EXTRACRANIAL CAROTID DISEASE: RISK FACTORS AND MANAGEMENT
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Identifying The Patients For Treatment
Carotid angioplasty and stent placement are becoming increasingly popular interventions for carotid artery disease. It is important for clinicians to become familiar with clinical and radiological factors that stratify patients to treatment with angioplasty, angioplasty-assisted stenting, or CEA. More importantly, it is imperative that clinicians understand the risk of stroke associated with treatment versus observation alone. As is the case for most other surgical and interventional procedures, minimizing morbidity is achieved by thoughtful analysis of the patient’s neurological condition followed by exquisitely careful patient selection. Treatment for carotid stenosis has undergone rigorous scrutiny involving many multicenter trials for both asymptomatic and symptomatic stenosis. The data obtained from these studies has been used by clinicians to create treatment algorithms. We will review some of these trials, specific angiographic data, and technical developments of carotid stenting that may help to reduce the risk of stroke for specific cohorts with carotid stenosis.
Among the many trials examining stroke risk following treatment of carotid stenosis, the North American Symptomatic Carotid Endarterectomy Trial (NASCET) attempted to quantify stroke risk following CEA in medically-treated patients with symptomatic carotid artery disease.121 At 30 days from the time of surgery, the incidence of death was 1.1%, disabling stroke was 1.8%; and nondisabling stroke was 3.7%.122 Among 26 variables evaluated for stroke risk, the following criteria were found to portend increased risk of stroke: contralateral carotid occlusion, hemispheric TIA, left-sided procedure, ipsilateral ischemic lesion on CT scan, and irregular or ulcerated ipsilateral plaque. Other stroke risk factors included diabetes and elevated diastolic blood pressure. 122 Interestingly, previous cardiac intervention for coronary artery disease was found to reduce the risk of stroke. Results from NASCET demonstrated that patients with 70% or more stenosis had a 17% reduction in stroke following CEA as compared to medical treatment alone.121 Symptomatic stenosis in the 50 to 69% range was associated with a 5-year rate of ipsilateral stroke of 15.7% among patients treated surgically and 22.2% among those treated medically. No benefit of surgery was found for patients with less than 50% stenosis.122 We caution that these findings, as well as factors that portend increased stroke risk, were found in a post-hoc analysis of the NASCET data set.
In an analysis of patients randomized to CEA in the European Carotid Surgery Trial (ECST), the risk of major ischemic stroke or death following surgery was 7% and did not vary substantially with degree of stenosis.123 Conversely, the risk of major ischemic stroke ipsilateral to the unoperated symptomatic carotid artery did increase with severity of stenosis, most notably with stenosis in the 70 to 80% range. For patients with more than 80% stenosis, the Kaplan-Meier estimate of the frequency of a major stroke or death at 3 years was 26.5% for the medically-treated group and 14.9% for the surgery group, an absolute benefit from surgery of 11.6%. It is important to note that measurements of 80% stenosis in the ECST corresponded to approximately 60% stenosis in the NASCET.122
Treatment of carotid stenosis in asymptomatic patients has been extensively studied. Of the 721 asymptomatic patients with 60% or more carotid stenosis who underwent CEA in the Asymptomatic Carotid Atherosclerosis Study (ACAS), 1 patient died and 10 others had strokes within 30 days (1.5%).124,125 The estimated 5-year risk of ipsilateral stroke was 11% for the medical group and 5.1% for the surgical group. Risk factors for stroke included diabetes mellitus, contralateral siphon stenosis, radiation-induced stenosis, previous history of stroke, more than 60% contralateral stenosis, length of external carotid artery plaque, and use of local or regional anesthesia were associated with a higher risk of TIA and MI.126 In another analysis of asymptomatic patients with carotid stenosis, the combined incidence of ipsilateral neurological events was 8.0% in the surgical group and 20.6% in the medical group (P <0.001).127 The incidence of ipsilateral stroke alone was 9.4% in the medical group and 4.7% in the surgical group.
