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116 CAROTID TREATMENT: PRINCIPLES AND TECHNIQUES
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3-21
Complication—External
Carotid Artery Dissection
This single AP radiograph of a CCA injection was taken on the third post-operative day. The dilation of the
arterial repair from plaque removal with a thin residual arterial wall can readily be seen. This arteriogram was
performed when the patient experienced a single post-operative transient ischemic attack, and dissection of the
ECA is demonstrated. This dissection is the consequence of inadequate plaque removal in the ECA at the time of
arteriotomy and arterial repair. As mentioned earlier in the text, I do not hesitate at present to perform a separate
ECA arteriotomy and endarterectomy when I am dissatised with marsupialization of the plaque from the ECA.
When this is not done and a plaque remnant is left behind with a loose leading edge, an arteriogram such as this
can be the consequence. Although in most cases this is a benign occurrence and has not been considered justication for re-operation, I am familiar with one case in which an ECA dissection led to thrombosis of the common
and internal carotid arteries 10 days post-operatively, followed by a major and irreversible stroke. I have thus
developed a very low threshold for ECA arteriotomy and repair, and this technique is illustrated in Figs. 4-67 to
4-71, 4-82, 4-83, and 4-93.
CHAPTER 3: RADIOGRAPHIC STUDIES 117
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(From Loftus CM. Surgical management options to prevent ischemic stroke. Neurosurgery Quarterly 4(1): l–38, 1994.)
118 CAROTID TREATMENT: PRINCIPLES AND TECHNIQUES
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3-22
Morphology and Plaque Content
Satoshi Kuroda
Until recently, pre-operative diagnosis of carotid artery stenosis was mainly based on cerebral angiography (1).
Subsequently, non-invasive MR angiography in the 1990s and 3D CT angiography in the 2000s with the advent
of multi-sector CT systems can be used as an alternative to cerebral angiography. Because patients with carotid
artery stenosis have more complications from cerebral angiography, such as cerebral infarction, than patients
with other diseases, the widespread use of MR angiography and 3D CT angiography is extremely useful for
safe examination (2). However, the main purpose of all of these examination modalities has been to obtain morphological imaging information, such as plaque shape, presence or absence of ulcers, and degree of stenosis. In
particular, the degree of stenosis is a gold standard that has been used as a surrogate marker for inclusion criteria
and stratication in almost all randomized clinical trials conducted since the 1980s.
On the other hand, it has been widely known for many years that the nature of plaque content, in addition to morphological information, plays a crucial role in the pathogenesis of TIA and ischemic stroke. Thus,
approximately 20% (14/67) of cases of moderate stenosis (30%–69%) are symptomatic (3), and irregular plaque
shape and intra-plaque hemorrhage (IPH) are important factors in determining the occurrence of cerebrovascular events (3–5). In addition, some of these cases may have repeated cerebrovascular events unless CEA or other
measures are performed (6, 7). Based on a pooled analysis of RCTs for CEA, Rothwell et al. proposed a prediction score of the occurrence of ipsilateral stroke by using gender, degree of stenosis, plaque shape (irregular or
ulceration), and time since onset in 2005 (8).
Carotid Ultrasound
Until recently, the only modality that could visualize the nature of the plaque content was ultrasound. It is known
that ultrasound imaging can differentiate the nature of the plaque content by differences in plaque echogenicity.
Carotid ultrasonography is non-invasive and can be performed repeatedly at the bedside. Mainly, B-mode and
color Doppler mode can be used to assess plaque size, shape, surface, brightness, mobility, and blood ow velocity. The laminar structure observed between the arterial lumen and the outer membrane is an intima-media
complex, and the intima-media thickness (IMT) is normally less than 1 mm. IMT is known useful to predict the
severity of atherosclerosis in the whole body, and the thickened IMT is a risk factor for myocardial infarction (9).
A variety of drugs have been found to regress the IMT, but a recent systematic review has found that regression
of the IMT does not reduce the risk of myocardial infarction, stroke, or all-cause mortality (10).
Plaques are often classied as low-intensity (hypoechoic or echolucent), iso-echoic, or high-intensity
(hyperechoic). An acoustic shadow is observed in highly calcied lesions. Low-intensity plaques are unstable
plaques with a hematoma or necrotic core and are at high risk for stroke (11). According to a recent meta-analysis
of asymptomatic ICA stenosis, low-intensity plaques are a risk factor for ipsilateral stroke (relative risk 2.31),
regardless of the stenosis rate (12). However, a quantitative scale would be essential to determine echogenecity
of the plaque. Plaques with ulcers, plaques with irregular surfaces, and plaques with uneven interiors are also
at high risk of developing stroke (13). Ultrasonography is superior in its ability to assess plaque mobility due to
its high time resolution. Plaque mobility is associated with the development of stroke (14). Cases with mobile
plaques have been found to have larger areas of necrotic core and are more likely to suffer recurrent and progressive strokes (15). However, the disadvantage of ultrasonography is that the results of ultrasonography can be
inuenced by the examiners and there is a large amount of variability in the interpretation of the results.
