Carotid Artery Stenting: Technical Considerations

Carotid artery stenting (CAS) is currently being investigated as an alternative treatment to carotid endarterectomy (CEA) (1–6). The goal of both procedures is the prevention of stroke from extracranial carotid artery occlusive disease. Carotid stenting, compared with surgery, offers patients a less invasive and traumatic means of achieving this goal. The efficacy of carotid stenting in preventing stroke depends on the ability of the operator to achieve complication-free results. The purpose of this article is to describe the technical details and patient selection factors that have allowed us to improve the outcomes from this procedure.

Methods

Access Sheath Placement

Once the diagnostic study is completed and the stenotic internal carotid artery is identified, the 5F catheter is advanced, using the 0.038-inch glide wire, into the ipsilateral external carotid artery. The glide wire is then withdrawn and replaced with an extra stiff 0.038-inch exchange wire (0.038-inch Extra Stiff Amplatz Wire, 260 cm; Cook, Inc.). The 5F catheter is withdrawn, and the 7F 90-cm guiding sheath (Shuttle; Cook, Inc.) is then advanced into the common carotid artery (Figs 1A and 2D) over the exchange Amplatz wire, which is anchored in the external carotid artery. If the brachiocephalic diagnostic angiography has previously been performed and the target lesion identified, the stenting procedure begins by placing the 7F 90-cm Shuttle sheath, via the femoral approach, into the upper thoracic aorta. After withdrawing the inner dilator from the sheaths, the 125-cm 5F catheter (VTK Thorocon NB, 125 cm) is introduced into the 7F sheath. Care must be taken not to advance the 7F sheath too closely to the aortic arch because this will decrease the maneuverability of the 5F catheter. The common carotid artery is then catheterized with the 125-cm 5F catheter, and this catheter is advanced into the external carotid artery (road mapping is very useful). Using the appropriate guidewire (0.038-inch glide wire or extra stiff 0.038-inch Amplatz wire), depending on the arch extension and carotid artery tortuosity, the 7F sheath is advanced over the 5F catheter into the common carotid artery, just proximally to the stenosis. If the advancement of the sheath over the 5F catheter is not smooth, the 5F catheter is removed, replaced with the sheath's inner introducer, and then the sheath is advanced into the common carotid artery. There are modifications of this technique, especially if the stenosis is located in mid or distal segments of the common carotid artery or if the external carotid artery cannot be catheterized. The 5F catheter guidewire assembly, over which the 7F sheath is placed in the common carotid artery, is kept below the stenosis or bifurcation (Amplatz exchange J-wire is used). Exceptionally, in cases of significant aortic arch elongation or common carotid artery tortuosity, the stenosis is traversed with a glide wire and 4F or 5F catheter. Next, using an Amplatz wire, the 7F sheath is advanced proximally to the stenosis. This technique is also used in ostial and very proximal carotid stenoses. One should be aware that by placing the 7F sheath in the common carotid artery, especially if the carotid artery is tortuous (Fig 2A), the bifurcation is displaced upward and kinks can be created on the internal carotid artery (Fig 2D and E). These disappear once the sheath is withdrawn but can complicate the stenting procedure. As soon as the 7F sheath is placed into the arterial system, 4.000 to 5.000 units of heparin are administered through the sheath to raise the activated clotting time to no more than 250 s (Hemotec Company method).

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fig 1.

Angiograms from the case of an 80-year-old male patient with bilateral internal carotid artery stenosis.

A, Angiogram shows 80% stenoses in the left internal carotid artery (ICA) (curved arrow). A 7F sheath (7F) was inserted into the left common carotid artery (LCCA). Distal, independent stenosis on the internal carotid artery (thick black arrow) can be seen. ECA, external carotid artery.

B, Angiogram shows status after predilation (curved arrow) of the internal carotid artery with a 4-mm balloon over a 0.018-inch guidewire (white arrows). Spasm on the distal internal carotid artery can be seen.

