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129Arterial Pathology

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

Fig. A5.56 Downstream ﬂ ow patterns in hemodynamically rel- evant high-grade ICA stenosis. TCCS, color-mode image and corresponding Doppler spectrum analysis, transtemporal approach. (A) Lower pontine plane, C6-ICA: pronounced poststenotic ﬂ ow pattern (ﬂ ow velocity 21/10 cm/s, PI 0.6 and a markedly prolonged AT). (B) Midbrain plane, M1-MCA: mild poststenotic ﬂ ow pattern only (ﬂ ow velocity 63/25 cm/s, PI 1.1 and mildly increased AT) because of collateral ﬁ lling via the ACoA.

Fig. A5.57 Downstream ﬂ ow patterns in hemodynamically rele- vant high-grade ICA stenosis. TCCS, color-mode image and corresponding Doppler spectra. (A) Transorbital approach: antegrade OA ﬂ ow with mild poststenotic ﬂ ow pattern (ﬂ ow velocity 24/10 cm/s). (B) Transtemporal approach, lower pontine plane: similar ﬂ ow pat- tern in the C6-ICA (ﬂ ow velocity 20/10 cm/s).

• Near-occlusion with variable velocities and ICA/CCA

ratio and occlusion.

Fig. A5.58 Downstream ﬂ ow patterns in hemodynamically rel- evant high-grade ICA stenosis. TCCS, color-mode image and corresponding Doppler spectra. (A) Transtemporal approach, anterior coronal plane: M1-MCA with almost normal ﬂ ow pattern. (B) In contrast, a mild poststenotic ﬂ ow pattern is present in the A1-ACA. The best explanation is that the contralateral A1-ACA takes care of both ACA territories and the aﬀ ected MCA has more need of the remaining blood ﬂ ow from the ICA.

velocity parameters which have been adapted to the rough NASCET grading system (Alexandrov and Needleman 2012). According to a consensus report the following criteria were proposed (Grant et al 2003):

• <50% stenoses (peak systolic velocity <125 cm/s, ICA/ CCA ratio <2.0, end-diastolic velocity <40 cm/s, <50% diameter reduction).

• 50–69% stenoses (peak systolic velocity 125–230 cm/s, ICA/CCA ratio 2.0–4.0, end-diastolic velocity 40– 100 cm/s, ≥50% diameter reduction).

• Stenoses >70%–near-occlusion (peak systolic velocity >230 cm/s, ICA/CCA ratio >4.0, end-diastolic velocity >100 cm/s, ≥50% diameter reduction).

An adapted “sonographic NASCET index” has since been proposed, which also took the distal ICA ﬂ ow information into account and which consequently yielded better correlation with angiographic ﬁ ndings than the conventional peak systolic ﬂ ow velocity measurements alone (Hathout et al 2005). Nevertheless, the American Heart Association decided to recommend duplex ultrasound as a screening tool only and not as a possible sole examination technique before ICA intervention because of divergent published studies and its low sensitivity and speciﬁ city compared with other imaging modalities (Latchaw et al 2009).

Despite the above well-deﬁ ned grading criteria, they

still have to be applied with caution considering other potentially modifying aspects. The given cut-oﬀ val- ues for blood ﬂ ow velocities might not be applicable in patients with generally altered cerebral perfusion, e.g., in severe hyperemia, in young subjects who in general show higher blood ﬂ ow velocities of the brain- supplying arteries, or in elderly and hypertensive patients who have often generalized dilated vessels and subsequent lower ﬂ ow velocities. Furthermore, a contralateral high-grade ICA stenosis or ICA occlusion may lead to an ipsilateral compensatory raised ICA ﬂ ow and ﬂ ow velocity with subsequent overestimation of the stenosis (Henderson et al 2000). Vice versa, endarterectomy of a contralateral high-grade ICA stenosis often results in an ipsilateral decrease of intrastenotic blood ﬂ ow velocity. Following stent treatment, the mean observed drop of contralateral peak systolic velocity was reported to be

60.3 cm/s. In 71% of patients with the initial ﬂ ow veloc- ity-derived diagnosis of signiﬁ cant contralateral steno- sis, interventional angiography refuted the presence of any signiﬁ cant contralateral stenosis (Sachar et al 2004). In a CEA study, the intervention led to a contralateral decrease of blood ﬂ ow velocity in 52% of cases with

130 5 Vascular Pathology

NASCET (%) –15 0

ECST (%)

Diameter B-mode

Turbulence

ICA syst

ICA diast

ICA syst post

ICA/CCA

Prestenot. CCA

Poststenot. ICA

Poststenot. C6-ICA

IC collaterals

OA collateral

Fig. A5.59 Ultrasound grading of ICA stenosis at its origin according to the NASCET and ECST criteria. Flow velocities are given in cm/s. Occl. = occlusion; diameter = residual diameter assessed in cross-sectional plane; turbulence = aliasing in color-mode and/or systolic broadening in Doppler spectrum analysis; V within the stenosis; V CCA = prestenotic ﬂ ow pattern = reduced ﬂ ow velocity and increased pulsatility in CCA; poststenot. ICA = reduced ﬂ ow velocity, delayed systolic ﬂ ow acceleration and/or reduced pulsatility; poststenot. C6 = poststenotic ﬂ ow pattern = r e d u c e d ﬂ ow velocity, delayed systolic ﬂ ow acceleration and/or reduced pulsatility in C6-ICA; OA collateral = ↑↓: OA ﬂ ow may be nor- mal, absent, or retrograde; IC collaterals = intracranial collateral activation via communicating arteries: retrograde ipsilateral A1-ACA, raised ﬂ ow velocities in ipsilateral P1-PCA and PCoA and/or via leptomeningeal arteries: raised ﬂ ow velocities in ipsilateral P2-PCA and P3-PCA branches in variable combinations. ↑ ↓ = variable.

