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).

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.

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).

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.

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, A long 6F sheath is advanced over a dilator to the CCA. G, After removing the Amplatz wire and dilator, the lesion is crossed with a wire/filter device. H, Predilation. I, Stent placement. J, Stent deployment. The ostium of the ECA is often “jailed.” K, Postdilation. L, Final result.

An alternative to distal embolic protection is proximal protection. Two devices are available: the Gore flow reversal system (WL Gore & Associates, Flagstaff, AZ) and the Mo.Ma system (Medtronic, Minneapolis, MN). Both are positioned in a similar fashion. With the Gore device, the external carotid artery is accessed as described earlier and a balloon-tipped sheath is advanced over the 0.035-inch Amplatz wire into the CCA. This sheath has a port for an occlusion balloon to be placed in the external carotid artery. The external and common carotid balloons are inflated, arresting antegrade flow. The Mo.Ma system is similar but consists of a single sheath with two balloons: a proximal balloon in the CCA and a distal balloon in the external carotid artery. When the balloons are inflated, blood flow is arrested. In either system, once patient tolerance of balloon occlusion is confirmed, the internal carotid lesion is crossed with a 0.014-inch wire, dilated, and stented as described earlier. With the Mo.Ma system, blood is manually aspirated after the stenting procedure to clear the debris distal to the common carotid balloon. The Gore system, however, provides continuous flow reversal by having the arterial sheath connected to a venous sheath (Fig. 15-4). Although experience with these devices is limited, data indicate that they can provide excellent results.

Stents

There are two types of self-expanding stents: closed-cell and open-cell (Fig. 15-6). Open-cell stents are more flexible and may better navigate tortuous vessels. Closed-cell stents are more rigid but may better “cover” atherosclerotic plaque. Whereas some evidence suggests that the frequency of embolic complications in symptomatic patients is lower with closed-cell stents, others have found no significant correlation between stent design and outcomes. Typical stent sizes are 6 to 10 mm in diameter and 2 to 4 cm in length. Gentle postdilation with a ≤ 5-mm balloon is often performed to improve stent apposition with the vessel wall. There is no benefit to aggressive postdilation since the rates of restenosis and late loss are very low in the carotid artery. Balloons are conservatively sized (≤ 1:1) to minimize vessel trauma/dissection, plaque embolization, and stimulation of the carotid sinus. A poststent carotid diameter stenosis of ≤ 50% is an acceptable result. Figure 15-6C shows a carotid bifurcation lesion after self-expanding stent placement.

Figure 15-6 Closed- and open-cell stents. A, Closed-cell stents are less maneuverable but may better “cover” plaque. B, Open-cell stents have more “open” space and are more flexible. C, Baseline angiogram of right internal carotid artery stenosis (left); angiogram after self-expanding stent placement (right).

Following the procedure, if a filter-type EPD is used, the EPD is retrieved and final carotid and cerebral angiography is performed (Fig. 15-7). If a proximal protection device is used, the balloons are deflated and final angiography is performed. It is important to confirm that the carotid artery is free of dissection and that the cerebral vasculature is intact. Prior to removal of equipment, a neurologic exam assessing speech, movement, and mental status should be performed. If a neurologic deficit is found, a culprit lesion is sought and neurovascular rescue attempted.

Figure 15-7 Internal carotid artery (ICA) stenting. A, Baseline carotid angiography demonstrating ostial internal carotid artery (ICA) stenosis (arrow). B, Predilation with filter-type Embolic protection device (EPD) in place (arrow). C, Final angiography. The stent is placed across the ostium of the external carotid artery (ECA); ≤ 50% residual stenosis is an acceptable result.

Aorto-Ostial Interventions

Femoral access is obtained with a 6F to 9F sheath depending on the diameter of the balloon and stent that will be used. After anticoagulation (ACT ≥ 250 sec) and appropriate diagnostic imaging of the target lesion, a 5F diagnostic catheter is advanced through a guide catheter (i.e., JR4 or multipurpose guide) to the ostium of the target CCA. The ostial lesion is crossed with a steerable 0.035-inch hydrophilic wire. The diagnostic catheter is then advanced across the lesion into the distal vessel. The hydrophilic wire is exchanged for a stiff 0.035-inch Amplatz wire, and the guide catheter is carefully advanced over the diagnostic catheter until it engages the ostium of the CCA. The diagnostic catheter is then slowly removed.

