Historical Perspective

Mathias and colleagues performed the first reported angioplasty of a carotid bifurcation in 1980.⁸ The indications initially were mostly nonatherosclerotic disease (radiation-induced or inflammatory stenosis); however, soon there was a push toward atherosclerotic disease, and that resulted in the discovery of an inordinate risk for iatrogenic dissection (5% to 8%) and distal embolic complications (8% to 10%).^9,10 This initial finding resulted in the impetus for discovery of a distal embolic shower protection (DEP) device. The first attempts were simply distal occlusion of the internal carotid artery through a balloon parked in parallel to the more proximal stent delivery system, followed by aspiration of blood and debris after angioplasty. This was refined by the development of a wire-mounted balloon (PercuSurge GuardWire; Medtronic AVE/PercuSurge Inc., Sunnyvale, CA) that allowed a balloon to be passed through the lesion for angioplasty while there was distal flow arrest. However, the results from carotid angioplasty remained dismal, principally from the high rate of recurrent stenosis, as well as procedural complications. Parallel development of coronary and peripheral vascular stents eventually resulted in the trial of a stent at the carotid bifurcation with inherent jailing of the external carotid artery in 1990.¹¹ This step single-handedly jettisoned CAS into a viable solution initially for patients considered very poor candidates for CEA.

The revolution that ensued has seen a wide variety of balloons for angioplasty, stents designed specifically for the carotid anatomy, an array of distal protection devices, and most recently, an entirely new way of distal protection achieved through flow reversal from the internal carotid artery into the arterial guide sheath, which is the conduit for deployment of devices across the carotid bifurcation. The major impetus for advancement of CAS came with publication of the results of the Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial,¹² which effectively demonstrated that patients considered to be at high risk with CEA were less likely to have complications if treated by CAS. This trial resulted in Food and Drug Administration (FDA), Centers for Medicare & Medicaid Services (CMS), and Medicare approval of CAS as a viable option in such patients. This brings us to the current era, during which a large number of trials that have been completed and others that are ongoing continue to refine our understanding of the uses and restrictions of CAS. The future for CAS appears to be clear: it is here to stay.

Carotid Endarterectomy Trials

Indications for and outcomes of CEA have been extensively studied. Support for performance of CEA is generated from four well-designed multicenter, randomized clinical trials—NASCET,^2,3 ECST,^6,7 ACAS,¹³ and ACST.⁵ NASCET^2,3 and ECST^6,7 addressed the use of CEA for symptomatic patients with 70% to 99% carotid stenosis or selected patients with 50% to 69% stenosis (Table 351-1). These studies resulted in class IA indications for the use of CEA in symptomatic patients meeting the appropriate criteria.¹⁴ However, it is important to realize that the general population of patients with carotid stenosis has substantially different demographics than do those who met the strict eligibility criteria for these studies.¹⁵ For instance, NASCET excluded patients 80 years and older and those with intracranial carotid stenosis more severe than the surgically accessible lesion; liver, kidney, or lung failure; cardiac valve or rhythm disorder; previous ipsilateral CEA; uncontrolled hypertension or diabetes; recent myocardial infarction (MI); or major surgery.² Such patients were considered to have excessive perioperative morbidity (i.e., high risk). Since publication of the NASCET results, patients considered for carotid revascularization are often divided into low- and high-risk groups, and this surgical risk stratification has been applied as an integral part of the study design in recent CAS trials.