++ ++ ++

dist

ICA syst post

80 90 Occl.

40 50

= poststenotic ICA peak systolic ﬂ ow velocity; ICA/CCA = peak systolic velocity ICA/CCA ratio; prestenot.

(+)

90 95

(+)

>125

>210

>240

>330

>370

<100

>100

>50

<50 <30

(+)

+++

(+)

= peak systolic ﬂ ow velocity within the stenosis; V

ICA syst

Occl.

= end-diastolic ﬂ ow velocity

ICA diast

= poststenotic ﬂ ow pattern

dist

an average drop of 20% duplex-deﬁ ned stenosis grade (Busuttil et al 1996). It can be assumed that such eﬀ ects will only occur if the untreated ICA serves as a collateral vessel supplying blood via the ACoA before intervention. Interestingly, none of these studies analyzed the presence or absence of intracranial collaterals, which probably explains why this phenomenon was not observed in all of the patients.

Another potential pitfall to be considered is the occurrence of tandem stenoses, i.e., the simultaneous presence of an extra- and intracranial ICA stenosis. In such cases ﬂ ow velocity and therefore also the stenosis grade may be underestimated. A tandem stenosis should be considered if indirect signs of a hemodynamically relevant distal ﬂ ow obstruction are present, which cannot solely be explained by the ﬁ ndings of the extracranial ICA stenosis. Finally, it has to be mentioned that the stenosis categories are based on the presence of an isolated, short, and circumscribed ICA stenosis. In stenoses more than 2 cm in length, such as are often seen in dissection, ﬂ ow velocities lower than expected might be observed due to the increased ﬂ ow resistance.

A near-occlusion may be diﬃ cult to be distinguished from a vessel occlusion, especially if the site of the vessel obstruction is slightly distal to an otherwise not severely aﬀ ected bulb. In these circumstances the bulb may reveal a stump signal, but the following ICA segment may present a turbulent ﬂ ow pattern with variable

ﬂ ow velocities. A marked poststenotic waveform in the distal extracranial or intracranial petrosal ICA segment assures a near-occlusion of the ICA. Its clinical signiﬁ - cance is limited and mainly of interest in patients with enduring insuﬃ cient collateral function in whom open- ing of the near-occlusion may be indicated. In suspected proximal ICA occlusion sonographers should follow the ICA from its origin to the more distal segments, reduce the PRF and the size of the color box, and increase the color gain in both the longitudinal and transverse planes in order not to overlook near-occlusion (Fig. A5.60). For further details, see Case 1 and Case 11. For details of ICA near-occlusion, see Case 15 and Case 18.

Graduation of Stenosis after Stenting

Carotid artery stenting is a well-established alternative to carotid endarterectomy. Postinterventional duplex sonography allows assessing stent placement as well as comorbidities like dissection or residual or reoccurring stenosis (Fig. A5.61). Velocity criteria for in-stent restenosis evaluation are still not well established. Comparing carotid angiograms with duplex ultrasound for luminal stenosis, increasing peak systolic velocities and ICA/CCA ratios correlate with evolving restenosis within the stented carotid artery. However, application of velocity criteria for nonstented arteries leads to an overestimation of the stenosis grade. Analysis of ﬂ ow after

131Arterial Pathology

Fig. A5.60 Left: Ce-MRA, coronal rotated MIP showing an ICA near-occlusion stenosis (arrow). Note the collapsed poststenotic ICA (arrows). Right: Extracranial duplex, color-mode image, longitudinal plane with corresponding Doppler spectrum analysis:

Top: Stump signal in the carotid bulb suggestive for ICA occlusion. Bottom: Color-mode and Doppler spectra assessment with adapt-

ed PRF and gain reveal a turbulent ﬂ ow with moderate increase velocities (121/38 cm/s) corresponding to an ICA near-occlusion.

Fig. A5.62 Proximal ICA occlusion. Left: DSA, selective left CCA ﬁ lling, lateral view. Small blind sack ICA (arrow) followed by a complete absence of ICA contrast ﬁ lling. Right: Extracranial duplex. Top: B- and color-mode image, longitudinal view with corresponding Doppler spectrum analysis. Isoechoic intraluminal material ﬁ lling the ICA is seen which could be either an atherothrombotic plaque or subacute thrombus. Note the anechoic proximal area with absent color ﬁ lling corresponding to a nonperfused but still open vessel segment, the blind sack. Bottom: Doppler spectrum analysis. Alternating “to-and-fro” stump signal.

Fig. A5.61 Proximal ICA after stent treatment of a high-grade stenosis. Duplex ultrasound of the CCA and ICA. (A) B-mode image, longitudinal plane revealing the stent in situ, a large shadow of a calciﬁ ed plaque (arrowhead), and a residual hypoechoic plaque more distally (arrow). (B) Color-mode image, cross-sectional plane showing the CCA circumference. (C,D) Longitudinal color-mode image and simultaneous Doppler spectrum analysis of the proximal ICA revealing a mildly disturbed ﬂ ow without increase of velocities, indicating a mild residual stenosis. Note also the residual hypoechoic plaque (arrow).