C, Angiogram obtained after the CAS control study. A 10 × 20 Wallstent was used, dilated with a 5 × 20 Symmetry balloon. Minimal residual spasm can be seen. Independent distal stenosis persists (wide black arrow).

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fig 2.

Angiograms from the case of an 87-year-old female patient with occlusion of the right internal carotid artery and 65% symptomatic, ulcerated stenosis on the left common and internal carotid arteries.

A, Angiogram of the innominate artery (IA) shows a 90-degree take-off of the left common carotid artery (LCCA), with more distal tortuosity.

B, Anteroposterior projection angiogram of the left common carotid artery (LCCA) (5F catheter in the ostium). Sixty-five percent ulcerated stenosis (curved arrow) on the internal carotid artery (ICA) and on the common carotid artery (open arrow) can be seen. ECA, external carotid artery.

C, Lateral projection.

D, Anteroposterior projection angiogram of the left common carotid artery (LCCA), obtained through a 7F sheath placed in the distal left common carotid artery. By upward displacement of the bifurcation, kink (angled arrow) developed in the proximal internal carotid artery. 7F, distal tip of the 7F sheath; ECA, external carotid artery; open arrow, stenosis in the distal left common carotid artery; curved arrow, ulcerated stenosis in the internal carotid artery.

E, Lateral projection.

F, Anteroposterior projection angiogram of the left common carotid artery (LCCA), obtained after CAS was performed. A 10 × 20 Wallstent was used, dilated with a 5.5 × 20 Symmetry balloon. The 7F sheath is removed; the 5F catheter is in the ostium of the left common carotid artery. Open curved arrow, previous location of the ulcerated stenosis on the internal carotid artery.

G, Lateral projection.

Results

Discussion

CAS is an alternative revascularization technique for extracranial carotid stenotic disease. In September 1994, a multidisciplinary group of physicians, comprised of interventional neuroradiologists and interventional cardiologists (one of whom was board-certified in neurology), started to investigate CAS. From the beginning, the group based its technique on the premise that combining angioplasty with elective intravascular stent placement will increase the reliability and safety of the method. The first series of patients in this study who underwent stenting was reported in 1995 (3).

Refinements in patient and lesion selection and interventional technique as well as an increase in our understanding of several factors that improve outcome (15) have resulted in reducing the incidence of neurologic complications. From an 8.2% complication rate in 1994 to 1995, we reduced the complication rate to 4% in 1997 to 1998. On an annual basis, the incidence of minor embolic stroke has declined from 6.8% (1994–1995), to 5.8% (1995–1996), 5.3% (1996–1997), and 4% (including one retinal artery embolus 2 weeks after the intervention) (1997–1998).

In the clinical protocol, we place great emphasis on antiplatelet therapy before and after CAS. In our judgment, the low rate of acute and delayed stent thrombosis and elimination of acute poststenting embolic events is predicated on correct and compulsive doses of adjunctive antiplatelet therapy.

The patient selection was modified based on analysis of complications related to different groups of patients. Advanced age was the most important predictor of procedural neurologic complications, especially in patients older than 80 years (15). Patients with several comorbidities, especially those associated with significant hypertension, and patients who have recently suffered stroke, are also more prone to neurologic complications (11, 15). In our opinion, patients with severe brain atrophy/dementia and patients with Alzheimer's disease do not tolerate carotid stenting well. We do not accept patients with severe renal impairment, which precludes the safe use of a contrast agent, and we do not accept patients who are unable to tolerate appropriate doses of antiplatelet agents. On the other hand, our analysis showed that a number of higher risk situations for CEA represents ideal indications for CAS, such as restenosis after CEA (16), stenosis due to previous neck radiation and radical neck surgery (17), and lesions in distal internal carotid artery or involving high, retromandibular bifurcation. Sex, the presence or absence of neurologic symptoms, coronary artery disease, diabetes mellitus, hypercholesterolemia, smoking, and the presence of bilateral carotid lesions, ulcerations, or contralateral carotid occlusion do not significantly influence the incidence of neurologic complications (15).