The ACAS trial¹³ and the ACST⁵ addressed the use of CEA in asymptomatic patients. The degree of benefit from CEA for asymptomatic lesions is substantially less, and the indications for revascularization are still debated. ACAS and ACST demonstrated a 5.4% to 5.9% absolute reduction in risk over a 5-year period.^5,13 Therefore, periprocedural risks are particularly relevant to the decision analysis for the treatment of asymptomatic patients, with a morbidity rate higher than 3% minimizing any benefit. Nonetheless, as a result of publication of the ACAS trial, nearly 75% of CEAs in the United States are performed on asymptomatic patients.¹⁶

In the aforementioned trials, carefully selected low-risk patients were treated by highly experienced surgeons at high-volume medical centers. The low complication rates seen in NASCET and ACAS are often not obtained in the general population. Studies have shown perioperative stroke and death rates to range from 0%¹⁰ to 11.1%¹⁷ for symptomatic patients and from 0%¹⁸ to 5.5%¹⁷ for asymptomatic patients. In fact, a study of Medicare mortality data from hospitals participating in NASCET and ACAS demonstrated a 1.4% perioperative mortality rate¹⁵ as compared with 0.6% reported in NASCET² and 0.1% reported in ACAS.¹³ Perhaps equally concerning, CEA-related mortality rates have been demonstrated to be higher (2.5%) for low-volume hospitals,¹⁵ although other studies have argued that only small differences exist between mortality rates at high- and low-volume hospitals.¹⁹

Treatment decisions are also dependent on patient-specific factors. The presence of comorbid disease has a significant influence on outcome after CEA. Perioperative stroke and death rates for common comorbid conditions are 8.6% for congestive heart failure,^20,21 7.5% for age older than 75 years,^20,21 10.8% for postendarterectomy restenosis,²² 13.9% for ipsilateral carotid siphon stenosis,²⁰ 10.7% to 17.9% for intraluminal thrombus,^20,23 14.3% for contralateral carotid occlusion,²⁴ and 16.4% to 26.2% for CEA combined with CABG.^25,26 It is important to note that in the presence of such comorbidity, the natural history of carotid disease itself is grimmer. The investigators of the Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) “natural history” study monitored 1115 patients with asymptomatic internal carotid artery stenosis treated with medical therapy alone and identified significant differences in patient subgroups with respect to risk for stroke and death.²⁷ The highest risk group (82% to 99% stenosis according to NASCET criteria,² history of contralateral transient ischemic attack [TIA], and serum creatinine level >0.085 mmol/L) had a 4.3% annual ipsilateral stroke rate as opposed to 0.7% in the lowest risk group.^27,28

It should also be noted that since the aforementioned major randomized CEA trials began, best medical therapy has improved. In NASCET, the primary medical intervention was 1300 mg of aspirin on a daily basis.² This dose of aspirin is no longer used because lower doses have been proved to be equally efficacious with fewer side effects.^29–31 Other antiplatelet drugs, such as clopidogrel and ticlopidine, are also now available,^32,33 and the combination of aspirin and dipyridamole was shown to be more efficacious than aspirin alone.³⁴ Methods for blood pressure control were not specified in NASCET, whereas it is now known that blood pressure below 120 to 130/70 mm Hg is optimal for reduction of cardiovascular risk in patients with medical comorbid conditions^14,35,36 and that for primary stroke prevention, a 10–mm Hg reduction in systolic blood pressure produces a 31% reduction in the relative risk for stroke.³⁷ For secondary stroke prevention, angiotensin-converting enzyme (ACE) inhibitors^35,38 and the combination of a thiazide diuretic with an ACE inhibitor³⁸ have now been proved effective. Additionally, in the past decade, statins have assumed a prominent role in cerebrovascular and cardiovascular risk modification.^39–43 In a study of patients receiving medical therapy for severe carotid artery disease, statin use was associated with significantly lower rates of stroke, MI, and death.⁴⁴ It is likely that improvements in medical therapy for carotid atherosclerotic disease and related comorbidity should prompt periodic reevaluation and fine-tuning of the risk-benefit analysis for medical therapy versus surgical intervention.