The lesion is predilated with a balloon sized 1:1 with the CCA. As the balloon deflates, the guide is gently advanced or “telescoped” over the balloon and across the lesion. This will protect the stent as it is delivered to the lesion. The predilation balloon is removed, and a balloon-expandable stent is placed (in arteries protected by the axial skeleton, balloon-expandable stents are more often used). After positioning the stent at the target lesion, the guide catheter is withdrawn, uncovering the stent and placing it in contact with the target lesion. The proximal stent should protrude slightly into the aorta (≤ 1 mm) to ensure adequate lesion coverage. After verifying adequate placement with contrast injections through the guide catheter, the stent is deployed at nominal pressure (Fig. 15-8). As the balloon deflates, the guide is again gently telescoped over the balloon to allow further stents to be delivered distally if needed. Final angiography and neurologic assessment are performed. The access site is managed similarly to other interventional procedures. Sheath removal is performed when the ACT is ≤ 170 seconds if a closure device is not used.

Figure 15-8 Dilating and stenting aorto-ostial lesions. A, The lesion is crossed with a 0.035-inch wire and a predilation balloon is placed. B, The lesion is predilated, and as the balloon deflates, the guide catheter is advanced, thus “swallowing” the balloon. C, The guide is now distal to the lesion. D, The balloon is removed. E, A balloon-expandable stent is placed, although a portion of it remains within the guide. F, The guide is withdrawn, uncovering the stent and leaving it in contact with the lesion. G, The stent is deployed. If a stent is required distally, the stent balloon is “swallowed.”

Stroke

In a review of more than 54,000 patients, the 30-day risk of stroke during or after CAS was 3.9%. Symptomatic patients were twice as likely to have an adverse event as asymptomatic patients. While providing a good general idea of the stroke risk, this review found significant heterogeneity between studies, and stroke risk differs among patients depending on lesion severity, symptomatic status, and other factors such as renal function.

Most events occur within 24 hours of the procedure. If the patient develops a focal neurologic deficit during the procedure, an embolic event is assumed. Immediate cerebral angiography should be performed, and rescue intervention should be attempted. Typically these emboli are plaque elements and not amenable to thrombolytic agents. Attempts at revascularization with angioplasty and stenting and/or thrombectomy are recommended. Mental status changes after the procedure warrant evaluation by means of computed tomography to rule out intracranial bleeding or hyperperfusion syndrome (see the following section below).

Hemodynamic Instability

Stimulation of the carotid sinus baroreceptor is common during carotid interventions and can cause hypotension and bradycardia. Typically, patients who are most sensitive will react negatively to predilation of their lesion. Acute hypotension can lead to brain hypoperfusion and neurologic symptoms due to impaired cerebral autoregulation.

Atropine (0.4–1 mg) is used to treat acute bradycardia. A prophylactic dose may be considered before stent deployment if the patient was sensitive to predilation, but there is a risk of urinary retention in men. The dose may be repeated if necessary. Aggressive fluid administration is important in treating hypotension, but vasopressor medications are often needed to maintain a systolic blood pressure of 120 mm Hg. We use IV phenylephrine in repeated boluses of 50 to 100 mcg as needed. A continuous infusion may be required if hypotension persists. In most patients, however, phenylephrine can be weaned within several hours of the procedure, and the patient can ambulate in preparation for discharge the next day. Midodrine 2.5 to 10 mg three times daily can be useful to support blood pressure in the setting of prolonged hypotension. Adjusting the patient’s antihypertensive regimen will be necessary over the short term. Keep in mind that as in any interventional cardiovascular procedure, access site bleeding is a common cause of hypotension and should be ruled out in these patients.

Hyperperfusion Syndrome and Intracranial Hemorrhage

The opening of a stenotic carotid artery can lead to significant increases in cerebral blood flow, sometimes to levels more than twice the preprocedure flow. Hyperperfusion syndrome occurs in <1% of carotid stent patients and is defined clinically by the presence of an ipsilateral throbbing headache, a seizure, or a focal neurologic deficit. A chronically stenotic carotid artery can cause the cerebral vasculature to remain in a state of constant, maximal vasodilation. When the stenosis is suddenly alleviated, cerebral autoregulatory mechanisms fail to control blood flow, a problem exacerbated by hypertension. The resulting elevated cerebral perfusion pressure can lead to cerebral edema or, worse, intracranial hemorrhage.

Neurologic symptoms from cerebral edema are usually transient but must be addressed. A neurology consultation and head CT should be obtained if this diagnosis is entertained. When diagnosed, strict control of blood pressure is critical, and consideration of mannitol, diuretics, or antiepileptic medications (depending on presentation) is warranted. Medications that cause cerebral arterial vasodilation (i.e., hydralazine) should theoretically be avoided. Intracranial bleeding is life threatening. If it occurs, antiplatelet medications should be stopped and a neurosurgical team consulted. Strict blood pressure control (goal systolic pressure of 120–140 mm Hg) may decrease the risk of hyperperfusion syndrome and intracranial bleeding.

