Carotid Artery Stenting

15 Carotid Artery Stenting



Jonathan A. Rapp, Pranav M. Patel, Christopher J. White


Nearly 800,000 strokes occur each year in the United States, and more than 130,000 Americans die annually from stroke. Stroke is the third leading cause of mortality in the United States, and among survivors, 15% to 30% are permanently disabled. Warning symptoms, such as a transient ischemic attack (TIA), historically defined as a neurologic event lasting <24 hours, precede a minority (15%) of all strokes. A new, tissue-based definition of TIA has been formalized, but most of the studies referred to in this chapter predate its publication. Following a TIA, the 90-day risk of stroke is 15%, and the 6-month risk of a stroke, TIA, or death is as high as 30%. Therefore, TIAs should be treated as medical emergencies.


Approximately half of all strokes occur in the distribution of the carotid artery, and carotid artery disease (CAD) amenable to revascularization accounts for as high as 12% of new strokes. Although occlusion of the carotid artery due to plaque burden can cause a stroke, the more common scenario is for carotid plaque to rupture resulting in distal embolization and cerebral infarction. Because more than 80% of strokes have no warning symptoms, stroke prevention with management of asymptomatic carotid atherosclerosis and carotid revascularization for high-risk patients is important.


Roughly 5% to 10% of patients over age 65 have a carotid stenosis >50%, and only 1% have a stenosis ≥75%. The natural history of carotid artery disease depends on the patient’s symptomatic status and lesion severity. In the Asymptomatic Carotid Atherosclerosis Study (ACAS), among medically treated asymptomatic patients with stenosis ≥60%, the 5-year risk of ipsilateral stroke or any stroke or death within 30 days of randomization was 11%.


Symptomatic patients with carotid atherosclerosis have a much worse prognosis than asymptomatic patients. In the North American Symptomatic Carotid Endarterectomy Trial (NASCET) trial of symptomatic carotid lesions, the 5-year risk of ipsilateral stroke in those medically managed was 18.7% among those with lesions <50% in severity. Results were similar in the European Carotid Surgery Trial (ECST). The risk of stroke increased with severity of stenosis, with the 3-year risk of ipsilateral stroke in those with stenosis >80% being 26.5%.


Medical therapy for carotid atherosclerosis should focus on preventing stroke and stabilizing atherosclerotic lesions to prevent plaque rupture and atheroembolization. Blood pressure control with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are of particular benefit in stroke prevention. In addition, a review of more than 70,000 patients with, or at high risk for, cardiovascular disease found that statins significantly lower the risk of stroke. Current American Heart Association/American Stroke Association (AHA/ASA) stroke guidelines endorse the National Cholesterol Educational Program (NCEP III) recommendations for the use of statins. The Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) study showed that rosuvastatin treatment in patients with normal cholesterol levels but elevated levels of C-reactive protein is effective in reducing the rate of stroke and is indicated for patients with carotid artery disease.


Antiplatelet medications are a critical component of primary stroke prevention. In secondary prevention, aspirin reduces the risk of future strokes by 15% to 25%. High-dose aspirin provides no more benefit than lower doses (160–325 mg daily) but is associated with more side effects. The Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management, and Avoidance (CHARISMA) trial included more than 4300 patients with a prior TIA or stroke and found that aspirin 75 to 162 mg daily was as effective as aspirin plus clopidogrel in preventing future myocardial infarction (MI), stroke, or cardiovascular death. AHA/ASA guidelines recommend that all patients with carotid atherosclerosis be placed on antiplatelet medications. Aspirin 50 to 325 mg daily, aspirin-dipyridamole, or clopidogrel should be initiated for secondary prevention of stroke. The combination of aspirin and dipyridamole is recommended over aspirin alone, however. The combination of aspirin and clopidogrel is not recommended.



Clinical Presentation


Patients with carotid artery stenosis may be asymptomatic or exhibit ischemia in one of three vascular territories: retinal, hemispheric, or global. In symptomatic patients, the history, neurologic exam, and imaging studies can often localize a lesion to a particular vascular territory. The National Institutes of Health Stroke Scale (NIHSS) should be performed in all symptomatic patients to quantify the neurologic deficit and predict outcome.