With the great deal of complexity regarding risk assessment in this complex patient population, current standards are limited to minimizing overall surgical risk to maximize the probable benefit from surgery. Currently, the guidelines of the American Heart Association/American Stroke Assocation¹⁴ and the Canadian Neurosurgical Society⁴⁵ have established an upper limit of 6% for perioperative risk in symptomatic patients¹⁴ and a 3% upper limit in asymptomatic patients, assuming a life expectancy exceeding 5 years.²⁶

Publication of Carotid Angioplasty and Stenting Study Data

The results of trials comparing endovascular and surgical treatment of carotid stenosis are summarized in Table 351-2.^46–56 The first randomized trial comparing these treatments, the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), included 504 patients enrolled between 1992 and 1997 and was designed to compare balloon angioplasty alone with CEA.⁴⁶ Stents, when they became available, were incorporated as well but accounted for only 26% of cases. Twenty-four centers in Europe, Australia, and Canada participated, and as in previous CEA trials, high-risk surgical patients were excluded from enrollment, including those with recent MI, poorly controlled hypertension or diabetes mellitus, renal disease, respiratory failure, inaccessible carotid stenosis, or severe cervical spondylosis. CAVATAS demonstrated no statistically significant difference between endovascular and surgical treatment in the rates of disabling stroke or death within 30 days (6.4% for CAS versus 5.9% for CEA) and no significant difference in 3-year ipsilateral stroke rates. It is interesting to note that only 26% of patients randomized to endovascular treatment actually received stents. This becomes even more pertinent when one considers the 3-year ipsilateral stroke rates. These early encouraging results generated a great deal of interest in CAS, and further studies were undertaken.

The Wallstent trial,^47,48 the first multicenter randomized trial designed from inception to evaluate CEA and CAS equivalence, enrolled a total of 219 symptomatic patients with 60% to 99% stenosis. Thirty-day stroke or death rates were 12.1% with CAS and 4.5% with CEA (P = .049). Additionally, 12.1% of CAS patients suffered ipsilateral stroke, procedure-related death, or vascular death at 1 year versus 3.6% of CEA patients (P = .022), and as a result, the trial was halted by the Data Safety and Monitoring Committee after an interim analysis demonstrated worse outcomes for the CAS group. Critical to interpreting these results is the fact that distal protection devices were not used in the Wallstent trial. A significant proportion of major CAS neurological complications are due to embolization of atheromatous material.^57–60 Devices that capture embolic debris released during CAS have significantly improved procedural safety.^57,60–64

One of the first trials to use embolic protection was Carotid Revascularization Using Endarterectomy or Stenting Systems (CaRESS),^54,55 a multicenter, nonrandomized, prospective study comparing CAS with embolic protection (n = 143) and CEA (n = 254) in symptomatic (32%) and asymptomatic (68%) patients at low and high surgical risk. An important feature of CaRESS was that the treatment procedure was chosen by the treating physician and the patient, not randomized. Although this study design probably introduced selection bias, the CaRESS trial represents a generalized perspective on carotid revascularization and more closely represents its “real-world” application. Baseline group demographics were similar, except that patients with previous carotid interventions more often underwent CAS. No statistically significant difference between 30-day and 1-year death or stroke rates existed between CAS and CEA (2.1% versus 3.6% and 10.0% versus 13.6%, respectively), nor were significant differences found for restenosis, residual stenosis, repeat angiography, and need for carotid revascularization. Overall morbidity and mortality approached NASCET^2,3 and ACAS¹³ standards and represent the lowest rates among the major CAS trials to date. The low stroke and death rates may be attributable to the ability of the treating physician to consider patient-specific factors and successfully assign each patient to the safest therapy.

