Preparation

One of the most important steps for any successful procedure is preparation. For CAS, the clinical and imaging evaluation of the patient to determine the suitability of the procedure is essential. The symptomatology determines whether a patient will be low or high risk, or is perhaps not even a candidate for CAS.

The patient’s imaging must be reviewed to evaluate both the vasculature and the intracranial contents. If the patient is symptomatic, it is important to determine that the symptoms are caused by ischemia, rather than something else. A recent CT or MR image will detect an infarction or hemorrhage while excluding other processes such as a tumor. Evidence of an infarction may also determine the timing of the procedure. Large areas of damage may lead to hemorrhagic conversion when the supplying carotid artery patency is restored. If the patient has not recovered significantly, or if the infarct volume by imaging is more than one third the territory of the stenotic carotid distribution, the authors usually perform angioplasty and stenting 1 month after the incident. This waiting period seems to allow the injured vasculature and brain to heal sufficiently to lessen the risks of hemorrhage after revascularization. The risk of this delay is that the patient may have further ischemic events despite antiplatelet agents. In fact, the tightly stenotic carotid artery may even occlude during the waiting period. In the NASCET study, the nearly occluded (“string sign”) symptomatic patients seemed to do reasonably well with medical therapy, with a 1.7% cerebrovascular accident (CVA) rate at 1 month that increased to 11.1% at 1 year, and those undergoing CEA had a stroke rate of 6.3% . Of course, as yet no data exist on angioplasty and stenting in these patients.

During the clinical evaluation, the interventionalist can determine the patient’s ability to cooperate. Most procedures are performed with conscious sedation, but some patients may have difficulty cooperating when sedated. In addition, the patient must be able to sustain an open airway while supine under normal (unchallenged) circumstances. Patients who have a history of a contrast allergy should be premedicated with prednisone, 50 mg, by mouth every 6 hours for three doses ending 1 hour before the procedure; just before the procedure, diphenhydramine, 25 mg IV, and an H2 blocker such as cimetidine, 300 mg IV, will prevent and lessen adverse contrast reactions in allergic patients. In cases of severe contrast reactions, intubation for airway control can prevent the respiratory effects of laryngospasm or bronchospasm. Assessment of the patient’s renal function will also assist in the selection of an appropriate contrast agent (non-ionic isosmolar) (Visipaque, Amersham PLC, Little Chalfont, Buckinghamshire, UK) for those at risk for the development or worsening of renal failure. In these circumstances, administration of a bicarbonate drip (3 amps bicarbonate in 1 L normal saline at 3 mL/kg for 1 hour before the procedure and 1 mL/kg during the procedure and for 6 hours afterwards) may lessen the incidence of postprocedural renal failure. In addition, the administration of n-acetylcysteine, 600 mg by mouth twice daily the day before and the day of the procedure, may be helpful.

Antiplatelet agents are initiated 5 days before elective procedures: 325 mg of aspirin and 75 mg of clopidogrel bisulphate daily. If the patient has gastrointestinal upset, enteric-coated aspirin can be substituted. For more urgent situations, the patient can be loaded with 300 to 450 mg of clopidogrel bisulphate several hours before the procedure. Intravenous IIb/IIIa inhibitors seem to increase the risk of intracranial hemorrhage and are not recommended for routine CAS .

