Indications and Patient Selection

There is irrefutable evidence that for certain patient populations CEA offers an advantage over best medical treatment (BMT) alone. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) generated prospective, randomized data demonstrating symptomatic patients with carotid stenosis greater than 70% and a perioperative stroke or death rate below 6% are best treated by CEA over BMT alone.^13,14 The Veterans Affairs Cooperative Studies Program (VACSP) also found a beneficial effect of CEA when compared to BMT.¹⁵ The Asymptomatic Carotid Atherosclerosis Study (ACAS) proved asymptomatic patients with carotid stenosis of greater than 60% could benefit from CEA with a reduction in 5-year ipsilateral stroke risk, provided that their perioperative stroke or death rate was less than 3% and their modifiable risk factors were aggressively treated.¹⁶ Based on the preceding results, the Stroke Council of the American Heart Association has published guidelines and indications for CEA.¹⁷ However, these key trials excluded patients deemed to be high risk for CEA. The initial indications for CAS were some of the key exclusion criteria from NASCET, VACSP, and ACAS, including restenosis after CEA, contralateral internal carotid artery (ICA) occlusion, previous neck irradiation, advanced age, renal failure, chronic obstructive pulmonary disease, and severe cardiopulmonary disease. The increasing use of CAS has led investigators to question whether either revascularization procedure is more beneficial over the other. Over the last 10 years, multiple studies have attempted to answer that question; however, variability in study design, technology used, and patient selection have made a comparison between CAS and CEA difficult.^12,18–22 It is beyond the scope of this chapter to detail individual study design flaws, results, and criticisms; however, several study trials have helped influence patient selection for CAS in my practice. The trial that led to U.S. Food and Drug Administration approval for CAS was the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE). The SAPPHIRE study led to a general sense that CAS was at least equivalent to CEA in high-risk patients. SAPPHIRE 30-day myocardial infarction (MI), stroke, and death rates were 4.8% in the CAS arm versus 9.8% in the CEA arm (P = 0.09).¹² One-year MI, ipsilateral stroke, and death rates were 12.2% in CAS versus 20.1% in CEA (P = 0.048). The 3-year incidence of stroke was 7% for both CAS and CEA. The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) randomized 1326 symptomatic and 1196 asymptomatic patients to CAS or CEA with a median follow-up period of 2.5 years. This study recently concluded that among patients with symptomatic or asymptomatic carotid stenosis, the risk of the composite primary outcome of stroke, MI, or death did not differ significantly in the groups treated by CAS from those treated by CEA.¹⁸ This study did find a higher risk of periprocedural stroke with stenting (4.1% vs. 2.3%, P = 0.01) and periprocedural MI with endarterectomy (1.1% vs. 2.3%, P = 0.03). Further, quality-of-life analyses among survivors at 1 year indicated that stroke had a greater adverse effect than did MI on a range of health-status domains. It is the current practice of my colleagues and I to offer CAS to asymptomatic or symptomatic patients who would benefit from CEA but are deemed to be too high a surgical risk for CEA.

Preoperative Preparation

All patients in our surgical practice undergoing CAS are reported in ongoing clinical registries. Pretreatment patient evaluation consists of a noninvasive study suggesting carotid stenosis and a neurologic assessment performed by a neurologist or neurosurgeon. On the day of the procedure, the patient’s National Institutes of Health Stroke Scale is assessed and recorded. Preoperative laboratory results include hematocrit, hemoglobin, platelet count, white blood cell count, serum creatinine, prothrombin time, and activated partial prothrombin time obtained within a week of intervention. My colleagues and I also routinely obtain a baseline 12-lead electrocardiogram. Further cardiac or pulmonary evaluation is performed case by case as deemed medically necessary. MI is always a primary or secondary endpoint for clinical trials; thus, postprocedure creatine kinase, creatine kinase-MB, and troponin-I levels are routinely collected the morning after the procedure. All patients have a baseline brain computed tomography or magnetic resonance imaging to document preexisting infarctions.

In our practice, all patients considered for CAS are started on aspirin at a dosage of 325 mg daily at least 5 days prior to the procedure. My colleagues and I also start clopidogrel at least 24 hours prior to the procedure but preferably 3 to 5 days prior to intervention. Clopidogrel is loaded as a 300-mg dose the day before or 75 mg daily 5 days prior to intervention. Some evidence suggests the combination of aspirin and clopidogrel decreases restenosis by inhibiting myointimal proliferation.^23–25 In emergent cases in which patients are not pretreated, patients are loaded the day of surgery with aspirin at 325 mg and clopidogrel at 300 mg. After the angiogram is completed and the determination to proceed with CAS is made, 4000 U of heparin is administered intravenously and redosed at 1000 U every hour until completion of the stenting procedure. Although not a standard of care, many surgeons check activated coagulation times with the practice of anticoagulating to achieve the goal of doubling these times.