Diagnosis of Carotid Artery Disease: Anatomical Imaging


Duplex ultrasonography is most often the initial test used to assess the severity of carotid artery stenosis. Carotid ultrasound also has a high accuracy for carotid restenosis after endarterectomy. Numerous criteria have been proposed to diagnose severe carotid stenosis. In most cases >80% stenosis correlates with systolic velocity >300–400 cm/sec, diastolic velocity >100–135 cm/sec, and ratio of internal carotid artery/common carotid artery (ICA/CCA) systolic velocity of >3.5. Factors such as contralateral occlusion, diminished cardiac output from severe left ventricular dysfunction, aortic stenosis, and common carotid artery stenosis may make these measurements less reliable. Magnetic resonance angiography and computed tomography angiography are the other noninvasive imaging studies that are helpful in identifying carotid artery stenosis. Duplex imaging is often the test of choice given its safety profile, low cost, and wide availability. Imaging that can define the aortic arch and the circle of Willis is useful in planning endovascular procedures. The particular noninvasive method used should reflect local availability and expertise.


Digital subtraction angiography (DSA) is the gold standard for defining carotid anatomy with the NASCET method of stenosis measurement the most widely used (Fig. 15-1). Cerebral catheter-based angiography carries a risk of cerebral infarction of 0.5% to 1.2%; therefore, noninvasive imaging should be the initial strategy for evaluation.


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Figure 15-1 Methods of carotid stenosis assessment. The NASCET method is the most widely used.



Surgical Therapy


Current AHA/ASA guidelines give a class I indication for CEA in symptomatic patients with stenosis of 50% to 99% if the risk of perioperative stroke or death is <6%. In asymptomatic patients, AHA/ASA guidelines give a class IIa indication to CEA in patients with stenosis of >70% if the risk of perioperative stroke, death, or MI is low, historically defined as <3%. Patients considered especially high risk for CEA include those with:



• Carotid artery stenosis after prior radical neck surgery


• High cervical carotid artery lesions that are surgically inaccessible


• Sequential lesions of the proximal to distal ICA


• Lesions of the common carotid artery and associated ICA lesions


• Recurrent stenosis of the carotid artery after CEA


• Non-atherosclerotic cause of carotid artery stenosis (e.g., fibromuscular dysplasia, Takayasu’s arteritis)


• Ipsilateral stenosis due to prior radiation therapy to the neck


• Increased operative risk due to concomitant illnesses such as CAD requiring coronary artery bypass surgery


• Contralateral occlusion and concurrent high-grade ipsilateral stenosis



Carotid Artery Stenting


Carotid artery stenting (CAS) was developed as a less invasive alternative for carotid revascularization. The interventionalist should be part of a multidisciplinary team that includes neurologists and/or vascular medicine specialists that can provide valuable pre- and postprocedure care. Additionally, it is necessary for the operator to possess the ability, or have access to an on-site expert, to perform neurovascular rescue procedures in the event of a complication, a standard of care not met by CEA.



Medications


Aspirin (81–325 mg daily) is begun at least 24 hours prior to the procedure and is continued indefinitely. Clopidogrel 75 mg daily (or alternatively ticlopidine 250 mg twice daily) should be given for 5 consecutive days preceding stent placement and continued for at least 1 month after stent deployment. Minimal, if any, sedation is used during the procedure because the patient requires neurologic assessments during the procedure. Because of potential hypotension during angioplasty or stenting, antihypertensive medications should be held the morning of the procedure.


Intravenous unfractionated heparin should be given such that the activated clotting time (ACT) is ≥ 250–300 seconds. Additional boluses of heparin may be required during the procedure. Unless another indication exists for it, anticoagulation is not used following the procedure.



Procedural Techniques



Baseline Aortography and Cerebral Angiography


Vascular access is most commonly obtained from the femoral artery although brachial or radial access may be used. Prior to selective angiography, an arch aortogram is performed with a pigtail catheter placed in the proximal ascending aorta to define the anatomy of the aortic arch, which is critical to the success of the stent procedure. This is done in the 45º left anterior oblique position with a large-format image intensifier (12-inch to 16-inch) using DSA (15 mL/sec for 3 sec) and a power injector.