If an arteriogram was performed previously, review of it will demonstrate the aortic arch, the target carotid artery in the neck, and the blood supply to the ipsilateral cerebral hemisphere. The degree of elongation of the aortic arch will help to determine the likelihood of success of a transfemoral approach or the need for an alternative transbrachial or transradial puncture. If the line of origin of the brachiocephalic vessels arises parallel to the upper convexity of the aortic arch (type I aortic arch), the desired carotid artery may be selected using the transfemoral approach with almost no difficulty ( Fig. 1 ). Similarly, if the brachiocephalic vessels arise from the aortic arch between the outer and inner convexities of the aortic arch (type II aortic arch), selecting the desired vessel will be only slightly more difficult ( Fig. 2 ). It is only with the type III aortic arch, where the innominate artery arises below the level of the inner convexity of the aorta, that catheterizing the innominate artery, right common carotid artery, or left common carotid arteries is difficult ( Fig. 3 ). In this instance, it may be difficult to exchange the diagnostic catheter for a guiding catheter or long sheath. Origin of the left common carotid artery from the innominate artery (the so—called “bovine arch”) may cause problems for selective catheterization, similar to the type III aortic arch. In these two situations, the transbrachial or transradial approach may be appropriate. (All the authors’ CAS procedures have been performed transfemorally.) The direct carotid approach should be used only in patients who are non-CEA candidates and have high lesions and no other access. In these patients, the access site is closed operatively so that the carotid artery is not compressed in an attempt at hemostasis. Successful hemostasis is essential with the direct carotid approach because hematoma formation may compromise the airway. Finally, the carotid artery itself is evaluated because tortuosity of the common carotid artery may cause problems for catheterization. Tortuosity of the internal carotid artery may alter the choice and placement of an embolic protection device (EPD) and the type and site of the stent to be deployed, and even preclude performance of the procedure itself if there are extreme elongation and loops in the carotid artery at or near the treatment site (see Fig. 3 ). In these circumstances, CEA may be the more prudent choice. Other anatomic CAS exclusionary criteria include thrombus at the treatment site ( Fig. 4 ), long subtotal occlusion (string sign), and, of course, total occlusion.

A 47-year-old woman with left carotid transient ischemic attacks. ( A ) Left anterior oblique arteriogram of the aortic arch, demonstrating a type I arch with a small left internal carotid artery. ( B ) Anteroposterior right common carotid arteriogram, demonstrating irregular, alternating dilation of the right internal carotid artery, which is a diagnostic of fibromuscular hyperplasia. This finding demonstrates the value of examining the opposite carotid artery. ( C ) Lateral left common carotid arteriogram, demonstrating a near occlusion of the internal carotid artery approximately 2 cm above its origin. ( D ) Lateral left common carotid arteriogram after placement of a 6-mm × 20-mm Precise stent. The self-expanding stent dilated the internal carotid artery, so an angioplasty was not necessary.

A 78-year-old man who had bilateral CEAs years previously. He now has left carotid transient ischemic attacks. ( A ) Left anterior oblique arch aortogram, demonstrating heavy calcifications due to atherosclerosis within the aortic arch and a type II–type III origin to the brachiocephalic vessels. Extremely slow flow in the left carotid artery causes it to fill poorly. ( B ) Anteroposterior left common carotid arteriogram after a Simmons 2 catheter was exchanged for a 6F Shuttle sheath, demonstrating severe recurrent atherosclerosis with an ulcerated plaque in the distal left common carotid artery and a very high-grade stenosis in the internal carotid artery, 2 cm beyond its origin. The flow in the internal carotid artery is very slow. ( C ) Anteroposterior left common carotid arteriogram after angioplasty with a 5-mm × 40-mm Savvy balloon and placement of a 10-mm × 40-mm Precise stent across the bifurcation, revealing patency of the internal carotid artery and smoothing of the irregularities in the distal left common carotid artery. The guidewire can be observed across the CAS site with its tip in the petrous carotid artery.

A 79-year-old woman who had active right carotid distribution transient ischemic attacks and was not a candidate for CEA because of her severe chronic obstructive pulmonary disease, hypertension, and severe peripheral vascular disease. ( A ) Left anterior oblique arch aortogram, demonstrating a type III arch configuration and an occluded left subclavian artery. The right common carotid artery is very tortuous and the right vertebral artery is extremely tortuous. ( B ) Anteroposterior right common carotid arteriogram, demonstrating a high-grade stenosis in the right internal carotid artery, which extends beyond the level of the mandible, increasing the risk for CEA. ( C ) Anteroposterior right common carotid arteriogram after angioplasty with a 4-mm × 40-mm Savvy balloon and placement of an 8-mm × 30-mm Precise stent, demonstrating restoration of a normal lumen. ( D ) Anteroposterior right common carotid arteriogram of the head before the CAS, demonstrating poor filling of the intracranial right carotid distribution because of the internal carotid artery stenosis in the neck. The right anterior cerebral and right posterior cerebral arteries show no filling, and the right middle cerebral artery has unopacified blood mixing with the contrast. ( E ) Anteroposterior right common carotid arteriogram after the CAS, demonstrating filling of the right A1 segment, filling of the right posterior cerebral artery, and now excellent filling of the right middle cerebral artery. Frequently, after angioplasty of high-grade lesions, there is increased flow in the distribution. Because of this, blood pressure must be monitored and controlled tightly.

