig. 5.56a–c (Atlas) High-grade ICA origin stenosis.
a Echolucent, smooth plaque (P) at the origin of the internal carotid artery (ICA) is dicult to delineate from owing blood (leftmost image). There
is aliasing in the longitudinal color ow image with a peak systolic velocity (PSV) of 3m/s, indicating high-grade stenosis. Blue indicates normal
ow direction toward the brain (away from transducer); red indicates turbulent ow with retrograde components. The transverse view (rightmost
image) displays the sonomorphologic appearance of the echolucent, eccentric plaque in the carotid bulb (ICA, indicated by calipers) and the
resulting high- grade luminal narrowing. The external carotid artery (ECA) and jugular vein (V ) are seen lateral to the ICA.Accurate stenosis grading is not possible from transverse views (see . Fig.5.53 (Atlas) and 7 Sect. 1.2.3); a rough estimate is that the diameter reduction is >80%.
b Angiogram: High-grade stenosis (arrow) of the ICA caused by eccentric plaque.
c Eccentric high-grade ICA stenosis, which, unlike the stenosis in a, is caused by a calcied plaque (P) with acoustic shadowing (PSV of 380cm/s).
In this example, the color coding follows the convention adopted in some textbooks on vascular ultrasound to invariably depict arteries in red
and veins in blue. Therefore, the arteries are displayed in red although the blood ow direction is away from the transducer. Also seen are turbulent ow components (see . Fig.5.22a)
5.10 · Atlas: Extracranial Cerebral Arteries
a
363
5
b
c
. Fig. 5.57a–e (Atlas) Evaluation of plaque morphology (. Figs.5.14, 5.15, and 5.18).
a Example of a partially calcied plaque with echolucent noncalcied portions and a bowl-shaped defect at the distal end. The sharp demarcation
of the defect with a bright boundary is more in keeping with a harmless defect niche rather than fresh ulceration (and was conrmed intraoperatively). The peak systolic velocity (PSV) of 2.5m/s indicates >70% stenosis by ECST criteria (equivalent to >50% stenosis by NASCET criteria; see
. Fig.5.9b and . Table5.9). Mix of red and blue within the defect indicates eddy currents (see . Fig.5.18a, e).
b Echogenic plaque (P) protruding into the lumen at the internal carotid artery (ICA) origin (longitudinal image on the left, transverse image
on the right). Acoustic shadowing indicates calcication of the plaque. The stenosis has no hemodynamic relevance and does not explain the
patient’s symptoms (TIAs), which are attributable to a oating portion (F) identied by real-time ultrasound. (In unclear cases, the time-motion
mode can be used to demonstrate plaque motion, see . Fig. 2.57 (Atlas).)
c Color duplex (left) and contrast-enhanced ultrasound (CEUS) (right) of echolucent eccentric plaque (P) causing high-grade stenois at the ICA
origin. The fact that no contrast microbubbles enter the plaque in the CEUS examination indicates absence of neovascularization and hence a less
vulnerable plaque. However, this very eccentric plaque may be highly vulnerable because it is prone to intralesional hemorrhage. The echolucent
plaque is dicult to dierentiate from surrounding blood in B-mode ultrasound (rightmost image), and color duplex is necessary to delineate the
eccentric plaque from owing blood (leftmost image). If no gray-scale median (GSM) analysis is performed, the echogenicity of the plaque can be
evaluated by comparing it with that of the sternocleidomastoid muscle anterior to the artery (closer to the transducer). The low echogenicity of
the plaque in this example corresponds to a GSM<20.
d Echolucent, eccentric plaque (P) causing moderate stenosis (Doppler waveform) at the ICA origin (color duplex on the left, CEUS on the right).
CEUS clearly shows signs of (mild) plaque neovascularization (arrows; grade 2). This example also illustrates the discrepancy between the risk of
embolism resulting from plaque thickness (arrow in transverse view on the left; 5.5mm versus 8mm bulb diameter) and the hemodynamic relevance of the stenosis (PSV of 160cm/s, consistent with approx. 60% ECST stenosis and 40% NASCET stenosis).
e Six months later, color duplex ultrasound reveals nearly unchanged plaque thickness (not shown), while CEUS shows increased neovascularization (grade 3) of the proximal plaque portion (site of high shear stress) but little neovascularization in the distal portion (grade 1). This plaque is
homogenenous in terms of echogenicity but inhomogeneous in terms of neovascularization