CAS was well established as a treatment option for high-risk patients by SAPPHIRE,¹² a randomized, multicenter trial designed to determine CAS noninferiority to CEA in high-risk patients. Eligible patients (n = 334) had symptomatic stenosis of at least 50% or asymptomatic stenosis of at least 80%. The 30-day MI, stroke, or death rate was 4.8% for CAS and 9.8% for CEA (P = .09). Much of this difference was secondary to MIs occurring in the CEA group, and although not reported in the SAPPHIRE publication, the 30-day rate of stroke and death was approximately 4.8% for CAS patients and around 5.6% for CEA patients. At 1 year, 12.2% of CAS patients had suffered stroke, MI, or death versus 20.1% of CEA patients (noninferiority analysis: P = .004; superiority analysis: intention to treat, P = .053; as treated, P = .048). MI and major ipsilateral stroke rates were significantly better after CAS than after CEA (2.5% versus 8.1%, P = .03; 0% versus 3.5%, P = .02; respectively).

Because SAPPHIRE had shown such clear noninferiority in high-risk patients, the Stent-supported Percutaneous Angioplasty of the Carotid artery versus Endarterectomy (SPACE) trial⁵⁰ set out to establish noninferiority for CAS versus CEA in low-risk patients. In this multicenter trial, the safety and efficacy of CAS and CEA were compared in 1183 randomized patients with symptomatic carotid artery stenosis (≥70% by duplex ultrasonography, ≥50% by NASCET criteria,² or ≥70% by ECST criteria⁶). The 30-day rates of ipsilateral stroke or death were 6.84% for CAS and 6.34% for CEA (P value not significant).⁵⁹ It is important to note that embolic protection was not required and was used in just 27% of patients, although a subgroup analysis did not demonstrate a significant difference between patients with embolic protection and those without. Despite these encouraging results, “SPACE failed to prove the non-inferiority of carotid-artery stenting”⁵⁰ statistically. This is because the trial was halted more than 700 patients shy of its goal enrollment of 1900 as a result of an interim analysis demonstrating that 2500 patients would be needed to reach significance given the results up to that point. The steering committee acknowledged a “lack of funds”⁵⁰ to expand the trial to an enrollment of 2500 patients and therefore halted the trial. In essence, the study was underpowered to demonstrate noninferiority because of incorrect estimation of the anticipated effect sizes. Still, although its a priori goals were not realized, the 0.51% difference observed in perioperative stroke or death between CAS and CEA was not statistically significant and is well within the published differences between individuals, institutions, and variations of CEA.

The SPACE results, even though they were negative, were still quite encouraging to CAS proponents. Unfortunately, a second multicenter, randomized trial to assess the noninferiority of CAS versus CEA in patients with more than 60% stenosis, Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S), was ended after interim analysis (n = 527) demonstrated the 30-day rate of any stroke or death to be significantly higher in the CAS group (9.6%) than in the CEA group (3.9%) (P = .01).⁵² Importantly, early in the trial the use of embolic protection was not required. Patients treated without embolic protection experienced a 25% 30-day rate of stroke or death (5 of 20 patients), which prompted changes in protocol by the EVA-3S safety committee. Additionally, EVA-3S compared groups of physicians with unequal experience. Surgeons performing CEA had performed at least 25 endarterectomies in the year before trial entry, yet endovascular physicians were certified after completing as few as 5 to 12 CAS procedures (5 CAS among at least 35 stent procedures on supra-aortic vessels or 12 CAS). Endovascular physicians were also allowed to enroll study patients while simultaneously undergoing training and certification. Subgroup analysis based on CAS physician experience demonstrated a 12.3% stroke and death rate for endovascular physicians tutored in CAS during the trial,⁵² 7.1% for those tutored in CAS during their endovascular training, and 10.5% for physicians with experience in CAS. The resulting overall rate of stroke and death (9.6%) is substantially higher than that in other randomized trials. Therefore, it is hard to accept such an elevated complication rate as representative of the practice of CAS in general. It is more likely that EVA-3S emphasizes the importance of embolic protection, as well as rigorous training and credentialing for CAS physicians. The implied importance of embolic protection in EVA-3S has been further supported by numerous imaging studies examining the frequency of (mostly small, asymptomatic) ischemic lesions on postoperative magnetic resonance imaging (diffusion-weighted imaging [DWI]). These studies have demonstrated the following: a reduction in the frequency of lesions seen on DWI with distal embolic protection (49% versus 67%)⁶² and fewer lesions noted on DWI after CEA than after CAS (11.6% versus 42.6%, no significant clinical difference) with current embolic protection devices,⁶⁵ as well as a low frequency of DWI-confirmed lesions with more recent embolic protection devices, such as the Parodi flow reversal system (NeuroProtection System, W. L. Gore & Associates, Flagstaff, AZ),⁶⁶ at a rate not significantly different from that incurred by diagnostic cerebral angiography alone (18.2% versus 11.5%).⁶⁷