Once the morphology of the aortic arch is determined (Fig. 15-2), catheters are chosen for selective angiography of the cervical arteries supplying the brain (right and left carotid and vertebral arteries) and the cerebral vasculature. In a type I arch, Berenstein or Judkins right (JR) catheters are often used. In type II or III arch morphologies, shepherd’s crook–shaped catheters (i.e., Simmons or Vitek catheters) may be best (Fig. 15-3).


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Figure 15-2 Aortic arch morphologies. Arch morphology is defined based on the origin of the great vessels. A, Type I arch: all vessels originate at the superior margin of the arch. B, Type II arch: at least one vessel originates between the superior and inferior margins of the aortic arch. C, Type III arch: at least one vessel originates below the inferior margin of the aortic arch.


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Figure 15-3 Catheters for accessing the carotid artery. Berenstein or JR4 catheters are usually best for a type I arch. Shepherd’s crook catheters may be best for type II or type III arches.


Angiograms are obtained to delineate the anterior and posterior circulation supplying the brain. The intracranial and extracranial portions of each vessel are studied. Generally, two views of each are obtained, one in the anteroposterior projection and one in the lateral projection. Alternatively, some operators use rotational angiography. It is important to demonstrate the circle of Willis to define any baseline abnormalities. DSA may be performed with a 50/50 mix of saline and contrast. An external reference object is used with carotid angiograms in order to accurately measure the diameter of the artery.



Internal Carotid Intervention


A diagnostic catheter is used to engage the common carotid artery (CCA), and a roadmap angiogram is made of the carotid bifurcation. A 0.035-inch stiff-angled hydrophilic wire is advanced into the external carotid artery, and the diagnostic catheter is advanced over the wire. The hydrophilic wire is exchanged for a 0.035-inch stiff Amplatz wire over which an 8F guiding catheter or a 6F sheath may be advanced to the target vessel CCA. Care must be taken to avoid plaque disruption with wires and catheters, and at this point in the procedure, the plaque in the ICA should remain untouched.


For procedures performed with a filter-type distal embolic protection device (EPD), the target lesion is crossed with the EPD. Although there are no randomized trials comparing stenting with EPDs to stenting alone, one study found that 57% of EPDs contained debris upon retrieval. EPDs are standard of care in the United States, and several types exist (Fig. 15-4). If the distal EPD will not cross the lesion, the stenosis may be crossed with a conventional 0.014-inch guidewire and subsequently predilated with a small (2.5 mm) balloon. Then the EPD should be placed. After distal EPD deployment, the lesion is often predilated with an undersized coronary balloon, typically 3 to 4 mm in diameter. A self-expanding stent is then placed across the lesion. The stent is sized to fit the CCA, and as a general rule, self-expanding stents are typically sized at least 1 mm larger than the reference diameter. There is no demonstrated benefit for using tapered stents. It is common practice, when treating an internal carotid bifurcation lesion, to place the stent across the ostium of the external carotid artery (Fig. 15-5).


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Figure 15-4 Embolic protection devices (EPDs). A, Filter-type device. B, Balloon occlusion of internal carotid artery (ICA). C,D, Proximal protection with flow reversal. See text. ECA, external carotid artery.


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Figure 15-5 Stenting of the internal carotid artery (ICA). A, The common carotid artery (CCA) is accessed with a diagnostic catheter and standard 0.035-inch J wire. B, The catheter is advanced over the J wire but remains in the CCA. C, The J wire is exchanged for a hydrophilic stiff-angled 0.035″ wire. D, The catheter is advanced to the ECA and the hydrophilic wire is removed. E, A stiff Amplatz wire is advanced to the ECA and the c atheter is removed. F,

Related posts:

  1. Aorto-Ostial and Branch Ostial Lesions and Unprotected Left Main Percutaneous Coronary Interventions
  2. Angiography for Percutaneous Coronary Interventions
  3. Carotid Artery Stenting
  4. Peripheral Vascular Intervention

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Jun 4, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Carotid Artery Stenting

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