Increased Operative Stroke and Morbidity Risk
Many factors (mentioned above) portend an increased perioperative risk of stroke for patients undergoing CEA. Some of these same risk factors pertain to endoluminal carotid revascularization. Of these, pseudo-occlusion, or “slim” or “string” sign (angiographic indication of near-complete occlusion of the carotid artery) has been postulated to be of increased risk. According to a post-hoc analysis of the NASCET data, 106 patients with near-complete occlusion of the carotid artery were subdivided into those with (n=29) and those without (n=77) a string-like lumen. Of patients with near occlusion treated with surgery, 6% had perioperative strokes, similar to the group of patient with 70 to 94% stenosis. Only one of the medically-treated patients (1.7%) with near occlusion had a stroke within the first month. This data suggests that CEA is not needed on an emergency basis for patients with such lesions and that it does not portend increased stroke rates for this population as compared to patients with 70 to 94% stenosis.128
Intracranial or extracranial stenoses (such as those found with extracranial tandem lesions) portend an increased stroke risk for medically-treated patients with carotid stenosis but do not increase the perioperative risk.129 Although the results from ACAS suggest that contralateral intracranial carotid stenosis increases surgical morbidity, the presence of intracranial stenosis did not increase the surgical risk for a similar subset of NASCET patients. One hundred and fifteen (8.1%) patients enrolled in NASCET had 142 medical complications.130 The complications were MI and other cardiac disorders (8.1%), respiratory complications (0.8%), transient confusion (0.4%), and other complications (0.7%). Five patients died from these perioperative complications. These results suggest that patients with significant medical comorbidities may be better managed with stent placement versus CEA.
Identifying High Risks
The question arises whether it is possible to identify high-risk patients in need of carotid revascularization who may benefit from angioplasty-assisted stenting and avoid the surgical morbidity of CEA. What is clear are the risk factors that increase the incidence of stroke and the morbidity of surgery following CEA, but more evidence is needed to demonstrate whether stent placement significantly decreases the periprocedural morbidity in this subset of patients. Current prospective multicenter trials are underway to evaluate the effectiveness of carotid stenting in high-risk patients. Some evidence exists that there is a similar morbidity rate but an overall lower cost and shorter hospital stay following stenting versus CEA. In one study of nonrandomized groups with similar patient populations, major ipsilateral stroke and death occurred more frequently in the surgical group (2.9%) than in the stent group (0%), but the difference was not significant.131 The stent group also had a significantly shorter length of stay in the hospital. In a multicenter registry of 5,210 endovascular carotid stent procedures involving 4,757 patients, technical success was achieved in 98.4%.132 TIAs occurred at a rate of 2.82%, with a minor stroke rate of 2.72%. A major stroke rate of 1.49% and a mortality rate of 0.86% were observed. Restenosis rates of carotid stenting were 1.99% and 3.46% at 6 and 12 months, respectively. Roubin et al. reported their experience of more than 500 carotid stent procedures in a group of asymptomatic and symptomatic patients.133,134 There was a 0.6% fatal stroke rate and a 1% death rate from causes other than stroke during the 30-day periprocedural period. The major stroke rate was 1%, and the minor stroke rate was 4.8%. Over the 5-year study period, the periprocedural stroke rate improved from 7.1% to 3.1%.
Selection and Timing
Patient selection and timing of carotid stenting may minimize stroke risk. Recent radiographic evidence of a large infarction or a hemorrhage should delay elective carotid stenting for at least 6 weeks. Bovine or tortuous arches with ostial stenoses, inability to tolerate even temporary anticoagulation, severely tortuous carotid arteries, and poor routes of peripheral access (due to severe peripheral vascular disease) are vascular characteristics that may make CEA a more desirable option. Conversely, patients who have restenosis following a previous endarterectomy, contralateral carotid occlusion, a carotid bifurcation at the level of C2 or higher, dissecting lesions, severe coronary artery disease, or have undergone radiation therapy to the neck may be more likely to derive greater benefit from stenting. In a recent study by Lopes et al., the rate of stroke following both stenting and delayed coronary artery bypass surgery was 11%.135 This stroke rate was lower than that for CEA and coronary bypass surgery (performed either simultaneously or sequentially).