Plaque MRI
Since the mid-1990s, plaque imaging using MRI has been challenged, because of its high spatial resolving
power, which makes it useful to observe the presence and thickness of necrotic core, IPH, and brous cap (16).
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FIGURE 3-22
Representative MR ndings and intra-operative view during CEA. (A) Note that the lesion with iso-intensity on T1-weighted image (T1WI,
arrow) and source image of time-of-ight (SI-TOF, arrow) most likely represents brous plaque. (B) Note that the lesion with high intensity
on T1WI (arrow) and iso-intensity on SI-TOF (arrow) represents lipid-rich plaque with necrotic core. (C) Note that the lesion with high intensity on T1WI (arrow) and SI-TOF (arrow) represents unstable plaque with IPH.
Althougha variety of imaging methods have been reported, the imaging ndings of MRI are known to greatly
vary depending on the imaging method: in the case of T1-weighted images (T1WI), spin-echo technique without ECG coupling results in a high signal intensity of the plaque in the order of IPH, necrotic core, and brous
plaque, which is the most reliable way to differentiate these three types of plaques. On the other hand, magnetization-prepared rapid acquisition with gradient echo (MPRAGE) and 3D-TOF MRA source image (SI-MRA)
reduces its diagnostic accuracy. Thus, although the signal strength of the IPH is strong, the signal intensity of
the necrotic core and brous plaque is approximately equal, making it difcult to differentiate the vulnerable
necrotic core from the stable brous plaque (17). A combination of T1WI and SI-MRA can provide a sensitive diagnosis of plaque characteristics (18). Representative MR ndings and intra-operative photographs are
presented in Fig. 3-22.
Recent reports have shown that the nature of the plaque content is closely related to the occurrence of
cerebrovascular events. Thus, symptomatic moderate (30%–69%) ICA stenosis predisposes patients with IPH
on MRI to recurrent ipsilateral cerebral infarction or TIA (19); plaques with a high signal on T1WI and SI-MRA
are at high risk for embolic complications during CAS (20, 21). Dynamic contrast-enhanced MRI is useful in
detecting the development of vasa vasorum in the outer membrane and correlates with the presence of IPH (22).
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FIGURE 3-23
This diagram demonstrates the relationship among % stenosis, plaque content, cerebral hemodynamics, and localization of cerebral infarct
in patients with carotid artery stenosis (see the text).
Kashiwazaki et al. (2015) precisely analyzed the ndings on diffusion-weighted images, plaque MR images, and
cerebral blood ow (CBF) images in 48 patients with TIA/ischemic stroke due to carotid artery stenosis. As the
results, cortical infarction (n = 18) was closely related to lipid-rich plaque or IPH, suggesting that artery-to-artery
embolism played a key role in the occurrence of cerebrovascular events. Borderzone infarction (n = 3) was signicantly associated with hemodynamic insufciency, i.e., reduced CBF and cerebrovascular reactivity (CVR) to
acetazolamide (see later). On the other hand, mixed-type infarction (n = 17) was characterized by both of factors
(Fig. 3-23). The results strongly suggest that the combination of MRI and blood ow study such as SPECT and
PET would allow us to specify the mechanism of TIA/ischemic stroke and determine ideal treatment strategy in
individual patients with carotid artery stenosis (18).
18
F-Fluorodeoxyglucose (FDG) PET
The role of inammation in atherosclerosis has received much attention in recent years. Because the activated
macrophages in the plaques have high glucose metabolism, 18F-FDG PET can non-invasively detect plaques with
high inammation (inamed plaques) (23). In fact, carotid plaques with a high accumulation of 18F-FDG are
lipid-rich plaques with a necrotic core and a large number of histologically activated macrophages (Fig. 3-24); the
diagnostic rate of lipid-rich, inamed plaque is even higher when 18F-FDG PET is combined with plaque MRI(24).