Carotid registries are nonrandomized outcome records for symptomatic and asymptomatic high-risk CAS patients. These registries include Arbeitsgemeinschaft Leitende Kardiologische Krankenhausarzte (ALKK); ACCULINK for Revascularization of Carotids in High-Risk patients (ARCHeR); Boston Scientific EPI: A Carotid Stenting Trial for High-Risk Surgical Patients (BEACH); Carotid Artery Revascularization using the Boston Scientific FilterWire EX/EZ (CABERNET); Carotid Acculink/Accunet Post Approval Trial to Uncover Unanticipated or Rare Events (CAPTURE); Carotid Artery Stenting with Emboli protection Surveillance—Post Marketing Study (CASES-PMS); and Carotid Revascularization with ev3 Arterial Technology Evolution (CREATE) (Table 351-3).^68–75 Although registries do not provide direct comparison data, they do help establish true adverse event rates in high-risk CAS patients and are a crucial component for improving our understanding of the risks associated with CAS. The collaborators of CABERNET found a 4.0% 30-day rate of death, stroke, and MI (N = 446 patients),⁷¹ whereas the investigators of ARCHeR (N = 581 patients) found a 30-day stroke or death rate of 6.9%, as well as a 1-year composite outcome (30-day rate of MI, stroke, or death plus the 1-year rate of ipsilateral stroke) of 9.6%.⁶⁹ CREATE (N = 419 patients) demonstrated a 6.2% 30-day rate of MI, stroke, and death.⁷⁵ The CAPTURE registry (N = 3500) determined that the post-CAS incidence of stroke, MI, and death was 6.3% for patients treated with the Acculink/AccuNet CAS system (Abbott Vascular, Santa Clara, CA), as well as a rate of major stroke or death of 2.9%.^72,73 The BEACH investigators (N = 747 patients) found a 30-day MI, stroke, or death rate of 5.8%.⁷⁰ These results were similar to those in the CASES-PMS registry (5.0%), which examined the use of distal protection by endovascular carotid surgeons who either had previous experience with the device (AngioGuard XP, Cordis Endovascular, Warren, NJ) or underwent formal training (N = 1493).⁷⁴ Under these rigorous conditions, the 30-day major adverse event rate did not vary significantly between symptomatic and asymptomatic patients and among physicians with high and low volume or differing level of experience with the specific distal protection device. The German ALKK registry (N = 1888 patients), which included patients with standard risk, demonstrated an in-hospital death and stroke rate of 3.8%.⁶⁸ Interestingly, when this risk was stratified by time, the investigators saw improvement from 6.3% in 1996 to 1.9% in 2004 (P = .021). Continued effort to maintain rigorous registries such as those just described is critical to our eventual understanding of appropriate patient selection and procedural risks.

TABLE 351-3 Carotid Angioplasty and Stenting Registries

ALKK, Arbeitsgemeinschaft Leitende Kardiologische Krankenhausarzte; ARCHeR, ACCULINK for Revascularization of Carotids in High-Risk patients; BEACH, Boston Scientific EPI: A Carotid Stenting Trial for High-Risk Surgical Patients; CABERNET, Carotid Artery Revascularization using the Boston Scientific FilterWire EX/EZ; CAPTURE, Carotid Acculink/Accunet Post Approval Trial to Uncover Unanticipated or Rare Events; CASES-PMS, Carotid Artery Stenting with Emboli protection Surveillance—Post Marketing Study; CREATE, Carotid Revascularization with ev3 Arterial Technology Evolution; MI, myocardial infarction.

