Carotid Artery Revascularization
Fatemeh Malekpour
Gerardo Gonzalez-Guardiola
Sooyeon Kim
Melissa L. Kirkwood
INTRODUCTION
Although the stroke rate among the aging U.S. population has declined over the last decade, stroke remains one of the leading causes of morbidity and mortality in this country. Approximately 795,000 people suffer a stroke each year; in 140,000 of these cases, it results in mortality. In addition, there are roughly 7 million stroke survivors with varying degrees of disability.1 The socioeconomic impact of cerebrovascular accidents (CVAs) has been well-documented. The annual economic burden of stroke is approximately US$34 billion.1 Thus, prevention is the most important aspect of cerebrovascular care.
Approximately 70% of CVAs are caused by ischemia, the majority of which originate from extracranial atherosclerosis leading to shower emboli.1 Other sources of cerebral ischemia include lacunar stroke owing to occlusion of the small perforating arteries (eg, lenticulostriate, thalamoperforating, and pontine perforating) as well as cardioembolic stroke frequently associated with atrial fibrillation or advanced left ventricular dysfunction. Equipped with the knowledge of both medical management and surgical therapies for extracranial cerebrovascular diseases, vascular surgeons are integral members of the health care team.
PATHOGENESIS
Cardiovascular risk factors, such as advanced age, obesity, diabetes mellitus, and hypertension, have been linked to the development of atherosclerosis. These atherosclerotic plaques are subject to constant high-shear stress within this stenotic environment. This leads to macrophage infiltration and lysis, chronic inflammation, plaque ulceration, neovascularization with intraplaque hemorrhage, and thrombus formation. Such progressive changes result in further luminal narrowing, plaque rupture, or occlusion. Ruptured plaques then recruit platelets and procoagulants, such as plasminogen activator inhibitor-1 and tissue factor, leading to thrombus formation and subsequent embolization. Carotid plaque ulceration and thrombus are more prevalent in symptomatic carotid stenosis.2
Atherosclerosis at the carotid bifurcation is the most common source of emboli (38%), followed by cerebral arteries (33%), proximal vertebral arteries (20%), and branch vessels of the aortic arch (9%).3 About 50% of patients with transient ischemic attacks (TIAs) have hemodynamically significant carotid stenosis.4
CLINICAL PRESENTATION
Asymptomatic Carotid Disease
Patients with significant cardiovascular risk factors are at increased risks of developing carotid artery stenosis. Routinely associated physical examination findings, such as carotid bruits, are neither sensitive nor specific for detecting significant carotid artery stenosis. Carotid bruits may be present in approximately 5% of the general population over 50 years of age regardless of the atherosclerotic burden of the carotid artery.5 Only 23% of bruits are found to be associated with hemodynamically significant stenosis.5 Therefore, a carotid Doppler ultrasound is the initial diagnostic modality of choice for the workup of carotid artery disease.
Although routine screening of carotid arteries in the general population is not recommended, when carotid stenosis is detected in asymptomatic patients, about 10% to 15% may progress to severe carotid stenosis (>70%), warranting intervention.6 Surveillance with serial carotid duplex examinations and cardiovascular risk modifications are important in these patients.
Symptomatic Carotid Stenosis
Symptoms indicative of thromboembolic events from the carotid artery or anterior cerebral circulation include hemiparesis, hemianesthesia, transient monocular blindness, or aphasia. Prompt diagnosis and treatment should be a priority when the patients present with such neurologic deficits.
Transient Ischemic Attack
TIA is defined as acute neurologic symptoms lasting less than 24 hours with no irreversible neurologic sequelae. TIAs can present with isolated motor, ocular, or language deficits or a combination. However, isolated sensory symptoms in only part of one extremity or face can be a diagnostic dilemma especially in the absence of motor, visual, or language deficits. In patients who experience TIAs, the risk of early stroke is 4% at 1 month and 30% to 50% at 5 years.7,8
Cerebrovascular Accident
CVA is defined as neurologic symptoms lasting longer than 24 hours with imaging evidence of cerebral infarction. Although advanced age is an important risk factor for cardiovascular morbidity, 31% of first strokes occur in patients younger than 65 years.1 Within 5 years after the initial stroke,
5% to 20% of these younger patients will experience a fatal recurrent CVA.1 The mortality association is even more pronounced in older patients. Approximately one in three patients aged ≥75 years will succumb to death within 1 year after their first stroke, and 50% to 70% within 5 years.1
5% to 20% of these younger patients will experience a fatal recurrent CVA.1 The mortality association is even more pronounced in older patients. Approximately one in three patients aged ≥75 years will succumb to death within 1 year after their first stroke, and 50% to 70% within 5 years.1
Crescendo Transient Ischemic Attack
A phenomenon in which TIAs occur in increasing frequency while maintaining the complete recovery of neurologic symptoms between events.