CEREBRAL HEMODYNAMICS
15
O Positron Emission Tomography (PET)
PET is often used to assess cerebral perfusion pressure (CPP) or cerebral circulatory reserve, mainly in patients
with severe stenosis (>70%) or occlusion of the major cerebral arteries. PET has the advantage of measuring cerebral oxygen extraction fraction (OEF) in occlusive carotid artery diseases. However, the use of 15O-PET requires
the installation of a cyclotron in the facility and is not feasible in all hospitals.
The utility of PET in occlusive carotid diseases was strongly recognized in 1981 when Baron et al. rst
reported a case of misery perfusion syndrome (25). Since then, the stage classication proposed by Powers
et al. (26), using CBF, cerebral blood volume (CBV), and OEF as indices, has been frequently used (Fig. 3-25).
Powers et al. dened the condition as Stage 0, which is characterized by the normal range of CBF, CBV, CMRO2,
and OEF in patients with well-developed collateral circulation, even if the ICA is tightly stenotic. Powers et al.
dened the condition as Stage I, which is characterized by normal CBF, CMRO2, OEF, but elevated CBV because
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FIGURE 3-24
Typical ndings of unstable, inamed carotid plaque. Plaque MRI strongly suggests the presence of lipid-rich plaque with necrotic core
on T1-weighted image (T1WI, arrow) and source image of time-of-ight (SI-TOF, arrow). 18F-uorodeoxyglucose (FDG) PET/CT reveals
high accumulation of 18F-FDG in the plaque. Intra-operative photograph during CEA clearly shows that the plaque is fragile and lipid-rich
property. Immunostaining against CD68, which is specic for activated macrophage, detects a huge number of activated macrophages in
the plaque.
compensatory arterial dilation occurs in response to inadequately developed collateral circulation and moderately low CPP. Furthermore, in cases with poorly developed collateral blood circulation, maximum arterial dilation can no longer maintain CPP within the normal range, and CBF start to decrease. In this situation, oxygen
diffusion from the blood to the brain is enhanced above normal, i.e., cerebral oxygen metabolism is maintained
in a compensatory manner by an increase in OEF. Therefore, theoretically, this condition can be identied as a
FIGURE 3-25
Typical 15O-gas PET ndings of Stage-0, Stage-I, and Stage-II patients with right carotid artery occlusion. All parameters are within normal
in Stage-0 patients (upper). In Stage-I patients, CBF is kept normal by autoregulation-induced vasodilatory compensation, which leads to
CBV elevation (arrow, middle). In Stage-II patients, CBF is no longer maintained normal due to poorly developed collaterals, causing CBF
decrease, CBV elevation, and OEF elevation (arrows, lower). OEF elevation can be recognized as metabolic compensation to keep oxygen
metabolism normal.
122 CAROTID TREATMENT: PRINCIPLES AND TECHNIQUES
=× −%CVR 100 (CBFunderloadCBFatrest)/CBFatrest
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reduced CBF, elevated CBV, normal CMRO2, and increased OEF, which is dened as Stage II. This condition is
believed almost identical to misery perfusion syndrome reported by Baron et al. (25).
Elevated OEF is a strong parameter to predict an increased risk of recurrent stroke. Two independent studies have proven that patients with elevated OEF due to carotid artery occlusion are about 6–7 times more likely
to suffer recurrent ipsilateral ischemic stroke than those without (27, 28).
Single Photon Emission Tomography (SPECT)
SPECT differs from PET in that it uses radioisotopes with relatively long half-lives, such as
99m
Tc, and can be performed in many hospitals. SPECT is often used to quantify acetazolamide CVR as well
133
xenon,
123
I, and
as resting CBF in patients with occlusive carotid diseases. Acetazolamide (ACZ) rapidly increases CBF within
2 minutes after intravenous infusion and has a maximum increase in CBF after 10–25 minutes (29). Rapid intravenous infusion of ACZ inhibits the action of carbonic anhydrase (CA) in erythrocytes within 1 minute, which
inhibits the transport of CO2 from the brain, causing the brain tissue to become acidotic, and nally induces
the dilation of arterioles; ACZ decreases extra-cellular pH by 0.2, a phenomenon equivalent to a 15–18 mmHg
increase in arterial blood CO2 pressure (PaCO2) (29).
Since Vorstrup et al. (30) reported that the measurement of ACZ reactivity can accurately detect hemodynamically compromised ischemia even with SPECT, this test method has been widely used. In most cases, ACZ
reactivity can be calculated quantitatively with the following equation.