In general, it should be noted that more systemic factors and comorbidities increase the risks associated with CEA, whereas local anatomic and lesion factors increase the risks associated with CAS. At the beginning of our experience, the only contraindication for CAS was pedunculated thrombus at the lesion site (thrombi are more easily seen on 7.5 or 15 frame/s cine angiograms than on digital subtraction angiograms). By analyzing our complications, it became apparent that the lesion severity (≥90% diameter stenoses) and the length and multiplicity of the stenoses were associated with more embolic complications (15). In our experience, patients at higher risk of neurologic complications are those with severely tortuous, calcified, and atherosclerotic carotid vessels and carotid stenosis with severe concentric calcifications. Significant kink, tortuosity, and angulated take-off of the internal carotid artery brings significant technical difficulties to CAS and is also prone to more complications. We completely abandoned recanalizations of occluded internal carotid arteries, not because they were associated with more embolic complications but because of a high rate of postrecanalization intracerebral hemorrhages.

Despite the presence of “difficult” lesions and anatomic situations and the presence of thrombotic, friable, atherosclerotic plaque in many patients with carotid disease, meticulous technique can minimize the risk of cerebral emboli. The initial complete brachiocephalic angiography not only remains the most reliable method for assessment of the precise degree of carotid artery stenosis but also reveals all anatomic conditions that are unfavorable to CAS and that will indicate that surgical therapy should be the intervention of choice. Preprocedural knowledge of contralateral carotid stenosis occlusion and the conditions of intracranial circulation (isolated hemisphere, collateral supply) can subtly modify the CAS technique (shorter balloon inflations). Significant distal and intracranial internal carotid artery stenosis that slows the blood flow is unfavorable to CAS, because slow flow is prone to acute stent thrombosis.

The coaxial technique with guiding sheath placement ascertains continuous access to the common carotid artery. This is important when the access to the bifurcation is more difficult (elongated arch, tortuosity of the common carotid artery), when the passage of the guidewire through the stenosis is difficult (eccentric stenosis, ulcerations, internal carotid artery kinks and tortuosities, angulated take-off of the internal carotid artery), and when complication develops (dissection, intracranial embolism). The disadvantages of using a coaxial system (sheath or guiding catheter) are as follows: 1) there is wider access into the common femoral artery; 2) the placement of the sheath can prolong the time of the intervention; 3) the sheath can change the anatomy of the bifurcation; and 4) eventually, dissection can be created in the innominate or common carotid artery by careless advancement of the sheath. The access sheath we use is thin-walled and kink- and pressure-resistant, with good flexibility. The sheath has an open-ended Tuohy-Borst manual adjusting valve seal, which permits unimpeded catheter or guidewire introduction and ease in avoiding air or thrombus entrapment. The side-arm fitting allows intermittent or continuous flushing and contrast injection and also allows for continuous intraarterial blood pressure monitoring. The sheath can be also used as a basis for precise measurement of the internal and common carotid artery size (quantitative carotid angiography) (a sheath outer diameter of 3 mm = 9 F). Heparin is injected through the sheath. This prevents formation of the clots within the sheath. The activated clotting time is raised to no more than 250 s. A higher rate could increase the tendency toward brain hemorrhage.