Current Studies

The two major most recently completed randomized trials of CAS versus CEA are the Carotid Revascularization Endarterectomy versus Stent Trial (CREST) and the International Carotid Stenting Study (ICSS). CREST was a National Institutes of Health–funded, multicenter randomized trial that enrolled 2502 patients with greater than 50% symptomatic carotid stenosis or greater than 70% asymptomatic stenosis for randomization to CEA or CAS.^76–80 Primary end points included death, stroke, or MI at 30 days and ipsilateral stroke within 60 days. CREST maintained a rigorous credentialing phase for CAS providers. CREST demonstrated no significant difference in the primary endpoint (30-day MI, stroke and death rate) between CAS (5.2%) as compared with CEA (4.5%) (p = 0.38). The major differences between the two treatments were that minor strokes (not major) were more common following CAS (3.2 vs. 1.7%, p = 0.01) whereas MI (1.1 vs. 2.3%, p = 0.03) and cranial never injury (0.3 vs. 4.7%, p < 0.0001) was more common after CEA. ICSS resulted from the favorable results of CAVATAS and is also known as CAVATAS-2. ICSS⁸¹ randomized 1713 patients; in this study, the primary endpoint, similar to CREST, were more common after CAS (8.5% vs. 5.2%, p < 0.006). However, similar to SPACE and EVA-3S, there were issues regarding credentialing being more rigorous for the group performing CEA, as compared to CAS.

ICSS resulted from the favorable findings of CAVATAS and is also known as CAVATAS-2.⁸¹ It is a multinational prospective trial randomizing symptomatic patients equally suited for CAS or CEA. Additionally, lessons learned from EVA-3S are being applied. Attendance at a CAS training course is required, as well as mandatory proctoring for centers with limited experience admitted to the trial on a probationary status. Furthermore, embolic protection is recommended whenever the endovascular physician believes that a protection device can be safely deployed.

An additional ongoing study is the Asymptomatic Carotid Stenosis, Stenting versus Endarterectomy Trial (ACT I), a randomized trial consisting of low-risk patients with asymptomatic 80% to 99% carotid stenosis at multiple centers across North America.⁸² The primary outcomes will be 30-day MI, stroke, and death rates and 5-year stroke-free survival. Another study, the Transatlantic Asymptomatic Carotid Interventional Trial (TACIT) will randomize standard- and high-risk patients with asymptomatic carotid stenosis into one of three treatment arms: optimal medical therapy only (antiplatelet, antilipidemic, antihypertensive, strict diabetes control, and smoking cessation), optimal medical therapy plus CEA, or optimal medical therapy plus CAS with embolic protection.⁸³ Planned enrollment is 2400 patients with a primary end point of occurrence of stroke and death at 3 years. Secondary end points include rates of TIA and MI, economic cost, quality-of-life analysis, neurocognitive function, and carotid restenosis.

Most recently, preliminary results have been made available for the Parodi flow reversal system (Gore Neuroprotection System) in the Embolic Protection with Reverse Flow (EMPiRE) trial, which demonstrated a 30-day rate of TIA, stroke, MI, and death of 4.5%.⁸⁴ Additionally, the results of the Evaluating the Use of the FiberNet Embolic Protection System (EPS) in Carotid Artery Stenting (EPIC) trial demonstrated a 30-day rate of 3% for TIA, stroke, MI, and death (N = 237 patients) when using the FiberNet distal embolic protection system (Lumen Biomedical, Plymouth MN).⁸⁵ Continuing efforts and eventual completion of these trials or publication of the final results of these trials will improve our understanding of the relative indications for and contraindications to CAS and CEA.