Fig. A5.63 Proximal ICA occlusion. Left: Ce-MRA coronal rotated MIP. Note the large blind sack (arrow). Right: Extracranial duplex. Color-mode image, longitudinal view (top) with corresponding Doppler spectrum analysis (bottom). Note the anechoic intraluminal material. Here the blind sack ICA signal reveals a retrograde ﬂ ow. Note the aliasing eﬀ ect in the ECA, caused by the low PRF set- ting used for the detection of low residual ICA ﬂ ow.

stent placement in nonstenotic vessel segments found a 22% increase of in-stent peak systolic ﬂ ow velocity but no signiﬁ cant increase of end-diastolic velocity (Haki- mi et al 2012). The following ICA in-stent restenosis threshold criteria for peak systolic ﬂ ow velocity and ICA/CCA ratio have been proposed (Lal et al 2008): ≥20% (PSV ≥150 cm/s and ICA/CCA ratio ≥2.15); ≥50% (PSV ≥220 cm/s and ICA/CCA ratio ≥2.7); ≥80% (PSV 340 cm/s and ICA/CCA ratio ≥4.15). Similar thresholds were re-

ported by Stanziale et al (2005): ≥50% (PSV ≥225 cm/s and ICA/CCA ratio ≥2.5); ≥70% (PSV ≥350 cm/s and ICA/ CCA ratio ≥4.75).

In comparison to ultrasound and catheter angiography, MRA is of limited value in the evaluation of intracranial as well as extracranial vessels after stent implantation (Golshani et al 2013). In contrast, CTA was reported to yield similar results to color-coded duplex sonography (Nolz et al 2012). Further improvements in the assessment

132 5 Vascular Pathology

Fig. A5.64 Distal supraophthalmic ICA occlusion. Left: DSA, selective right CCA ﬁ lling, lateral view. (A) Early arterial phase: Proximal ICA contrast ﬁ lling but apparent contrast stops after 4 cm. (B) Late arterial phase demonstrates preserved contrast ﬁ lling of the whole ICA (arrows). Note: The ICA lumen is smaller than the ECA lumen. Right: Extracranial duplex. Top: Color-mode image, longitudinal plane. Preserved color ﬁ lling within the proximal ICA. Bottom: Dop - pler spectrum analysis: Small antegrade ﬂ ow with reduced ﬂ ow ve- locities and increased pulsatility resembling OA ﬂ ow pattern (ﬂ ow velocity 40/12 cm/s).

of intracranial stents might result from applying ﬂ at- panel cone beam CT—a high-resolution imaging technique based on projection radiography which lacks the typical beam-hardening CT artifacts (Hu et al 2015, Ott et al

2016). For further reading on stenting in ICA stenosis, see Case 15; for intracranial stenosis, see Case 26.

ICA Occlusion

ICA occlusion should be deﬁ ned according to its location in relation to the OA oﬀ spring. A proximal ICA occlusion below the origin of the OA (infraophthalmic occlusion) and near the carotid bifurcation is usually characterized by a missing color-mode and Doppler ﬂ ow signal. The most frequently observed cause in near-bifurcation occlusion is atherothrombotic pathology. In cases with a small remaining “blind sack” a stump signal (low-amplitude, alternating “to-and-fro” Doppler signal) with a short anterograde systolic ﬂ ow and a retrograde diastolic ﬂ ow or only a retro- grade ﬂ ow can be seen. If the PRF settings are low, a weak color signal may be present (Fig. A5.62 and Fig. A5.63). In distal infraophthalmic occlusions, e.g., near the skull base— as typically seen in dissections—the ICA may initially remain open from its origin up to the occlusion site. However, as no relevant vessel branch is present, a stump signal and weak color signal may be obser ved over the whole visible course. If the occlusion persists, the remaining ICA usually occludes by thrombus formation starting from the occlusion site and advancing in a stepwise manner toward the carotid bifurcation. The diameter of the CCA subsequently decreases (Kubis et al 2001). In distal ICA occlusion, adaptive diameter reduction is also observed in the ICA itself. In acute and subacute occlusions, the vessel walls are usually well delineated; in chronic occlusion, no clear vessel borders can be distinguished. The latter is caused by the less

Fig. A5.65 ICA dissection. Left: DSA, selective right CCA ﬁ lling, lateral view. (A) Proximal ICA dissection with typical ﬂ amed-like occlusion. Intracranial collateral ﬂ ow was assured by a cross-ﬂ ow via the ACoA. (B) 6 months later, ICA reopened (arrows). Note: The ICA lumen is smaller than the ECA lumen. Angiographically a cross-ﬂ ow persisted despite the recanalization of the ICA. Right: Extracranial duplex corresponding to B. Top: Color-mode image, longitudinal plane. Preserved color ﬁ lling within a slim ICA. Bot- tom: Doppler spectrum analysis: Small antegrade ﬂ ow with re- duced ﬂ ow velocities and increased pulsatility resembling OA ﬂ ow pattern (ﬂ ow velocity 30/6 cm/s).

well delineated or abolished intima-media complex. Flow patterns in the depending distal vessel segments, i.e., the carotid siphon, MCA and ACA depend on the presence and quality of collateral pathways (for further details, see “Collateral Pathways” below). For further details on infraophthalmic ICA occlusion, see Cases 11–13, Case 20, Case 24, Case 28, Case 39, and Case 40.