Stroke-In-Evolution
There is no resolution of symptoms, but rather they wax and wane indicating ongoing neuron ischemia at risk for infarction.
Transient Monocular Blindness (Amaurosis Fugax)
Amaurosis fugax is classically described as a “shade coming down over the eye” that lasts for seconds to minutes secondary to thromboembolism to the ophthalmic artery, the terminal branch of the internal carotid artery. In 25% of the patients with symptomatic carotid disease, such visual disturbances are the presenting symptom. Amaurosis fugax is the most common ocular manifestation, but transient hemianopias and other subtle visual field defects may also occur. Following amaurosis fugax, the risk of stroke was thought to be about 10% per year, but the risk of stroke in patients with confirmed retinal artery occlusion was found to be less than 1% annually according to new studies.9
Jaw Claudication
Although uncommon, symptoms of jaw claudication with eating may occur because of poor perfusion of the masseter muscle from the stenotic external carotid artery (ECA). This can be seen in severe carotid artery atherosclerosis.
Aphasia
Aphasia denotes language disturbances and more commonly involves the left carotid circulation as Broca area is typically located in the left frontal operculum with Wernicke area in the left posterior superior temporal gyrus.
DIAGNOSIS
According to the 2016 American College of Radiology (ACR) Appropriateness Criteria, imaging is indicated in asymptomatic patients with significant cerebrovascular risk factors or a carotid bruit on physical examination.10 In this setting, ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) can be utilized for initial evaluation. However, in symptomatic patients, cross-sectional imaging is preferred.
Ultrasound
Advantages of this modality include ease of access, low cost, high accuracy, low risk, and ability to evaluate hemodynamics. Limitations of this modality, as opposed to cross-sectional imaging, include the inability to assess arch vessel origins and intracranial vasculature and its operator variability.
The ACR, American Institute of Ultrasound in Medicine (AIUM), Society for Pediatric Radiology (SPR), and Society of Radiologists in Ultrasound (SRU) published joint recommendations for technique performing an ultrasound of the extracranial arteries.11 Briefly, the examination should include grayscale imaging (B-mode), color Doppler imaging, and spectral Doppler velocity measurements. The study should interrogate the entire course of the common carotid arteries, carotid bulbs, internal carotid arteries, vertebral arteries, and ECA origins. One should describe plaque morphology including composition and intima-media thickness; it is thought that noncalcified plaque may be at increased risk for thromboembolism. It should document the specific location of plaques at areas of increased velocity concerning stenosis with associated post-stenotic turbulence.12 The internal carotid artery end-diastolic velocity (ICA EDV), peak systolic velocity (PSV), and internal carotid artery to common carotid artery PSV ratio (ICA/CCA PSV) are useful adjuncts to quantify the severity of the disease.12 These are particularly useful when evaluating persons with heart failure, as their absolute velocities will be decreased in this condition, thereby making ICA/CCA ratios a more reliable metric. The ultrasound characteristics in assessing carotid artery stenosis are described in Tables 91.1 and 91.2.
A stenosis ≥50% is considered significant in symptomatic patients for evaluation for surgery. For asymptomatic disease, greater than or equal to 70% is widely accepted as a threshold for repair (see Figure 91.1A,B).
Computed Tomography
CT has proven an invaluable tool for procedural planning. Advantages of CT include ease of access; high accuracy; specific description of the location; composition and length of lesions; anatomic variants; and detection of incidental comorbidities such as coronary artery disease, chronic obstructive pulmonary disease, vasculitis/vasculopathy, prior cerebral infarct, or cerebral aneurysm. Disadvantages include a modest dose of ionizing radiation, iodinated contrast with a risk of contrast-induced nephropathy, and potential for allergic reactions. Additionally, although CT may quantify the degree of stenosis, it cannot infer whether the lesion is hemodynamically significant.
