doi: 10.1161/01.STR.0000125713.02090.27
(Stroke. 2004;35:e112.)
© 2004 American Heart Association, Inc.
Special Report |
Reporting Standards for Carotid Artery Angioplasty and Stent Placement
From University of California (R.T.H.), San Francisco; Columbia University (P.M.M.), New York, NY; Royal Perth Hospital, (C.C.P.), Australia; Miami Cardiac and Vascular Institute (J.J.C.), Fla; Mid-South Imaging and Therapeutics (J.D.B.), Memphis, Tenn; The Reading Hospital and Medical Center (D.S.), West Reading, Pa.
Correspondence to Philip M. Meyers, 710 W 168th St, Neurological Institute, New York, NY 10032. E-mail pmm2002{at}columbia.edu
 |
Introduction |
|---|
 Top Introduction Carotid EndarterectomyEndovascular Treatment of...Summary: Carotid StentingComplicationsComparison Between Treatment...CostsConclusionGlossary of Terms:References |
|---|
Cerebrovascular disease is the third leading cause of death in the United States.1,2 Approximately 750 000 people have a stroke annually, costing an estimated $45 billion in treatment and lost productivity.3,4 Carotid occlusive disease is responsible for 25% of these strokes.5 Large population-based studies indicate that the prevalence of carotid stenosis is approximately 0.5% after age 60 and increases to 10% in persons older than age 80 years. The majority of cases are asymptomatic.6–8 Surgical carotid endarterectomy is currently the accepted standard of treatment for revascularization of extracranial carotid occlusive disease.9 This has been validated by multiple, randomized, controlled trials that have demonstrated its efficacy over best medical therapy. However, in the past several years, carotid artery stenting has emerged as a potential therapeutic alternative to carotid endarterectomy for the treatment of atherosclerotic carotid artery disease. The future status of this endovascular approach will be determined by randomized trials directly comparing carotid artery stenting to endarterectomy, as well as by the potential for further innovation and improvement in endovascular devices, techniques, and safety. Comparisons of carotid stenting and endarterectomy are difficult because of differences in patient selection, the use of case series rather than randomized controlled trials for stenting, differences in definitions of outcomes and complications, and observer bias. The suggested reporting standards for carotid endarterectomy have not been uniformly followed up for surgical trials and not used in trials of carotid stenting.10 It is the purpose of this document to standardize reporting of carotid stent trials and recommend trial designs so that carotid stenting and endarterectomy may be fairly compared. This document is a consensus statement of the Technology Assessment Committees of the American Society of Interventional and Therapeutic Neuroradiology and the Society of Interventional Radiology.
|
Carotid Endarterectomy |
|---|
|
TopIntroductionCarotid EndarterectomyEndovascular Treatment of...Summary: Carotid StentingComplicationsComparison Between Treatment...CostsConclusionGlossary of Terms:References |
|---|
In 1953, DeBakey performed the first successful carotid endarterectomy for the treatment of an occluded cervical carotid artery.11 In 1954, Eastcott performed the first successful carotid endarterectomy in which the circulation to the brain was intentionally interrupted to remove a stenotic plaque.12,13 Despite only anecdotal evidence of efficacy,
1 million carotid endarterectomies were performed worldwide between 1974 and 1985.14,15 There was a temporary decline in the mid 1980s, when a number of critical reports suggested unacceptable rates of perioperative stroke or death,16–21 and a high rate of endarterectomy performed for inappropriate indications.22 Rates of carotid endarterectomy in the United States and Canada have again increased since the publication of favorable, well constructed clinical studies, beginning in 1991 with the North American Symptomatic Carotid Endarterectomy Trial (NASCET).23,24 In 1996, 130 000 carotid endarterectomies were performed in the United States; twice that of 1991; in 2000, it was estimated that 174 000 carotid surgeries were performed.25 Because endarterectomy is considered the gold standard of carotid revascularization, the major trials that document its safety and efficacy are summarized by the following text.