In supraophthalmic ICA occlusions (distal to the OA origin) the ICA provides blood for the OA only, but therefore remains open. In this constellation the ICA can be considered as an extended OA. Consequently, the ICA lumen collapses to a level below the ECA diameter and the ﬂ ow pat- tern resembles that of the OA with low ﬂ ow velocities and a higher pulsatility but preserved diastolic ﬂ ow (Fig. A5.64). For further reading on supraophthalmic ICA occlusion, see also Case 37. It is noteworthy that in ICA dissection and ICA occlusion with collateral ﬂ ow via the ACoA and/or PCoA an “extended OA” and collateral ﬂ ow via the communicating arteries may persist even after recanalization of the ICA, as we have observed for many years (Fig. A5.65).

CCA Stenosis and Occlusion

In contrast to the ICA, an exact grading system for CCA stenoses does not exist. However, the relation of diameter and area assessments as well as the diameter/ﬂ ow velocity relation, the criteria for local ﬁ ndings, and the pre- and poststenotic ﬂ ow alterations apply similarly to the NASCET-adapted criteria for ICA stenoses while a bulb is not present (see “ICA Stenosis” above). Stenoses in the mid- and distal CCA are easily accessible to duplex ultrasound (Fig. A5.66). Proximal low- and medium-grade CCA stenoses are probably often missed as the CCA origin is not directly accessible and a poststenotic ﬂ ow pattern can only be seen in high-grade stenoses (>70–80%).

133Arterial Pathology

Fig. A5.66 Extracranial duplex. (A) B-mode image, longitudinal plane: Large mixed-echoic structure in the CCA. (B) Color-mode, cross-sectional plane: Diameter of the vessel (8.8 mm), residual lumen (4.4 mm) with a resulting stenosis of 50%. (C) Colormode, longitudinal plane: Delineation of the remaining perfused lumen and confirmation of the plaque extension. (D) Doppler spectrum analysis revealing a spectral broadening and increased velocity in moderate CCA stenosis (flow velocity 168/53 cm/s).

In CCA occlusion, two patterns may be observed:

• Complete CCA, ICA, and ECA occlusions resulting in totally absent ﬂ ow signals.

• Proximal CCA occlusion with patency of ICA, ECA, and distal CCA or carotid bulb leading to ICA ﬁ lling by ret- rograde ECA ﬂ ow (Fig. A5.67; see also Video

A5.9).

ECA

ICA

Fig. A5.67 Left: Ce-MRA coronal view revealing a midpart CCA occlusion (arrow). Note the marked ECA ﬂ ow (curved arrow) indicat- ing ﬁ lling of the ICA. There is only a mild decrease of ICA diameter, which suggests a good collateral ﬁ lling (arrows). Right: Extracranial duplex. Color-mode image, longitudinal plane and Doppler spectrum analysis: Top: Retrograde ECA ﬂ ow (90/45 cm/s). Bottom: Antegrade ICA ﬁ lling (56/18 cm/s). Both vessels show a marked poststenotic ﬂ ow pattern. Note the bidirectional ﬂ ow in the distal CCA, also ﬁ lled up by the ECA (arrowhead).

In the latter, the retrograde ECA ﬂ ow either derives from ipsilateral VA anastomoses or from ECA anastomoses, e.g., via the superior thyroid artery, and its anastomoses to the contralateral ECA may be observed. In distal CCA occlusion, thrombus formation starting from the occlusion site advances in a stepwise manner toward the CCA origin at the aortic arch. For further details of CCA occlusion, see Case 3 and Case 30.

ECA Stenosis and Occlusion

ECA stenoses and occlusions are usually of little clinical relevance. Only in severe steno-occlusive ICA disorders might a hemodynamically relevant ECA stenosis be of interest, if it serves as a collateral pathway via a retrograde OA. Then it might not only have a direct eﬀ ect on cerebral perfusion but might also be a possible source of cerebral emboli. Patients being considered for extra-intracranial bypass surgery, e.g., in extracranial ICA occlusion, also require diligent ECA evaluation. If the ECA is already activated as a collateral (via a retrograde OA), an ECA bypass operation cannot be performed. For ultrasound evaluation of ECA stenoses the same general diagnostic criteria as in ICA stenosis can be applied. Main stem ECA stenoses can be graded according to the peak systolic velocity into moderate (140 ± 49cm/s) and high-grade stenoses (230 ± 95 cm/s) (Päivänsalo et al 1996). High ﬂ ow velocities may, however, also be found in nonpathologic conditions and should therefore be interpreted with caution. Only

Fig. A5.68 Left: Doppler spectrum analysis with a turbulent ﬂ ow signal and increased velocity in moderate ECA stenosis (ﬂ ow veloci- ty 190/20 cm/s). Right: Corresponding color-mode image. Aliasing phenomenon at the ECA origin. Note the superior thyroid artery (arrow).

if an evident lumen reduction or spectral broadening and turbulence are visible a stenosis can be diagnosed (Fig. A5.68). In hemodynamically relevant ECA stenoses a poststenotic ﬂ ow pattern has to be present (Fig. A5.69). ECA occlusions are usually well compensated for by the available collaterals and might easily be overlooked if distal segments are aﬀ ected and the main stem is spared.