The experimental work of Ohki et al (18) has shown that embolic debris is potentially released with “primary stenting” without predilation and during lesion dilation with large, peripheral-type balloons. Our experience from coronary angioplasty taught us to use same technique for CAS. We never cross the stenosis with a wire larger than 0.018 inch. The Nitinol tips of the 0.014- and 0.018-inch wires are conveniently radiopaque, soft, flexible, and nontraumatic to the internal carotid artery. Throughout all steps of CAS, we are very careful to keep the position of the tip of the wire close to the skull base; the wire must be advanced through all kinks and tortuosities in the internal carotid artery. The position of the wire provides us the assurance that if a dissection develops distally to the stent, it can be easily approached and repaired. For routine predilation, we use low-profile coronary 4 × 40-mm balloons, which accept 0.018-inch wires. Four-millimeter balloon predilation does not cause major occlusive dissections and is sufficient for passage of the stent (Fig 1B). The inflation pressure we use is nominal, and the deflation should be slow and full before withdrawing the balloon. The length of the balloon (40-mm) is advantageous in that it prevents the balloon from sliding out from the stenosis during inflation. As mentioned, the 0.014-inch wire, if used, is exchanged for a 0.018-inch wire before stent placement. First, it is easier to advance and accurately place the stent over the stiffer wire, and second, the more robust wire straightens the internal carotid artery, again facilitating the delivery and deployment of the stent (Fig 1B). We do not practice primary stenting without predilation; it is our impression that later postdilation of the constricted stent is associated with more “scissoring” of the stent wires on plaque and eventual subsequent embolization. After predilation control arteriography is performed, predilation and placement of the 0.018-inch wire can change the anatomic characteristics of the bifurcation in relationship to the osseous neck structures, which we use for stent placement.

For stenting we use self-expanding stents. A balloon-expandable stent has several disadvantages when deployed within the carotid bifurcation or its vicinity. Frequently, more than one stent is needed. The stent has to be differentially expanded to accommodate the size of the internal carotid artery, bifurcation, and common carotid artery; thus, more than one balloon is needed for appropriate dilation. The delivery balloon can rupture while deploying the stent; there may be difficulties in advancing the balloon-stent assembly (especially a 20-mm stent) through the guiding sheath if the aortic arch is significantly distended or the proximal common carotid artery is tortuous. The balloon-expandable stents tend to occlude the external carotid artery more frequently. They may also undergo deformation (13) with appropriate restenosis. Three exceptions when using the balloon-expandable stent have been noted (see “Stenting: Stent Deployment and Postdilation”). In heavily calcified stenosis, the postdilation recoil is common (even with 5-mm balloon predilation), and forcing the current, relatively high profile stent delivery systems through the stenosis may break off plaque and cause embolization. In this situation, a short Palmaz (P104) stent or AVE (5-mm) stent is placed to hold the stenosis open before passing a definitive self-expanding stent.