High Surgical Risk Patients

The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial is the only randomized trial comparing high surgical risk (HSR) patients treated with CEA to those treated with CAS. Patients (N = 334) with a symptomatic stenosis of ≥ 50% or an asymptomatic stenosis ≥ 80% (~30% were symptomatic) were randomized to either CEA or CAS. The primary end point of death, stroke, or MI at 30 days plus ipsilateral stroke or death from neurologic cause between day 31 and 1 year occurred in 12.2% of patients in the stenting group and 20.1% in the CEA group (P = 0.004 for noninferiority; Fig. 15-9). The 30-day stroke and death rate among the asymptomatic patients was 4.6% for the CAS group and 5.4% for the CEA group. At 3 years, there were no differences between the groups.

Figure 15-9 Freedom from major adverse events at 1 year in the SAPPHIRE trial.

(From Yadav JS, Wholey MH, Kuntz RE, et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004;351:1493–1501. Reprinted with permission.)

Most of the contemporary registry data focuses on HSR patients, and data from more than 10,000 HSR patients have been published. These registries generally include symptomatic patients with ≥ 50% stenosis and asymptomatic patients with ≥ 70–80% stenosis. Data from some of these studies are summarized in Figure 15-10.

Figure 15-10 Thirty-day outcomes from U.S. carotid artery stenting (CAS) studies/registries of high surgical risk patients.

Usual Surgical Risk Patients

Four large randomized studies in average or usual surgical risk patients compared CAS to CEA. The Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) trial found that the 30-day incidence of stroke or death was 9.6% in the CAS group and 3.9% in the CEA group. The Stent-Supported Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy (SPACE) trial noted that the 30-day rate of ipsilateral stroke or death was not different between the two groups (6.8% in the CAS group and 6.3% in the CEA group, P = 0.09 for noninferiority). However, the 2-year outcomes for this trial demonstrated a statistically significant benefit for CAS over CEA in patients <68 years of age (Fig. 15-11). The International Carotid Stenting Study (ICSS) published only their interim safety analysis, which demonstrated that the 30-day rate of death, stroke, or MI was 7.4% in the CAS group and 4% in the CEA group (P = 0.003). The rate of death and stroke alone also favored CEA (7.4% vs. 3.4%, P = 0.0004).

Figure 15-11 Two-year outcomes from SPACE. Age <68 years had better outcomes with carotid artery stenting (CAS) compared to carotid endarterectomy (CEA). Age ≥68 years appeared to have better outcomes with CEA.

The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) is the largest randomized trial published comparing CAS with EPD to CEA (Fig. 15-12). The primary outcome of periprocedural stroke, death, or MI or follow-up ipsilateral stroke was not significantly different between the two groups (7.2% for CAS and 6.8% for CEA). The 30-day risk of stroke was higher for CAS (4.1% vs. 2.3%, P = 0.01), whereas CEA was associated with a higher 30-day risk of MI (2.3% vs. 1.1%, P = 0.03). CAS appeared safer than CEA for patients ≤ 69 years of age while CEA yielded better outcomes in those >70 years of age.

Figure 15-12 Results from CREST. CAS, carotid artery stenting; CEA, carotid endarterectomy; MI, myocardial infarction.

CREST differed from the previous three trials in three significant ways. Most importantly, the European trials, EVA-3S, SPACE, and ICSS, allowed inexperienced operators to treat patients. All allowed stent operators, but not surgery operators, to be “tutored” during the randomized trial. CREST requirements were more stringent. In fact, many of the “experienced” CAS operators in the first three trials were not very experienced. The fact that so many neurologic events involve the nonculprit carotid circulation is testament to the importance of catheter skills, and the value of experience cannot be overstated. Second, CREST mandated the use of EPDs, whereas the other trials did not. Lastly, just over 50% of the patients in CREST were symptomatic, whereas the other trials were specifically for symptomatic patients. When taken together, the message from these four trials is that CAS with embolic protection is a legitimate alternative to CEA for average surgical risk patients but only when performed by experienced operators. The Asymptomatic Carotid Trial (ACT-1) will further help evaluate CEA vs. CAS in asymptomatic, usual surgical risk patients. Preliminary data have been reported (Table 15-2).

^{Table 15-2} Preliminary Data From ACT-1

ACT-1, Asymptomatic Carotid Trial; MI, myocardial infarction.

^* Hierarchical: only the most serious event is counted.

The 2011 AHA guidelines on the treatment for extracranial carotid and vertebral artery disease give carotid stenting a class I indication in patients with symptomatic carotid stenosis of >70% by noninvasive imaging or >50% by catheter-based angiography if the periprocedural rate of stroke or death is <6%. This recommendation is independent of surgical risk. CAS in asymptomatic patients is given a class IIb indication if the degree of stenosis is >70% by catheter angiography. Carotid revascularization is contraindicated in those with a total occlusion of the target carotid artery and those with severely disabling strokes.