Extracranial Posterior Circulation

VA Stenosis

V0/V1-VA: The origin of the VA is considered to be the second most common location of atherosclerotic s t e n o s i s . I n c o n t r a s t w i t h t h e I C A o r i g i n , h o w e v e r , t h e

134 5 Vascular Pathology

Fig. A5.69 Left: DSA, elective CCA injection, lateral view, revealing a pronounced ECA stenosis (arrow). Right: Ex tr ac ra ni al du pl ex of t he ECA, longitudinal plane, Doppler spectrum analysis on the left, corresponding color-mode image on the right. Top: Intrastenotic turbulent ﬂ ow and increased velocity (350/88 cm/s). Note the tapping eﬀ ects assuring the ECA insonation. Middle: Serrated ﬂ ow signal indicating proximal high-grade stenosis. Bottom: Poststenotic ﬂ ow pattern further distal of the stenosis.

Fig. A5.71 Left: Contrast-enhanced MRA, oblique projection: VA origin stenosis (yellow circle). Right: Extracranial duplex. Top: Longitudinal plane, color-mode image of the SA, V0-VA, and V1-VA. Note the color-aliasing at the VA origin (arrow). Bottom: Doppler spectrum analysis, intrastenotic ﬂ ow velocity 134/43 cm/s, meas- ured with angle correction because of the straight vessel course.

Fig. A5.70 VA o rig in (yel low cir cle) . Left: Contrast-enhanced MRA, coronal MIP aggravating a stenosis at the VA origin. Right: CTA, coronal MIP demonstrating a calciﬁ ed plaque but no relevant stenosis. (Duplex sonography of VA origin was not possible because of its deep origin from the SA.)

VO-VA

V1-VA

Fig. A5.72 Extracranial duplex, longitudinal plane: Left: Colormode image of the V0-VA and V1-VA segments. Note the color-aliasing at the VA origin (arrow). Right: Top: Doppler spectrum analysis and color-mode image of the V0-VA segment: 186/19 cm/s. Bottom: V1-VA segment distal to the stenosis: 64/25 cm/s with a mild poststenotic ﬂ ow pattern. Velocity ratio: 2.9. Considering the criteria of Hua et al (2009) a ≥50% stenosis can be assumed. Note the problematic angle correction in the elongated vessel segment.

V0/V1 segment is less easily accessible to duplex ultrasound due to its anatomic location behind the clavicle (for further details, see Chapter 2, “V0/V1 Segment” under “Special Arterial Anatomy and Ultrasound Anatomy”). This may be the main reason why established ultrasound grading criteria are missing. Compared with ce-MRA and CTA, duplex ultrasound is clearly less sensitive in detecting a stenosis of the VA origin (Khan et al 2009). MRA tends to overestimate VA stenosis or to consider a stenosis in an otherwise normal vessel (Fig. A5.70). Even in those cases with an ultrasound-detectable VA origin, plaque visualization or measurement of vessel diameter is usually not possible. In terms of the multiparametric approach to grading stenoses de-

scribed earlier, raised velocities and intrastenotic ﬂ ow turbulences may be observed in stenosis even below 50%. Poststenotic ﬂ ow patterns, especially an increased AT, can be expected in hemodynamically relevant stenoses of more than 70–80% which may become more obvious in more distant VA segments (see Fig. A5.44). In hemodynamically relevant stenosis, a secondary distal VA ﬁ lling may be observed via small cervical branches of the ECA (see also “VA Occlusion” under “Extracranial Pathology” below). If either both VAs have a large caliber or a stenosis occurs in a unilaterally hypoplastic vessel, a marked increase of ﬂ ow velocity may be absent as the contralateral or dominant VA compensates for it. In contralateral VA hypoplasia or when the contralateral VA

135Arterial Pathology

Fig. A5.73 (A) Contrast-enhanced MRA, lateral projection: V2VA s teno sis (ar row) . (B,C) Extracranial duplex, longitudinal plane. (B) Color-mode image and Doppler analysis proximal to the stenosis (ﬂ ow velocity 76/17 cm/s). (C) Color-mode image and Dop- pler analysis within the stenosis (ﬂ ow velocity 319/61 cm/s). The velocity ratio (pre- and intrastenotic) is 4.2. Also note the mildly increased prestenotic pulsatility, altogether indicating a hemodynamically relevant stenosis of at least 70–80%. A poststenotic vessel segment was not studied.

Fig. A5.74 Extracranial duplex of the V2-VA, longitudinal plane, Doppler spectrum analysis on the left, corresponding color-mode image on the right. Top: Intrastenotic turbulent ﬂ ow and increased velocity (295/49 cm/s) in the proximal V2-VA between the transverse processes of C5 and C6. Middle: ser rated ﬂ ow signal between C4 and C5 (93/24 cm/s). Bottom: Mild poststenotic ﬂ ow pattern (increased AT, decreased PI) between C3 and C4 (67/24 cm/s) indicative of a hemodynamic relevant proximal high-grade stenosis.