In the late 1980s, Kuroda et al. proposed a simple and easy-to-understand classication method to classify
patients into four types based on the quantitative values of CBF and CVR (31–34). Representative ndings on
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I-IMP SPECT are shown in Fig. 3-26. In Type-1 cases, CPP is nearly normal due to well-developed collateral
blood vessels, and CBF and CVR are both within the normal range, almost identical to Powers’ Stage 0. On the
other hand, in cases with inadequate collateral blood vessels, a moderate reduction in CPP induces autoregulatory vasodilation to compensate the reduced CPP, leading to normal CBF but reduced CVR on SPECT (Type 2).
This is considered almost identical to Powers’ Stage I on PET. Furthermore, in cases with even more inadequate
development of collateral blood vessels and highly reduced CPP, vascular compensation fails to maintain CBF,
and CBF is dependent on a decrease in CPP. In such cases, both CBF and CVR may be reduced on SPECT
FIGURE 3-26
123
Typical
normal limits in Type-1 patients. Only CVR is reduced in Type-2 patients (arrows). Both CBF and CVR are decreased in Type-3 patients
(arrows). On the other hand, only CBF is decreased, while CVR is kept normal in Type-4 patients (arrow).
I-IMP SEPCT ndings of Type-1, Type-2, Type-3, and Type-4 patients with left carotid artery occlusion. Both CBF and CVR is within
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FIGURE 3-27
Radiological ndings of a 78-year-old male with left severe (>90%) carotid artery stenosis. At onset, he had no cerebral infarct. Blood ow
studies revealed that he had Stage-II and Type-3 ischemia in the whole cerebral hemisphere on the left side, especially temporo-parietal lobes
(arrows). One month later, he suffered serious ischemic stroke in the left temporo-parietal lobes with Stage-II and Type-3 ischemia at initial
presentation.
(Type3). Finally, in the area of reduced CBF and normal CVR (Type 4), the following results have been found: (1)
transient and eventual improvement in CBF after revascularization, (2) minimal recurrence of ischemic stroke
during medical treatment, (3) normal range of OEF and reduced CMRO2 on PET, and (4) reduced neuronal
integrity on 11C-umazenil PET. This indicates that the Type-4 region is a “matched hypo-metabolism” in which
metabolic demand has already been reduced due to reduced neuronal density (Kuroda et al., 1993 [32]; Kuroda
et al., 2001 [33]; Kuroda et al., 2004 [34]).
Like OEF on PET, CBF, and CVR are useful parameters to predict the risk of recurrent stroke. In cases of
internal carotid or middle cerebral artery occlusion, patients with Type-3 ischemia have an eight fold higher
risk of recurrent ipsilateral cerebral infarction than other patients (33). A representative case is presented. This
78-year-old man, who presented with a TIA, was diagnosed with severe stenosis of the left ICA. 15O-gas PET
showed decreased CBF and increased OEF throughout the left cerebral hemisphere (misery perfusion syndrome). In addition,
123
I-IMP SPECT also showed decreased CBF throughout the left cerebral hemisphere, as well
as decreased CVR (Type 3). However, while waiting for CEA to be performed, the patient had a large recurrent
stroke in the left temporal to parietal lobe, where the OEF was elevated and the CVR was reduced (Fig. 3-27).
Hyperperfusion Syndrome after CEA/CAS
In recent years, it has become clear that post-operative hyperperfusion after CEA/CAS may occur more frequently than previously considered. Post-operative hyperperfusion may be silent in some cases, but when it
becomes symptomatic, it readily causes migraine-like headache, facial and ocular pain, seizures, and focal cerebral hemispheric symptoms (so-called hyperperfusion syndrome). In the most severe cases, intra-cerebral hemorrhage may occur, which can be fatal. A typical case is shown in Fig. 3-28.
Recent studies have revealed the frequency of hyperperfusion syndrome following CEA/CEA: cerebral
hemorrhage or hyperperfusion syndrome occurred in 5 of 450 patients (1.1%) who underwent CAS (35). According to a joint study in Japan, the frequency of the hyperperfusion syndrome after CEA/CAS procedures was
1.9% and 1.1%, respectively. Intra-cerebral hemorrhage occurred in about 40% of these cases. The fatality rate of
intra-cerebral hemorrhage is as high as 36%–63% (36). The hyperperfusion syndrome most often appears after
6 days in the case of CEA and within 12 hours in the case of CAS. The occurrence of intra-cerebral hemorrhage
is the same (36). Several factors have been reported as predictors of hyperperfusion after CEA/CAS procedures,
but prolonged, dense cerebral ischemia due to poorly developed collaterals would be most responsible for the
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FIGURE 3-28
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I-IMP SEPCT ndings before and after right CEA in a 68-year-old male with severe (>90%) carotid artery stenosis. Before surgery, both CBF
and CVR were critically reduced in the right cerebral hemisphere. Repeated SPECT just after right CEA demonstrated an abnormal elevation of CBF in the right cerebral hemisphere, suggesting post-CEA hyperperfusion (arrows). He complained of severe headache on the right
side, so systolic blood pressure was strictly controlled below 100 mmHg. His headache gradually resolved, and hyperperfusion completely
disappeared 3 days after surgery.