Anesthesia and Intraoperative Monitoring

CAS can be performed under monitored anesthesia care (MAC) or conscious sedation in the majority of cases, with only the rare need to convert to general endotracheal anesthesia. In my practice, my colleagues and I have not needed to convert to general anesthesia in any case. MAC allows us to monitor the patient’s neurologic status throughout the case; thus, we have not found the need to use other physiologic monitoring, such as electroencephalogram or intraoperative transcranial Doppler. MAC is also preferable because many candidates we evaluate for CAS are high-risk surgical patients due to an underlying cardiopulmonary disease rather than an anatomic consideration. The decision on arterial line blood pressure monitoring is based on the patient’s cardiopulmonary status, but all arterial lines are removed immediately after the procedure.

Procedure

Arterial access is gained through the femoral artery using the Seldinger technique to place a 6-French (Fr) sheath over a guidewire. Next, a 5-Fr diagnostic catheter is used to catheterize the common carotid artery (CCA). If needed, catheterization of the other vessels should be performed prior to the catheterization of the carotid artery needing treatment. Cervical carotid arteriography is performed to assess the degree of carotid stenosis. The intracranial circulation is also assessed at this point to characterize collateral flow, estimate delayed cranial perfusion secondary to stenosis, and identify any tandem lesions. Once measurements are performed and NASCET criteria are met for carotid stenting, a 0.035-inch exchange-length wire is passed under fluoroscopic road map guidance into the internal maxillary artery via the 5-Fr diagnostic catheter. The diagnostic catheter and femoral sheath are then removed over the exchange-length wire, and a 6-Fr, 90-cm sheath is passed under fluoroscopic guidance to a position 1 cm proximal to the cervical carotid bifurcation. If tortuous vessel anatomy does not allow the stiffer sheath to make the turn from the aortic arch into the right brachiocephalic or left CCA, a triaxial technique is used to advance the much stiffer sheath through this turn. This technique uses the 5-Fr diagnostic catheter over the exchange-length wire inside the 6-Fr sheath to give more support to the sheath through the turn. It is important on anteroposterior projections during positioning of the 90-cm sheath to visualize the projection over the chest. This ensures the sheath is taking a normal path through the turn from the aortic arch and not buckling.

The 0.035-inch exchange-length wire (and 5-Fr diagnostic catheter, if used) is removed, and more accurate measurements using a magnified cervical carotid arteriogram are performed using the 8-Fr outer diameter of the sheath as the measurement standard. The stenosis is determined according to NASCET criteria (Fig. 88-1A). The diameter of a straight portion of the ICA distal to the stenosis is determined to select the appropriate size of the distal protection device (DPD) and the appropriate diameter of the angioplasty balloon. The diameter of the CCA and the length of the stenosis are also determined to ensure selection of the appropriate length and diameter of the carotid stent. The carotid stent is sized so that it is 1 mm greater in diameter than the CCA.

FIGURE 88-1 A, Lateral arteriogram showing a calculation of extracranial ICA stenosis. This is expressed as the ratio of residual ICA lumen (labeled 2) divided by the estimated normal extracranial ICA diameter (labeled 1). B, Lateral fluoroscopic image demonstrating correct positioning of the DPD distal to the stenosis in the extracranial ICA. C, Anteroposterior fluoroscopic image demonstrating inflation of the angioplasty balloon within the stented extracranial ICA. D, Lateral unsubtracted arteriogram of the extracranial carotid artery following stent deployment and angioplasty of the ICA.

Next, the DPD is mounted on a 0.014-inch wire and advanced past the stenosis into the distal ICA under fluoroscopic guidance. The filter basket is deployed, with the surgeon taking care to position the filter distal enough to the stenosis to allow for positioning of the stent (Fig. 88-1B). My colleagues and I have found a very gentle curve on the guidewire tip helps the surgeon manipulate the wire past the stenosis. At this stage, we prefer to position and deploy the self-expanding carotid stent (Fig. 88-1C and D) in cases where the degree of stenosis will allow this, but we predilate with angioplasty if the degree of stenosis is severe enough to make stent passage difficult. If the lesion cannot be crossed with the DPD, the options are to perform the procedure without distal protection or the use of a proximal protection device that relies on flow reversal.²⁶ Once the stent is deployed and stent position is confirmed, the stent delivery system is removed over the 0.014-inch wire. Angioplasty is then performed under fluoroscopy (Fig. 88-1C). It is important to warn the anesthesia team prior to angioplasty, because this step can induce profound bradycardia, requiring treatment with atropine. This is particularly true when angioplasty involves the carotid bulb.