Fig. A5.75 Extracranial duplex, longitudinal plane, color-mode image and corresponding Doppler spectra in V0/V1 occlusion. (A) Absent color ﬁ lling and absent Doppler spectrum in the V0-VA segment. (B) Normal color signal and Doppler spectrum of the SA in the same patient.

has a PICA termination without relevant BA communication, the speciﬁ c criteria of stenosis should be eﬀ ective (Fig. A5.71 and Fig. A5.72). Several groups have published reference data for proximal VA stenosis, usually comparing them with results from conventional angiography; the largest set included 247 proximal VA segments. Best correlation was found with the peak systolic velocity yielding an accuracy of 94.5%, 96.2%, and 88.7% for the diagnosis of <50%, 50–69%, and 70–99% stenosis. The velocity ratio comparing the intrastenotic systolic ﬂ ow velocity and the velocity in the V2 segment may also be helpful (Hua et al 2009).

The reported cut-oﬀ values were:

• <50% stenosis: ≥85 cm/s, ratio ≥1.3

• 50–69% stenosis: ≥140 cm/s, ratio ≥2.1

• 70–99% stenosis: ≥210 cm/s, ratio ≥4.0.

Lower thresholds for the assessment of a ≥50% stenosis with a peak systolic ﬂ ow velocity of 114 cm/s and 108 cm/s have been reported by other groups (Koch et al 2009b, Yurdakul and Tola 2011). For further details, see Case 12, Case 23, and Case 45.

V2-VA: Stenoses of the V2-VA segment are rare, but in contrast to the VA origin (V0 segment) they are usually well accessible to duplex ultrasound. Because of this segment’s deep location and the small vessel size, it is not possible to measure the diameter or cross-sectional area in most instances. For assessment of stenosis, identical criteria as for the V0-VA segment are applied. Angle correction is usually possible and should be applied (Fig. A5.73; see also Video

A5.10). Evaluation of the prestenotic V1-VA segment as well as of the poststenotic vessel segment should be attempted and is feasible in most cases (Fig. A5.74). To assess the dimension of the stenosis, the velocity of the proximal VA can b e r ecor ded t o c alculat e a pr e- a nd in trast enot ic ratio (Alexandrov 2013).

V3-VA: Similar criteria apply to V3-VA stenoses which occur more frequently than those in the V2-VA segment especially in dissection but also in atherosclerotic pathologies. Exact angle correction is usually not possible because of its tortuous vessel course.

136 5 Vascular Pathology

Fig. A5.76 (A) DSA, selective SA ﬁ lling, posteroanterior view: Proximal VA occlusion (arrow). (B–D) Extracranial duplex, longitudinal plane, proximal V2-VA segment. (B) B-mode image: Typical image constellation with bilateral acoustic shadowing from the transverse processes between C5 and C6 and the hypoechoic signal of the VA. Dashed line: Estimated VA diameter. (C) Colormode image demonstrates a missing color-ﬂ ow signal within the occluded VA but a preserved ﬂ ow signal in the vertebral vein. Long and short dashed lines: Initially estimated and real diameter of the VA, re spec tiv ely. (D) Doppler spectrum of a normal vertebral vein.

VA Occlusion

The analysis of VA occlusions requires speciﬁ c anatomic knowledge to avoid diagnostic errors. In general, proximal and distal VA occlusions should be distinguished. The latter should be further separated into occlusion sites above or below the PICA origin. As in the diagnosis of ICA occlusion, an occluded vessel might be depicted by colormode sonography with absent color and Doppler signals (Fig. A5.75). Within the V1- and V2-VA segments the usually preserved blood ﬂ ow of the concomitant vertebral vein might be an additional diagnostic aid (Fig. A5.76).

In contrast with the extracranial ICA, which does not show secondary ﬁ lling from extracranial collaterals, the VA h as n um er ou s s egm en ta l c er vi ca l a na st om os es a t al l levels of its extracranial course which potentially serve as collaterals and usually prevent occlusion over its entire length. These are anastomoses from the thyrocervical trunk and muscular rami of ECA branches, especially from the occipital artery. Rarely, spinal rami of the contralateral VA al so p ar ti ci pa te in t he co ll ate ra l b lo od s up ply . I n c as e of a proximal VA occlusion these collaterals, depending on their quantity and quality, may cause a secondary VA ﬁ lling with “postocclusional” VA ﬂ ow of varying mag- nitude detectable in the distal VA segments (Fig. A5.77, Fig. A5.78, Fig. A5.79). In the presence of two equivalent VAs, the above-mentioned collateral pathways are rarely of importance as the contralateral VA will provide the blood supply to the posterior circulation and also retrograde via a vertebro-vertebral overﬂ ow toward the PICA of the af- fected VA. However, in case of contralateral VA hypoplasia or PICA termination, the extracranial anastomoses become relevant. The distal VA ﬂ ow is then usually anterograde with a typical poststenotic ﬂ ow pattern. Although the term “poststenotic” seems slightly inaccurate in a vessel segment distal to an occlusion, we suggest its use nevertheless, as it clearly illustrates the common problem of hemodynamic impairment in stenoses and occlusions.

Fig. A5.77 Left: DSA, selec tive t hyro cer vic al t runk ﬁ lling, LAO view. Proximal VA occlusion. Secondary segmental collateral ﬁ lling of the V2- and V3-VA segments from numerous muscle anastomoses. 1, 2, and 3 indicate corresponding VA segments in the duplex images. (1–3) Extracranial duplex, longitudinal plane. (1) V2-VA with minimal systolic and absent diastolic ﬂ ow; (2) Muscle branch anastomo- sis (ﬂ ow velocity 25/10 cm/s); (3) V3-VA with a poststenotic ﬂ ow pattern and low ﬂ ow velocities of V3-VA (ﬂ ow velocity 16/5 cm/s).