Self-expanding stents have several advantages; with exceptions, only one stent is needed. They are easily deployed, especially knowing that the distal end of the stent has to be deployed from within the healthy part of the internal carotid artery. It is not significantly important where the proximal end of the stent will be located in the common carotid artery. They can be easily deployed using vertebral bodies as landmarks and are easily postdilated. The unconstrained diameter of the self-expanding stent to be deployed should be at least 1 to 2 mm larger than the largest vessel segment to be covered by the stent (ie, usually the common carotid artery). In the past, we used 8- and 10-mm-diameter stents. Lately, we have used almost exclusively 10-mm-diameter stents (Figs 1C and 2F and G) because the stent mesh covering the diseased vessel is tighter, minimizing the possibility of emboli during postdilation. If the stent is placed only in the internal carotid artery, we use an 8-mm-diameter stent. Although the internal carotid artery is commonly 2 to 3 mm smaller than the common carotid artery, follow-up studies have shown that oversizing the stent in the internal carotid artery does not cause any acute or late problems (19). The length of the stent depends on the length of the stenosis being 20 to 40 mm. We try to avoid placing the distal end of the stent into kinks and tortuosities of the internal carotid artery. These cannot be eliminated and are only displaced distally and become more exaggerated. In the past, the only available self-expanding stents were Wallstents (Wallstent, 135-cm usable delivery length; Boston Scient. Vasc., Minneapolis, MN). More recently, we have gained experience with nonshortening Nitinol self-expanding stents (Memotherm, Angiomed Bard Inc.; Smart Stent, Cordis Corp.; Acculink, Guidant, Inc.). These stents are less rigid, do not straighten the internal carotid artery as much as the Wallstents do, and can be more precisely placed using the distal and proximal markers. An important technical point is to release 3 to 5 mm of the stent distally and wait for the stent to expand fully and stabilize against the vessel wall before releasing the remainder of the stent. All the Nitinol stents have the tendency to “jump” distally if released too fast. Some of the newer stents need only a 6F delivery system. In our experience, it is safer to underdilate than to overdilate the self-expanding stent. Overdilation with a high pressure squeezes the atherosclerotic material through the stent mesh, causing emboli. A 10% to 15% remaining stenosis does not cause hemodynamic problems. The self-expanding stents have a tendency for late, progressive expansion, especially if oversized (19). Importantly, it is not necessary to dilate the stent to obliterate segments of contrast-filled ulcerations or parts of the bulb external to the stent. This angiographic appearance is of no prognostic significance, and follow-up angiography has documented complete healing of these lesions over time (6). Inflation of the balloon across the distal end of the stent can cause dissection within the internal carotid artery (two occurrences with our materials; in both cases, the dissection was covered by an additional stent). If the distal end of the stent is folded inwardly and needs to be adjusted to the vessel wall, the inflation of the appropriately sized balloon has to be “soft” with no more than 1 to 2 atm. As already pointed out, it is important to keep the tip of the wire through the neck segment of the internal carotid artery up to the skull base throughout the entire procedure; the dissection can occlude the internal carotid artery. Pronounced spasm can also mimic dissection. Significant brady arrhythmias are not uncommon during predilation and stent postdilation, especially when the stenosis is ostial or within the bulb of the internal carotid artery. Bradycardia and asystole usually recover spontaneously after balloon deflation; however, occasionally, 0.5 to 1 mg of atropine is required for correction. All our patients, with one exception, responded to pharmacologic correction of bradycardia and hypotension. None had to be admitted to the intensive care unit for this reason. More prolonged bradycardia and hypotension were associated with balloon-expandable stents that place more sustained pressure on the receptors, especially when bilateral stenting was undertaken during the same procedure. No other arrhythmias were observed. We do not routinely use atropine for premedication because most of our patients are elderly and have coronary heart disease. Initially in our experience, when using balloon-expandable stents, transvenous pacemaker wires were routinely placed in the right ventricle. We have since abandoned this practice. Despite rare occurrence of significant, prolonged bradycardia, external or internal cardiac pacing has to be available. A modest fall in blood pressure requires no specific intervention. Occasionally, spasm can develop in the internal carotid artery (Fig 1B), especially after placement of the 0.018-inch wire with straightening of the artery or after stent placement. This condition can be treated with intraarterial nitroglycerin (100–200 μmg) or regresses with time.

Loss of consciousness can occur with balloon inflation, especially if the ipsilateral hemispheric blood supply is isolated or if the contralateral carotid artery is occluded. This phenomenon recovers spontaneously after immediate balloon deflation (20).

CAS has rapidly evolved into a less invasive procedure than CEA to treat patients with symptomatic and significant asymptomatic carotid stenosis. With today's equipment and techniques, stenting mortality and morbidity rates associated with stroke-related complications are in the range of 3%, similar or lower to those of comparable patient populations treated with traditional CEA (21–23), and there are no cranial nerve palsies. With both percutaneous stenting and endarterectomy, embolic stroke events can occur. With each technique, the incidence of ischemic or embolic stroke depends on meticulous procedural technique and expertise and is markedly dependent on the volume of cases performed. With the availability of dedicated carotid stenting equipment (low-profile stent delivery systems with a variety of different stent designs, better access sheaths, and specially designed wires and balloons) and carotid neuroprotective devices, current CAS results will likely be enhanced. The relatively straightforward endoluminal approach lends itself to the use of distal protection devices designed to minimize the risk of cerebral embolization. Two approaches are presently under investigation. The first, proposed by Vitek et al (24) and pioneered by Theron et al (4), involves the use of a distal occlusion balloon (4, 24, 25). The column of blood containing embolic particles within the proximal occluded internal carotid artery is aspirated. The second approach involves the deployment of a filter, which is removed after completion of CAS. The filter device seems more physiological; it provides constant cerebral perfusion. Carotid neuroprotective devices have the potential to enhance the safety of carotid stenting greatly.