Indications for Carotid Angioplasty and Stenting

The current indications for CAS are principally based on FDA and CMS approval for patients considered to be at high risk with CEA. As additional data become available from CREST, ICSS, ACT I, and other ongoing trials, further broadening of the indications for CAS is expected. However, at present, CAS should ideally be performed either in the setting of a patient with high surgical risk or after enrollment in an ongoing clinical trial. Guidelines for high surgical risk are principally derived from NASCET² and other CEA studies, as are indications for CAS. Therefore, CAS is approved for patients who are at high risk with CEA and have greater than 70% symptomatic carotid stenosis.

High-risk features for CEA include medical comorbid conditions, most prominently concurrent coronary artery disease causing angina and requiring CABG, recent or ongoing MI, and congestive heart failure (Table 351-4). Other medical risk factors extrapolated from NASCET include uncontrolled hypertension or diabetes and lung, liver, or renal failure. Additionally, CEA is considered high risk in patients older than 80 years. Surgical high-risk features include previous ipsilateral CEA or other perilesional surgery, previous neck irradiation, tracheostomy, or contralateral laryngeal palsy, all of which are related to the higher risk posed by surgical dissection during CEA. Anatomic considerations include a carotid bifurcation (lesion) located above the C2 vertebral body or below the clavicle or a very short neck and relatively high bifurcation, as well as severe neck arthritis causing a marked reduction in neck mobility during positioning for CEA. Another category of risk factors pertains to the available cerebrovascular reserve that renders CEA high risk, such as contralateral carotid occlusion and tandem lesions beyond the accessible cervical carotid artery. Similarly, neurological instability is also a recognized high-risk feature for CEA, including crescendo TIAs, stroke in evolution, TIAs while receiving heparin, multiple strokes, recent stroke, and acute occlusion.

TABLE 351-4 High-risk Features for Carotid Endarterectomy

Procedural Technique

CAS continues to evolve as a result of developing technology, evidence-based medicine, and operator experience. Here we describe our current routine for most CAS procedures; major steps for the procedure are illustrated in Figures 351-1 to 351-5. We briefly describe specific technologic considerations to entertain when planning CAS.

FIGURE 351-1 A 5 French diagnostic catheter is advanced into the external carotid artery on the affected side, and as the inset indicates, a stiff 0.35-inch exchange wire is left in the external carotid artery.

FIGURE 351-2 A 6 to 10 French guide is then brought into the common carotid artery over the exchange wire, and as the inset indicates, the wire and any introducer catheter are then removed from the guide sheath.

FIGURE 351-3 The lesion is then crossed with a 0.14-inch microwire (usually part of a distal embolic protection system). Once the lesion has been crossed, a distal embolic protection device is delivered through a microcatheter across the lesion and, as the inset indicates, unsheathed distal to the lesion.

FIGURE 351-4 After deployment of the distal protection device, a stent is brought up over the 0.14-inch microwire (left) and advanced across the lesion, where it is deployed, with the stenotic segment revealed as a waist apparent in the stent (right).

FIGURE 351-5 The stent delivery system is then retrieved, and an appropriately sized postdilation balloon is advanced over the wire and inflated briefly to its nominal pressure (left). Next, the balloon is retrieved and an angiogram is performed to confirm satisfactory revascularization. Once confirmed, the distal embolic protection device is recaptured and withdrawn (right).

The processes of angioplasty and stenting create intimal injury that promotes thrombosis.⁸⁶ Therefore, patient preparation with adequate antiplatelet and anticoagulation therapy is essential. Patients receive a dual antiplatelet regimen consisting of aspirin (325 mg daily) and a thienopyridine derivative (i.e., clopidogrel, 75 mg daily, or ticlopidine, 250 mg twice daily) for at least 3 days before stent treatment. A loading dose of clopidogrel (300 to 600 mg) administered early on the day of the procedure is an alternative for patients who are already taking aspirin. An intravenous bolus dose of heparin (50 to 60 U/kg) is administered after catheterization of the common carotid artery. An activated coagulation time of 250 to 300 seconds is maintained throughout the procedure. The heparin infusion is usually discontinued at the conclusion of the procedure.