A 54-year-old woman with a history of a recent right carotid distribution stroke and ongoing transient ischemic attacks despite antiplatelet therapy. She had received radiation therapy for a lymphoma 15 years previously and has had no evidence of recurrence. ( A ) Lateral right common carotid arteriogram in preparation for an angioplasty, demonstrating a high-grade stenosis in the internal carotid artery 1 cm beyond its origin. A filling defect just above the stenosis is a thrombus. ( B ) Lateral right common carotid arteriogram, demonstrating no change in the stenosis after anticoagulation for 1 month, but the thrombus has lysed in the now-asymptomatic patient. ( C ) Lateral right common carotid arteriogram after angioplasty with a 5-mm × 20-mm Savvy balloon and placement of a 9-mm × 30-mm Smart stent across the bifurcation, demonstrating restoration of a normal luminal diameter. ( D ) Lateral right common carotid arteriogram 4 years later, showing persistent patency of the common carotid artery. Slight intimal hyperplasia does not compromise the lumen. The external carotid artery remains patent.

Calcification at the angioplasty site can be problematic. Calcified plaque resists expansion and if it responds to the angioplasty, it is by fracturing, rather than by stretching or compressing. Expansion of the lumen occurs by stretching of the less involved (more normal) carotid wall. The goal of angioplasty when there is heavily calcified plaque at the angioplasty site is a reduction of the stenosis to less than 50%. Even if dilation to a more normal lumen has somehow been achieved with an aggressive angioplasty, this lumen will not be maintained by the stent because of the recoil of the residual artery wall. Attempts at overcoming the resistance of the heavily calcified arterial wall may lead to arterial rupture .

During the review of the patient’s arteriogram, the status of the opposite carotid artery and any vertebral collaterals is also informative and is particularly important if there are significant stenoses or occlusions and the operator is contemplating using flow reversal with the Parodi anti-embolism system. Although the patient may tolerate cessation or reversal of flow for short periods during the procedure, the risks could be higher than with the filter-type devices.

If the patient’s previous evaluation has been with Doppler ultrasound, MR angiography, or CT angiography, a formal arteriogram is performed immediately before the contemplated angioplasty and stenting. In most instances, the arteriogram is performed after placement of a 5F sheath in one of the femoral arteries. The 5F catheters are used for the arch aortography and the selective diagnostic arteriograms, which consist of an aortic arch, bilateral common carotid injections in the neck and head, and at least one vertebral artery (see Fig. 1 ). Evaluation of the intracranial circulation excludes more significant intracranial stenosis than the target carotid artery. Thus, the appropriateness of the proposed intervention and the suitability of the accompanying vasculature and planned access routes can all be determined before the procedure.

Embolic protection devices

EPDs have been approved recently for use with CAS. The theory behind their design is reasonable because most CVAs and transient ischemic attacks (TIAs) during CAS are caused by emboli. Whether the emboli are due to thrombus formation on the various catheters and devices, platelet aggregation, or liberated atheromatous debris does not matter because the effect is the same, obstruction of the cranial arterial vessels. Only rarely are procedural ischemic events related to hypoperfusion, which is usually due to hypotension and bradycardia. Therefore, the concept of embolic protection is reasonable.