Randomized Trials of Symptomatic Patients
North American Symptomatic Carotid Endarterectomy Trial
The North American Symptomatic Carotid Endarterectomy Trial (NASCET) was conducted at 106 centers in the US and Canada and analyzed 2885 patients with symptomatic carotid stenosis that were stratified into 2 groups: 30% to 69% stenosis (2226 patients)25 and 70% to 99% stenosis (659 patients).23 The degree of carotid stenosis was determined by the ratio between the luminal diameter at the point of greatest stenosis and the normal artery beyond the carotid bulb. The eligibility requirements for the NASCET were strictly defined. Patients with symptoms within 120 days of randomization were considered symptomatic. Patient exclusion criteria included a previous ipsilateral endarterectomy; an intracranial lesion that was more severe than the surgically accessible lesion; no angiographic visualization of both carotid arteries and their intracranial branches; or lung, liver, or renal failure. Temporary exclusion criteria included uncontrolled diabetes mellitus, hypertension or unstable angina pectoris; myocardial infarction within the previous 6 months; contralateral carotid endarterectomy within the previous 4 months; signs of progressive neurological dysfunction; or a major surgical procedure within the previous 30 days. These patients could be included if the disorder responsible for their ineligibility resolved within 120 days of their qualifying cerebrovascular event. Neurological classification was performed 30 and 90 days after the procedure with strokes (any new focal neurological deficit lasting >24 hours) categorized as disabling (modified Rankin score 
3) or nondisabling. If sufficient functional recovery occurred within 90 days, then the stroke could be reclassified from disabling to nondisabling.26
The authors reported a 5.8% incidence of perioperative stroke and death (0.6%) in the endarterectomy group. The inclusion of perioperative myocardial infarction (0.9%) increased the complication rate to 6.7%.23 There was an unequivocal benefit of surgery over best medical management in symptomatic patients with a severe carotid stenosis of 70%. Surgical intervention reduced the 2-year risk of any ipsilateral stroke in the medical group from 26% (annual event rate of 13%) to 9% in the surgical group, thus yielding an absolute risk reduction of 17%. Therefore, for every 100 patients undergoing surgery, 17 nonfatal strokes or deaths were prevented over a 2-year period. However, this risk reduction was not equal for all patients. The benefit was twice as great in patients with a stenosis of 90% to 99% as it was in those with a stenosis of 70% to 79%. At 8-year follow-up, the risk of an ipsilateral disabling stroke was 6.7%; of any ipsilateral stroke was 15.2%; of any stroke was 29.4%; and of any stroke or death was 46.6%. Therefore, despite the durability of endarterectomy in preventing an ipsilateral disabling stroke, the risk of any stroke or death over the ensuing 8 years was nearly 50%.25
The benefits of carotid endarterectomy in patients with symptomatic moderate stenoses of 30% to 69%, over a mean follow-up of 5 years, have also been reported. For patients with a stenosis of 50% to 69%, the 5-year rate of any ipsilateral stroke was 15.7% in the surgical group versus 22.2% in the medical group; an absolute risk reduction from any ipsilateral nonfatal or fatal stroke of 6.5% (1.3% per annum). However, among patients with 30% to 49% stenosis, the 5-year rate of any ipsilateral stroke was 14.9% for surgical patients versus 18.7% for medically treated patients, an insignificant risk reduction. The perioperative rate of disabling stroke and death was 2%.25
The surgical and medical complication rates for all patients (n=1415) undergoing carotid endarterectomy as part of the NASCET (30% to 99% symptomatic stenosis) have been reported.27,28 The overall rate of perioperative stroke and death (1.1%) was 6.5%. Five baseline variables were predictive of statistically significant increased surgical risk: hemispheric versus retinal transient ischemic attack as the qualifying event, left-sided procedure, contralateral carotid occlusion, ipsilateral ischemic lesion on CT scan, and irregular or ulcerated ipsilateral plaque. The incidence of perioperative wound complications was 9.3% and cranial nerve damage was 8.6%.27 Cardiovascular complications occurred in 8.1% of patients undergoing endarterectomy. Cardiovascular complications included myocardial infarction (1.2%), congestive heart failure (1.2%), and hypotension (2.1%). Patients with a history of myocardial infarction, angina pectoris, or hypertension were at significantly higher risk. Medical complications resulted in a prolonged hospitalization in 30% of cases.28
European Carotid Surgery Trial
The results of The European Carotid Surgery Trial (ECST), another large, multicenter, randomized controlled trial, were in accordance with the NASCET after adjustment for the different methods used to calculate the angiographic degree of carotid stenosis.29–31 The ECST method of calculating angiographic stenosis used an approximation of the normal carotid bulb diameter as the denominator rather than the distal cervical internal carotid artery, which was used in the NASCET, and resulted in overestimation of narrowing compared with the NASCET.