Fig. A5.78 Left: Ce-MRA, coronal MIP, anterior and oblique projection: Bilateral proximal VA occlusion with secondary V2- and V3-VA segmental ﬁ lling (mainly on the left side) from muscle anastomoses via the thyrocervical trunk. Right: Extracranial duplex, longitudinal plane, color-mode images with corresponding Doppler spectra. 1 Proximal V2-VA with minimal ﬂ ow: 10/3 cm/s; 2 Muscle branch anastomosis corresponding to the visible MRA branches, ﬂ ow ve- locity: 52/23 cm/s; 3 Distal V2-VA with poststenotic ﬂ ow pattern: 28/9 cm/s. In this case the PCA territories are fed by the PCoA of both sides (not shown).

A distal extracranial VA occlusion proximal to the PICA origin in contrast causes a stump signal, a highly pulsatile ﬂ ow signal with absent end-diastolic ﬂ ow or a biphasic or triphasic waveform comparable to an ECA branch, as its communication to these vessels usually remains open (Fig. A5.80). Again, it is important to mention that the en- tire length of the VA up to the occlusion site remain open because of the rope ladder–like anastomoses with ECA branches. In a study including 10 distal VA occlusions proximal to the PICA origin, all subjects had an open V2-VA with

137Arterial Pathology

Fig. A5.79 Left: DSA, selective right VA ﬁ lling, posteroanterior view. Occlusion of left proximal VA. The right VA ends as posterior inferior cerebellar artery. Note the secondary collateral ﬁ lling of the left VA via numerous segmental spinal anastomoses from the right VA (arrows). Right: Extracranial duplex, longitudinal plane, color-mode image and corresponding Doppler spectra. 1 Proximal left V2-VA (ﬂ ow ve- locity: 18/9 cm/s); 2 Left midpart V2-VA (ﬂ ow velocity: 22/10 cm/s);

3 Distal left V2-VA (ﬂ ow velocity: 27/10 cm/s). Note the improving ﬂ ow in distal segments with increasing number of collaterals.

a diastolic zero ﬂ ow (Saito et al 2004). Not only from a ra- diologic point of view but also considering clinical aspects, it has to be emphasized that the term “VA occlusion” alone is not suﬃ cient but has to be complemented by the exact location of the occlusion and the information about possible secondary VA ﬁ lling by collaterals distal to the occlusion. For further reading, see also Case 19, Case 35, and Case 41.

A special and rare condition aﬀ ecting the middle or

distal VA has to be mentioned. In the so-called “bowhunter syndrome” occlusion or stenosis of one VA occurs during head rotation. In case of a contralateral occlusion, hypoplasia, or PICA-ending VA variant without collateral ﬂ ow through one or both PCoAs, vertebrobasilar ischemia may occur. Patients usually report dizziness or vertigo, and also sensorimotor symptoms during head rotation. Ultrasound during head rotation may then show dynamic ﬂ ow changes with either stepwise reduced blood ﬂ ow velocities or even signal loss in the PCA, BA, or VA (Iguchi et al 2006, Sturzenegger et al 1994).

SA Proximal Stenosis and Occlusion

Direct signs of a hemodynamically relevant SA stenosis >50% are, as in all other arteries, raised ﬂ ow velocities and a turbulent ﬂ ow, which is often diﬃ cult to directly assess. In stenoses >70–80% and in proximal SA occlusion indirect hemodynamic signs can be observed within the d e p e n d e n t a x i l l a r y , b r a c h i a l , a n d r a d i a l a r t e r i e s . T h e s e v e s sels then show a poststenotic ﬂ ow pattern, i.e., a delayed systolic ﬂ ow rise, reduced ﬂ ow velocities, and a change from the typical triphasic ﬂ ow proﬁ le to a bi- or monopha- sic ﬂ ow signal. If a biphasic waveform is present on both sides the interpretation should be more cautious. A characteristic and pathognomonic sign of proximal high-grade SA stenosis or occlusion is a ﬂ ow alteration within the ipsilateral VA, which may serve as collateral for the blood supply of the arm. The ﬁ nding is called a “subclavian steal phenomenon” if no clinical signs are present. If there are

Fig. A5.80 Left: DSA, selective VA ﬁ lling, lateral view: Distal V3-VA o c c l u s i o n ( a r r o w ) . N o t e t h e o n l y o u t ﬂ ow pathway via a muscle supply- ing arterial branch presumably from the occipital artery. Right: Extracranial duplex of V2-VA with normal diameter of 4.0 mm (contralateral side 3.8 mm, not shown), longitudinal view: preserved color signal but highly pulsatile ﬂ ow on Doppler spectrum analysis with small retro- grade ﬂ ow component and no end-diastolic ﬂ ow (58/0 cm/s) indicat- ing that this vessel does not participate in brain perfusion and strongly suggestive of VA occlusion proximal of the PICA origin.

cerebral or brachial symptoms the term “subclavian steal syndrome” should be used (Fig. A5.81 and Fig. A5.82). The left side is mostly aﬀ ected in a ratio of ~4:1; this is usually explained by the acute angle of origin of the left SA which increases ﬂ ow turbulence and accelerates atherosclerosis (Labropoulos et al 2010, Nicholls et al 1991). In patients with the rare variant of a left VA originating directly from the aorta, no subclavian steal can be observed.