Currently, the four approved EPD systems are all filters with pores that allow blood to pass, but capture emboli or debris. They are mounted on a guidewire, the tip of which must first cross the stenosis; then, the restrained filter crosses the area. This procedure requires a residual lumen of approximately 2 mm. If the lumen is smaller, an unprotected angioplasty with a small balloon must be performed to allow passage of the guidewire and filter. In both instances, risks include obstruction of the lumen, dislodgement of debris (emboli), and dissection. The EPD wires and filters are not as readily maneuverable as standard .014- or .018-in guidewires. Moreover, the filter may not trap all the emboli because of imperfect apposition to the walls of the carotid. It may also become clogged with debris, which significantly obstructs flow. The four FDA-approved EPDs approved by the Food and Drug Administration (FDA) for CAS are available in varying sizes, depending on the size of the artery in which they are to be placed. They should be slightly larger than the internal carotid artery to assure wall-filter apposition. The first approved EPD was the Accunet, initially developed by Guidant (St. Paul, MN), which has been sold to Abbott (Abbott Park, North Chicago, IL) ( Fig. 5 ). Abbott also has an EPD named the Emboshield. Recently, approval for the Angioguard (Cordis Neurovascular, Miami Lakes, FL) ( Fig. 6 ) and the Spider (eV3, Irvine, CA) has been granted. A similar filter device approved for use in the heart but not for the carotid artery is the FilterWire EZ from Boston Scientific ( Fig. 7 ).

A 56-year-old woman with a right middle cerebral artery infarction 1 month previously, from which she has recovered. ( A ) Lateral right common carotid arteriogram, demonstrating a high-grade stenosis at the origin of the right internal carotid artery. Because the internal carotid artery is slightly smaller than the external carotid artery, the stenosis, by NASCET criteria, becomes 99%. ( B ) Lateral radiograph of the neck with a 5-mm Accunet EPD deployed in the internal carotid artery. ( C ) Lateral right common carotid arteriogram after angioplasty with a 4-mm × 20-mm Viatrac Plus balloon, and placement of a tapered 7-mm-to-10-mm–diameter × 30-mm–length Acculink stent across the bifurcation, revealing restoration of the normal luminal diameter at the origin of the internal carotid artery. The irregularity in the internal carotid artery above the angioplasty site is due to spasm.

A 65-year-old woman who had a left CEA 3 years previously because of TIAs due to carotid stenosis. She has had expansion of the internal carotid artery at the CEA site. In an attempt to prevent further expansion, stent placement was undertaken. ( A ) Lateral road-mapped image, demonstrating the dilated proximal left internal carotid artery just beyond its origin. A 7-mm Angioguard has been placed into the internal carotid artery above the site. ( B ) Lateral radiograph more clearly showing the guidewire and the expanded Angioguard. ( C ) Lateral road-mapped image showing positioning of the 7-mm × 40-mm Precise stent across the dilated CEA site and the bifurcation. ( D ) Lateral radiograph, demonstrating the stent bridging the dilated site. The Angioguard remains in place. ( E ) Lateral left common carotid arteriogram after the Angioguard has been collapsed and removed. The stent bridging the internal carotid artery and the dilated section, and in the common carotid artery, is readily apparent. ( F ) Lateral delayed image from the left common carotid arteriogram, demonstrating the slowed flow in the dilated segment. Presumably with time, fibrosis will restore a more normal lumen. The patient remained on aspirin and clopidogrel bisulphate for 3 months to ensure that this was a gradual process. ( G ) Computerized tomographic angiography 3 months poststenting, showing restoration of the normal lumen diameter. The pseudoaneurysm is filled with clot.

A 74-year-old man receiving coumadin for atrial fibrillation had three episodes of severe epistaxis requiring nasal packing. The last episode was so severe that angiography and embolization were requested. A diagnostic left common carotid arteriogram demonstrated a severe stenosis in the left internal carotid artery with retrograde flow in the left ophthalmic artery, which precluded embolization of the left internal maxillary artery. The high-grade stenosis in the left internal carotid artery was neurologically asymptomatic. ( A ) Lateral left common carotid arteriogram, demonstrating the tip of the 6F guide catheter in the left common carotid artery below the bifurcation. ( B ) Lateral road-mapped image with the EPD and its delivery catheter crossed the stenosis into the internal carotid artery. The EPD has not been deployed. ( C ) Lateral left common carotid arteriogram demonstrating the expansion of the EPD in a straight segment of the internal carotid artery above the stenosis. Note that the contrast passes through the EPD into the internal carotid artery above. ( D ) Lateral road-mapped image during placement of the self-expanding stent across the stenosis. Note how the stent has distorted the internal carotid artery so that it appears to be outside the vessel lumen. ( E ) Lateral road-mapped image during expansion of the stent across the stenosis. ( F ) Lateral road-mapped image after complete expansion of the stent. ( G ) Lateral left common carotid arteriogram after the CAS has been performed, restoring a near-normal lumen. The EPD remains in place. ( H ) Native lateral view of the neck, with the capturing catheter in place collapsing the EPD. ( I ) Lateral left common carotid arteriogram after the EPD has been removed, demonstrating slight irregularity due to spasm at the site of the EPD, but wide patency of the internal carotid artery.