The final step is removal of the DPD with a DPD recapture catheter. Occasionally, if the stent extends around a turn in the carotid, it can be difficult to pass the retrieval catheter. In this case, removal is aided by straightening the stented section of the ICA by gentle external manipulation of the carotid artery or by the use of a second 0.014-inch wire as a “buddy wire.” The basket should be inspected for any debris. Prior to removal of the sheath, a poststent arteriogram is performed (Fig. 88-2). My colleagues and I routinely perform a poststent cerebral arteriogram and compare it to our initial prestent arteriogram to assess for any thromboembolic events during the stenting or angioplasty.

FIGURE 88-2 A, Lateral cerebral ICA arteriogram demonstrating poor intracranial flow in a symptomatic patient with severe extracranial ICA stenosis prior to CAS. B, Lateral cerebral ICA arteriogram demonstrating improved intracranial flow in the same patient following CAS and angioplasty.

Postoperative Care

Following CAS, almost all postoperative patients are sent to monitored floor beds for overnight observation and discharged home the following day. If there was significant intraprocedural hemodynamic change or there continues to be profound hemodynamic aberrations postoperatively, my colleagues and I monitor the patient in an intensive care unit until hemodynamic instability has resolved.

The clopidogrel is discontinued 6 weeks after intervention, and patients are continued on an aspirin dosage of 81 to 325 mg daily indefinitely.

Patients undergoing CAS have carotid Doppler monitoring performed shortly after stenting to obtain a baseline and then are reassessed at 6-month intervals thereafter. If further follow-up noninvasive imaging is needed, my colleagues and I prefer computed tomography angiography because the stent artifact on magnetic resonance angiography makes the latter futile for assessing restenosis.

Complications

Following successful deployment of the carotid stent and removal of the DPD, a repeat cerebral arteriogram is performed and compared with the prestent cerebral arteriogram to assess for any large vessel occlusions. If a large vessel occlusion is identified, treatment options include intra-arterial tissue plasminogen activator or intra-arterial abciximab. Another option is mechanical thromboembolectomy using the Penumbra System (Penumbra, Alameda, CA).²⁷ In rare cases where thrombosis is seen in the stent, my colleagues and I have used intravenous abciximab, because the thrombus is felt to be an acute platelet aggregation (Fig. 88-3).

FIGURE 88-3 Lateral extracranial carotid arteriogram demonstrating acute thrombus (arrow) in a freshly deployed carotid stent.

Another potential complication that can be identified on the poststent arteriogram is dissection of the artery at the ends of the stent. If a dissection is identified, it needs to be treated with a second stent across the dissection.

Outcome Data

The endovascular technique for CAS presented here has produced acceptable results in asymptomatic and symptomatic high-risk patients with carotid stenosis.²⁸ In a review of treatment outcomes found by my colleagues and I for 101 consecutive patients (109 stents), in which DPDs were used in 72% of the cases treated, the overall in-hospital adverse event rate was 8.3%. Periprocedural events included, 2 patients (1.8%) experienced a hemispheric transient ischemic attack, 2 patients (1.8%) had transiently symptomatic acute reperfusion syndrome, and 1 patient (0.9%) died of an MI. The 30-day MI, stroke, and death outcome included 3 patients (2.7%) with minor strokes, defined as a modified Rankin score of less than 3, at 1-year follow-up and 1 patient (0.9%) with a major stroke, defined as a modified Rankin score of 3 or more, at 1-year follow-up.

Conclusions

We presented the technique and outcomes at our clinic for CAS treatment of high-risk patients with extracranial carotid disease. Despite the debate generated by several large trials attempting to compare CAS and CEA,^12,18–22 my colleagues and I feel that—with proper patient selection, evolving endovascular technology, and attention to interventional technique—CAS is a viable option for high-risk surgical patients. Improved periprocedural outcomes in both our data and the most recent CREST add credence to CAS for extracranial carotid disease in the high-surgical-risk population.