CT angiography is obtained from the aortic arch to the level of the Circle of Willis. Stenoses are generally described according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria as defined by the luminal diameter at an area of stenosis (A) relative to an immediately adjacent segment of the normal artery (B) using the following equation: (B – A)/(B) × 100.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) is becoming increasingly utilized in preprocedural evaluation. Advantages are similar to CT and include high accuracy and detection of anatomic variants and incidental comorbidities. Additionally, novel vessel wall imaging sequences are able to further characterize lesions such as dissection, intramural hematoma, or ulcerated plaques. Vessel wall imaging MRI is particularly valuable in patients with vasculitis, such as Takayasu or giant cell arteritis. Disadvantages are many and include increased length of
examination, which can be prohibitive in persons with claustrophobia, altered mental status, or inability to lay flat; susceptibility artifact from metallic hardware such as prior stents or spinal fusion; or MRI-unsafe hardware such as pacemakers or some aneurysm clips. Additionally, use of gadolinium contrast is associated with a small risk of allergic reaction and risk of nephrogenic systemic fibrosis. However, this can be readily circumvented with noncontrast time-of-flight angiography. Description of lesions is also performed according to the NASCET criteria.
examination, which can be prohibitive in persons with claustrophobia, altered mental status, or inability to lay flat; susceptibility artifact from metallic hardware such as prior stents or spinal fusion; or MRI-unsafe hardware such as pacemakers or some aneurysm clips. Additionally, use of gadolinium contrast is associated with a small risk of allergic reaction and risk of nephrogenic systemic fibrosis. However, this can be readily circumvented with noncontrast time-of-flight angiography. Description of lesions is also performed according to the NASCET criteria.
TABLE 91.1 Modified Washington Duplex Criteria | |||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||||||||||||
TABLE 91.2 Society of Radiologists in Ultrasound Consensus Criteria | |||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| |||||||||||||||||||||||||||||||||||||||||||||||||
 FIGURE 91.1 Carotid Doppler ultrasound demonstrating 70% to 99% stenosis with increased peak systolic velocity and end-diastolic velocity, post-stenotic turbulence, and a visible plaque in the proximal internal carotid artery. Panel A shows velocities in proximal right internal carotid artery and Panel B shows velocities in middle right internal carotid artery. (Courtesy of UT Southwestern Medical Center Vascular lab, Dallas, TX.) |
Arteriography
Although invasive, there are several situations where arteriography may improve diagnostic confidence such as with nondiagnostic or discordant noninvasive imaging results. The stroke risk associated with cerebrovascular arteriography is 1%. Access site and other complications can occur in up to 3% of patients.
MANAGEMENT OF THE PATIENT WITH CAROTID ARTERY STENOSIS
The primary goal in treating carotid artery stenosis is risk reduction and stroke prevention: by maximum medical therapy, endovascular therapy, or surgery. Regardless of the modality, a thorough understanding of the natural history of the disease is essential to formulating a rational and effective treatment strategy. Currently, the mainstay of management of extracranial cerebrovascular diseases includes medical management using antiplatelet and lipid-lowering agents as well as smoking cessation, carotid endarterectomy (CEA), carotid angioplasty and stenting (CAS), and transcarotid artery revascularization (TCAR) (see Algorithm 91.1).
 ALGORITHM 91.1 Approach to management of extracranial carotid artery stenosis. CAS, carotid artery stenting; CEA, carotid endarterectomy; TCAR, transcarotid revascularization. |
Medical Management
Medical management is the cornerstone of all treatments of extracranial carotid disease. All patients should begin medical optimization of their comorbidities. Antihypertensives should be considered to maintain blood pressure less than 140/90 mm Hg.1 Screening for diabetes or obstructive sleep apnea is recommended in this high-risk population. Initiation of a statin with a goal low-density lipoprotein cholesterol of less than 100 mg/dL is recommended.1 Lifestyle modifications, including smoking cessation, diet, and exercise, are also essential.
In the setting of acute ischemic stroke, thrombolysis with tissue plasminogen activator (tPA) within 3 hours of symptom onset has been shown to improve survival in carefully selected patients.13 In addition, as a mode of primary prevention of myocardial infarction (MI), antiplatelet therapy with aspirin (75-325 mg/day) is generally recommended. For secondary prevention of ischemic stroke, antiplatelet monotherapy with aspirin or clopidogrel (75 mg daily) is strongly recommended over anticoagulation.1 In select symptomatic patients with severe carotid stenosis, dual antiplatelet therapy (DAPT) with aspirin and clopidogrel for 3 months is a reasonable consideration.14 However, for those who are already on oral anticoagulation for indications such as atrial fibrillation or prosthetic heart valves, adding an antiplatelet agent may have a limited
benefit except for select cases in which unstable angina or coronary artery stenting is factored.14 Compared to warfarin, newer oral anticoagulants, such as dabigatran, may have a lower risk of intracranial hemorrhage, emerging as a more favorable option for many.15 Select medications commonly used in the management of extracranial carotid disease are described in Tables 91.3.
benefit except for select cases in which unstable angina or coronary artery stenting is factored.14 Compared to warfarin, newer oral anticoagulants, such as dabigatran, may have a lower risk of intracranial hemorrhage, emerging as a more favorable option for many.15 Select medications commonly used in the management of extracranial carotid disease are described in Tables 91.3.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