Three main grades of hemodynamic compromise can be distinguished which in part depends on the grade of SA stenosis: 1, a reduced systolic ﬂ ow (systolic deceleration); 2, an alternating (biphasic) ﬂ ow with the retrograde ﬂ ow in the systolic phase; and 3, a constant retrograde ﬂ ow in the ipsilateral VA may be observed. According to the extent of the collateral ﬂ ow the subclavian steal can be graded as grade 1, incipient; grade 2, incomplete; and grade 3, complete (Fig. A5.83 and Fig. A5.84). For further reading, see Case 23 and Case 28.

Brachiocephalic Trunk Stenosis (BCT)

Occlusive disorders of the brachiocephalic trunk (BCT) also called the brachiocephalic or innominate artery, are rare, occurring in less than 0.1% of patients routinely examined in a large Doppler laboratory (Brunhölzl and von Reutern

1989). Duplex ultrasound usually reveals a complete or partial steal phenomenon in the right VA and varying hemodynamic consequences in the right-sided carotids (CCA, ICA, ECA) (Fig. A5.85). A study including 12 patients with a BCT stenosis >70% diagnosed by catheter or MR angiography reported a complete resting VA ﬂ ow reversal (steal grade 3) in eight patients and a bidirectional ﬂ ow (steal grade 2) in the remaining four. Complete reversal of carotid ﬂ ow was seen in one patient only. A systolic deceleration (steal grade

1) in at least one of the carotid arteries was seen in all remaining 11 patients, mainly observed in CCA (8/11 = 73%), ICA (10/11 = 91%), and ECA (3/11 = 27%). No correlation was seen between degree of stenosis and the Doppler ﬁ ndings

138 5 Vascular Pathology

Fig. A5.81 Schematic of the two main variants of collateral ﬂ ow in case of a subclavian steal phenomenon. (A) Vertebro-vertebral overﬂ ow (regular type). (B) ICA-VA overﬂ ow (in cases with addition- al contralateral VA pathology). Further rare collateral variants have been described with conventional angiography, diﬃ cult to assess with ultrasound.

SA-R

V2-V

A-R

V2-VA-L

SA-L

Fig. A5.82 Subclavian steal phenomenon in left proximal SA occlusion. Left: DSA, selective right VA ﬁ lling, posteroanterior view. Ver- tebro-vertebral contrasts overﬂ ow from right to left. Right: Doppler spectrum analysis. SA-R: Right SA with normal triphasic ﬂ ow signal. V2-VA-R: Strong antegrade VA signal. V2-VA-L: Retrograde verte- bral ﬂ ow, which corresponds to a complete subclavian steal phe- nomenon grade 3. SA-L: Monophasic poststenotic distal SA signal.

Increasing proximal subclavian stenosis/occlusion

Fig. A5.83 (A,B) V2-VA duplex sonography, longitudinal plane, color-mode image, revealing an alternating ﬂ ow signal with a ret- rograde systolic ﬂ ow (A) and an antegrade diastolic ﬂ ow (B) in the aﬀ ected V2-VA corresponding to an incomplete subclavian steal phenomenon grade 2. (C) Corresponding Doppler spectrum showing the biphasic ﬂ ow during three cardiac cycles.

by this group (Grant et al 2006). Other authors proposed a classiﬁ cation according to the severity of hemodynamic changes. Type I presents a steal phenomenon (grade 1 or 2) in the right VA and minor changes in the carotid arteries, type II shows at least a grade 2 VA steal and a grade 1 steal in the carotid arteries, and for type III an additional carotid steal grade 2 or 3 has to be present (Brunhölzl and von Reutern 1989). Patients have a high incidence of clinical manifestations ranging from 50 to 75% and referable to both the posterior circulation (syncope and cerebellar infarcts) and the anterior circulation (right-sided amaurosis fugax or stroke) which may partly be explained by concurrent ipsilateral ICA disease (Brunhölzl and von Reutern 1989, Grant et al 2006). In patients with sustained clinical symptoms, stenting or angioplasty of the stenosis may be a therapeutic option (van Hattum et al 2007).

Systolic

Fig. A5.84 Ta bl e o f V 2-V A D op p le r ﬂ ow spectrum ﬁ ndings in in- creasing grade of subclavian steal (grades 1–3). N = normal.

slowing

Grade 1:

beginning

subclavian steal

Alternating

flow

Grade 2:

incomplete

subclavian steal

Retrograde

flow

Grade 3:

complete

subclavian steal

Intracranial Pathology

Stenoses

Intracranial atherosclerosis (ICAS) is the leading cause of stroke worldwide as it is of greater importance in Asian populations compared with the white population (Gorelick et al 2008). ICAS has been estimated to account for 40–60% of stroke and TIA in Asian populations (J.T. Kim et al 2006, Wong 2006). In asymptomatic subjects, the prevalence of MCA stenosis as one vascular risk factor was found to be as high as 12.6% (Wong et al 2007). In Asian stroke patients, the prevalence of intracranial stenosis is twice as high as the prevalence of extracranial stenoses (Tan et al 2005). Black people also seem to have a high prevalence of intracranial lesions (McGarry et al

1985). However, even in white people ICAS was seen

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