In a study of symptomatic and asymptomatic patients with carotid restenosis, the overall 30-day stroke and death rate was 3.7%.137 The minor stroke rate was 1.7%, and the major nonfatal stroke rate was 0.8%. The 3-year stroke-free rate was 96%. Another advantage of an endovascular approach in the setting of postsurgical restenosis is the lower incidence of cranial nerve palsies, which can be as high as 10% following CEA for restenosis.138 In a cohort of 62 high-risk patients with risk factors such as previous CEA, age greater than 80 years, previous neck irradiation, coronary artery disease, and significant contralateral carotid artery disease, carotid stents were successfully implanted (69 procedures in 62 patients).139 The major postprocedural complications included two minor strokes (2.9%), one major stroke (1.5%), and one fatal major stroke (1.5%).
As previously mentioned, several multicenter clinical trials are currently underway to investigate the efficacy of carotid stenting (with distal protection) compared to CEA, a time-tested procedure.
As carotid artery stenting continues to evolve, technology has become increasingly available to minimize stroke risk. Perhaps the most promising of these technologies involves distal protection with small, retrievable filters or balloons or techniques involving flow reversal. Examples include the PercuSurge Balloon (PercuSurge GuardWire, Medtronic AVE, Santa Rosa, CA), EPI Filterwire (Boston Scientific Embolic Protection Inc, San Carlos, CA), and Accunet (Guidant, Menlo Park, CA). Although the periprocedural incidence of neurological events is 5 to 9%, the incidence of embolic debris during carotid angioplasty and stent placement is substantially higher at 80 to 90%.132-134,140-147 The routine use of distal protection devices (available only for patients enrolled in clinical trials in which these devices are being evaluated – see Table 10) has demonstrated a 0 to 2% reduction in stroke rates. The protection device should be in place before stent deployment, as that has been shown to result in capture of the largest amount of embolic debris (versus at the time when the lesion is predilated and crossed with a wire). Clearly there will be high-grade stenoses that preclude the passage of high-profile distal protection devices before predilatation with an angioplasty balloon. In a review of 14 studies in which stents were placed to treat carotid artery stenosis, 73 (8.8%) of 834 patients had thromboembolic complications, of which 26 were TIAs and 47 (5.6%) were strokes, thereby demonstrating the clinical need for distal protection to prevent emboli.59 Several centers have described their techniques for carotid stent placement. It is often said that good judgment comes from experience and experience from poor judgment. On the basis of experience from more than 700 carotid artery stenting procedures, our group developed some techniques that maximize procedural success while minimizing morbidity. Our experience with carotid stent procedures has provided us with insight into complication avoidance and minimizing morbidity, while maximizing chances of successful revascularization. The following technical points will focus on stenting in the setting of irregular or complex anatomy, thus describing techniques which may avoid pitfalls that lead to common complications.
Tortuous aortic arches often pose significant challenges for maneuvering stents into the cervical carotid circulation. Without proper stabilization of the stent-delivery device, interventionists often lose position of the catheter and wire, potentially resulting in vessel injury. Techniques for straightening significant tortuosity or stabilizing guide catheters in bovine or wide arches include the use of “vascular scaffolding.” Difficult arches can be navigated by temporarily docking a guide sheath in the aortic arch and placing a stabilizing wire in the distal external carotid artery. The guide sheath and obturator are then advanced over this construct, proximal to the carotid artery lesion. A stabilizing, or “buddy,” wire may be left in place in the external carotid artery while crossing the stenosis with a 0.014 wire in the internal carotid lesion. Difficulty often arises in the setting of absent or diseased external carotid arteries. In this setting, the insertion of a 6-French sidewinder catheter (100 cm or longer) into the common carotid artery may provide sufficient support for subsequent advancement of the guide sheath over the catheter without wire assistance. As a last resort, or in the situation of tandem lesions involving the ostium of the common carotid artery, the guide sheath may be left in the aortic arch; and a stent can be navigated over a wire. Another situation for which stenting from the arch is an option is when there is guide catheter-induced flow arrest, which can result from excessive straightening of tortuous anatomy.
Reprinted with permission from Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA (eds): STROKE: PATHOPHYSIOLOGY, DIAGNOSIS, AND MANAGEMENT (4th edition), pp. 1475-1520 (chapter 78), Copyright Elsevier 2004. Permission has been granted to reproduce this material in online electronic format for non-exclusive world English rights.