Another not-yet-approved distal EPD is a microballoon, which is placed across the stenosis and inflated. The advantage is complete obstruction to distal embolization. The disadvantages are the resultant complete obstruction to internal carotid artery flow, which is not tolerated in about 5% of patients, and the need to cross the stenosis.

An entirely different concept that is not yet approved for use in the carotid artery is the Parodi anti-embolism system. With this device, the technique is changed; the lesion is not crossed until the EPD is in place ( Fig. 8 ). A large-bore guiding catheter with a balloon at its tip is placed in the common carotid artery. Through the guiding catheter lumen, a second, smaller balloon is positioned in the external carotid. Femoral venous access is also obtained. After the angioplasty device is ready to be positioned, the balloon in the common carotid artery is inflated, thereby obstructing flow. The balloon in the external carotid artery is also inflated. The balloon guide catheter then becomes a conduit for reversed flow from the opposite carotid artery or vertebral basilar system. This flow is directed through a filter and returned to the patient through the femoral vein. A standard angioplasty and stent procedure is then performed. At the conclusion of the CAS procedure, the balloon in the external carotid artery is deflated and removed. The guide catheter balloon is then deflated. The major advantage to this system is that the lesion does not have to be crossed without the protection in place. The major disadvantage is that not all patients have sufficient collateral supply to tolerate the occlusion, and a minor disadvantage is the larger-diameter 10F sheath necessary for insertion of the balloon guide catheter.

A 63-year-old man who had a left CEA 18 months previously for amaurosis fugax and is currently asymptomatic. ( A ) Anteroposterior left common carotid arteriogram, revealing a 95% stenosis at the origin of the internal carotid artery and a 50% stenosis of the distal left common carotid artery. Crossing this with a filter-type EPD was thought to be dangerous, so the Parodi anti-embolism system was used “off-label.” ( B ) Anteroposterior road-mapped image, demonstrating the guide balloon catheter in place, with the guide balloon inflated. Through the guide catheter, a second balloon has been placed into the external carotid artery and inflated. The distended 5-mm × 40-mm Savvy angioplasty balloon across the high-grade stenosis in the proximal internal carotid artery and the guidewire for the angioplasty balloon can be identified. ( C ) Anteroposterior left common carotid arteriography after the angioplasty, demonstrating significant dilation at the angioplasty site. The guidewire across the stenosis, the inflated balloons of the Parodi anti-embolism system in the external carotid artery, and the common carotid artery all can be identified. ( D ) Frontal view from a road-mapped image, demonstrating an 8-mm × 40-mm Precise stent across the angioplasty site in the internal carotid artery and more proximally into the common carotid artery. ( E ) Frontal radiograph, clearly showing the guidewire and the stent across the angioplasty site. The external carotid and common carotid artery balloons contain contrast. ( F ) Anteroposterior left common carotid arteriogram after the balloons have been deflated and withdrawn. The guidewire has also been withdrawn. This arteriogram demonstrates mild irregularity at the angioplasty site but wide patency of the common carotid and internal carotid arteries. Although the lumen is not dilated completely, one must remember that the self-expanding stent exerts some external expansile forces. If this result was not satisfactory, a further angioplasty through the stent with a larger balloon could be performed.

The authors have used EPDs for the past year and a half and found that the complication rate is slightly higher because of the learning curve with each EPD.

Although EPDs make intellectual sense, it is unclear whether their use results in a reduction in TIAs, CVAs, and death. Postulated reasons for untoward events despite EPDs include the necessity of crossing the lesion with the filter; movement of the guidewire and filter during the procedure, which may lead to spasm or intimal damage; failure to capture some of the emboli because of incomplete wall apposition; and overwhelming of the filter with debris. Operator inexperience and unfamiliarity with the device may also lead to complications.