occurrence of post-CEA/CAS hyperperfusion. Intra-operative monitoring of carotid blood ow, near-infrared
spectroscopy, and transcranial Doppler technique are reported useful to predict the appearance of hyperperfusion. The use of internal shunt and strict blood pressure control are important to reduce the frequency of the
hyperperfusion syndrome and intra-cerebral hemorrhage due to hyperperfusion (36).
For patients at high risk of post-operative hyperperfusion due to poor ipsilateral CBF and CVR, staged angioplasty (SAP), performed a few weeks after angioplasty with a small-diameter balloon, is an effective means to prevent
post-operative hyperperfusion (37). A recent multicenter study in Japan also found a lower frequency of hyperperfusion syndrome in the SAP group (4.4%) than in the usual CAS group (10.5%) and no difference in peri-operative
complications between the two groups (9.8% vs. 9.3%) (38). Please see the section on CAS for precise information.
NON-INVASIVE MRA AND CTA FOR SURGICAL PLANNING
In the past, cerebral angiography was considered as an essential pre-operative examination for treatment planning of CEA and CAS. However, cerebral angiography has been found to have a higher risk to cause cerebral
infarction than previously believed. In patients with carotid stenosis, the risk of cerebral infarction caused by
cerebral angiography has been found to be even higher (39, 40). On the other hand, the image quality and
accuracy of non-invasive MR angiography and three-dimensional CT angiography (3D-CTA) have dramatically
improved in recent years due to the improved performance of MR and CT systems and image analysis software
programs. Therefore, since around the mid-2000s, cerebral angiography has no longer been an essential preoperative examination for CEA and CAS. MR angiography can clearly detect intra-plaque hematoma with a long
T1 time, because MR angiography is often imaged using a time-of-ight technique (Fig. 3-29). In addition, since
CT scan sensitively detects bone and calcication, 3D-CTA is useful in detecting calcication within plaques
(Fig. 3-30). Because the carotid artery bifurcation is higher in Asians than in Europeans and Americans, it is
extremely useful to reconstruct and create a 3D-CTA together with the mandible and cervical vertebrae, so that
the relative position of the distal end of the plaque to the mandibular angle and cervical vertebrae can be ascertained before surgery. If the distal end of the plaque is located above the superior border of the second cervical
vertebra, the anatomical relationship between the plaque and the occipital artery should be checked (Fig. 3-31).
In addition, 3D-CTA is very useful to check the access routes from the femoral to the carotid arteries to
evaluate the anatomical risk of CAS (Fig. 3-32). The 3D-CTA and 3D-DSA are also useful to determine the size of
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FIGURE 3-29
Radiological and intra-operative ndings in a 76-year-old male with left carotid artery stenosis. MR angiography revealed severe stenosis
of the left internal carotid artery due to a high-volume plaque with high signal intensity (arrows). This plaque demonstrated high signal
intensity on both T1-weighted image and source image of time-of-ight (TOF), strongly suggesting that the main component of plaque was
intra-plaque hematoma (arrows). Intra-operative observation conrmed it.
stent and distal lter before CAS by quantifying the diameters of the CCA and the ICA at the most stenotic site
and distal to the plaque (Fig. 3-33). MRI plaque images help us to select the cerebral protection methods in CAS
(Figs. 3-34 and 3-35). A single distal lter protection will be enough for the stable brous plaque. Distal or proximal balloon protection (ow arrest method, Chapter 2) will be more effective for the unstable lipid-rich plaque. If a
large intra-plaque hematoma (most dangerous plaque) is detected, CEA will be rather recommended. If CAS is
necessary, protection by ow reversal method (Chapter 2) should be selected to avoid thromboembolic complication during CAS. Post-operative diffusion-weighted images provide the information of distal embolic ischemic
lesions after CAS (Fig. 3-36).
FIGURE 3-30
Radiological ndings in a 68-year-old male with right carotid artery stenosis. 3D-CTA clearly visualized a markedly calcied plaque of the
right internal carotid artery (arrow). Carotid ultrasound (US) showed typical acoustic shadow (arrow) and enhanced CT scan also demonstrated marked calcication of the right internal carotid artery (arrow).
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