The procedure is performed in an angiography suite with biplane digital subtraction and fluoroscopic imaging capability. The patient is sedated but arousable for neurological assessment. A Foley catheter and two peripheral intravenous lines are inserted. Blood pressure, oxygen saturation, and cardiac rhythm are monitored during the procedure. The carotid artery is generally approached percutaneously from the common femoral artery. The operator should also be familiar with radial and brachial approaches in the event that femoral artery access is not possible.

An aortic arch angiogram is obtained initially to define the atherosclerotic burden, as well as the anatomic configuration of the great vessels, which allows the operator to predict the feasibility of carotid cannulation and select the devices needed for the procedure. Selective carotid angiography is then performed and the severity of the stenosis defined. The diameters of the common and internal carotid arteries are measured, with attention paid to determining a landing zone for the embolic protection device. Intracranial angiography is also essential before the intervention because the presence of tandem lesions should be considered in the management strategy, as well as for comparison of preintervention and postintervention intracranial angiograms to confirm the absence of any vessel dropout suggestive of embolism.

Bradycardia occurs occasionally during angioplasty, and consideration may be given to administering glycopyrrolate (0.4 mg) before performing CAS. Atropine and vasopressors (e.g., dopamine and phenylephrine [Neo-Synephrine]) should be readily available should significant bradycardia and hypotension develop. Continuous intraprocedural monitoring of heart rate, blood pressure, and neurological status is essential. Therefore, we routinely transduce the arterial sheath in the femoral artery to maintain continuous arterial pressure monitoring.

After completion of the diagnostic angiogram and positioning of the catheter in the common carotid artery, road mapping of the cervical carotid artery is performed. An exchange-length 0.035-inch wire is positioned in the external carotid artery. The diagnostic catheter is exchanged over the wire for a 90-cm, 6 to 10 French sheath, which is then advanced into the common carotid artery below the bifurcation. For patients who have undergone complete diagnostic cerebral angiography before the stenting procedure, a combination of a 6 French, 90-cm shuttle over a 6.5 French Head-Hunter 125-cm slip catheter (Cook, Bloomington, IN) or a 5 French 125-cm Vitek catheter (Cook) can be used. In these cases, the shuttle is introduced primarily into the femoral artery over a 0.35-inch wire and parked in the descending aorta. The inner obturator and wire are removed. The 125-cm catheter is then advanced into the shuttle, and the target vessel is catheterized. The shuttle is brought over the wire and the catheter in the common carotid artery. The size of the shuttle is usually dictated by the profile of the embolic protection device and compatibility with the stent system. An optimal angiographic view that maximizes the opening of the bifurcation and facilitates crossing the stenosis should be sought. The lesion is crossed with the protection device. Predilation of the stenotic vessel segment is performed at the operator’s discretion. We avoid predilation whenever possible. If the lesion does require predilation, we prefer to undersize the balloon to simply facilitate crossing of the stent, usually with a 2- to 3-mm-diameter balloon. A 3- to 4-mm coaxial angioplasty balloon is advanced to the lesion over the 0.014-inch wire holding the protection device. On rare occasion, predilation needs to be performed before the introduction of an embolic protection device.

The diameter of the stent should be sized to the caliber of the largest segment of the carotid artery to be covered (generally 1 to 2 mm greater than the normal caliber of the common carotid artery). Oversizing of the stent in the internal carotid artery does not usually result in adverse events, but a tapered stent can better conform to the vessel wall. Particular attention should be paid to selection of a stent that is long enough to cover the entire lesion.