The ECST enrolled 3024 patients with symptomatic carotid stenosis stratified into 3 groups: 0% to 29%, 30% to 69%, and 70% to 99% stenosis, with a mean follow-up of 6.1-years. The ECST demonstrated that endarterectomy reduced the Kaplan-Meier 3-year risk of major stroke or death in patients with a symptomatic stenosis of 80% (60% as measured by the NASCET method) from 26.5% in the control group, with an annual event rate of 8.8%, to 14.9% in the surgical group, thus giving an absolute risk reduction of 11.6% at 3 years. The rate of nonfatal stroke, defined as symptoms lasting >7 days or death (1.3%) from surgery was 7%. The ECST did not specify rates of nonstroke surgical complications such as cranial nerve injury or cardiac events.31,32
Veterans Affairs Cooperative Carotid Trial
The Veterans Affairs Cooperative Symptomatic Carotid Stenosis Trial (VA-CSP-309) was a third randomized trial evaluating endarterectomy in symptomatic carotid stenosis, but it was prematurely terminated when the NASCET and ECST data were released.33 The VA-CSP-309 study enrolled 189 male patients, with a mean follow-up of 11.9-months, and demonstrated an absolute risk reduction for stroke or crescendo transient ischemic attacks of 11.7% in men with a carotid stenosis >50% who underwent endarterectomy (17.7% for stenosis >70%). They reported a perioperative surgical stroke and death rate of 5.5%. Among the 3 perioperative deaths, none was caused by ischemic stroke.
Randomized Trials of Asymptomatic Patients
Asymptomatic Carotid Atherosclerosis Study
The only large, well-constructed, randomized, controlled trial published to date comparing surgical endarterectomy with medical therapy in asymptomatic carotid stenosis is the Asymptomatic Carotid Atherosclerosis Study (ACAS), which enrolled 1662 patients at 39 centers with a median follow-up of 2.7 years.34 As in the NASCET, the inclusion criteria for the ACAS were stringent. Patients were excluded from the ACAS because of previous cerebral infarction; previous endarterectomy with restenosis; previous extracranial-to-intracranial bypass; any disorder that could seriously complicate surgery or prevent continuing participation over 5 years; long-term anticoagulation therapy; or a surgically inaccessible lesion.
Patients in the medical control group received 325 mg aspirin per day. Some authors have suggested this does not represent optimum medical therapy (the recommended dose in the NASCET was 1300 mg per day), because high-dose aspirin, ticlopidine, and aspirin combined with warfarin may be more effective.35 The ACAS reported an actuarial estimated 5-year risk, with a mean follow-up of only 2.7 years, for ipsilateral stroke and any perioperative stroke or death in patients with a carotid stenosis of 60%, of 5.1% for surgical patients versus 11%, with an annual event rate of 2.2% for medically treated patients, and yielded an absolute risk reduction of 5.9%. Therefore, over a 5-year period, 1 stroke per year was prevented for every 85 patients undergoing endarterectomy. However, the absolute risk reduction for disabling ipsilateral stroke was only 2.6%, which doubles the number of endarterectomies needed to prevent 1 ipsilateral disabling stroke compared with any ipsilateral stroke. This result was obtained with a very low 30-day perioperative stroke and death (0.1%) rate of 2.3%; 52% of these complications attributable to strokes were caused by diagnostic cerebral angiography (arteriography stroke rate of 1.2%). Stratification of data revealed no significant reduction in risk of stroke or death for females undergoing endarterectomy. Furthermore, no correlation between benefit and degree of stenosis was demonstrated.
Veterans Affairs Cooperative Study
The Veterans Affairs Cooperative Study (VA-CSP-167), a smaller multicenter trial that enrolled 444 males with asymptomatic carotid stenosis 50%, failed to demonstrate a statistically significant difference in the combined rate of stroke or death between the endarterectomy and medical groups at a mean follow-up of 47.9 months. The authors concluded that a modest effect could not be excluded because of the relatively small sample size. The 30-day perioperative rate of permanent stroke or death was 4.7%, which included a 0.4% stroke rate from diagnostic cerebral angiography.36 As in NASCET and ACAS patients undergoing endarterectomy for symptomatic carotid stenosis of 70%, cardiac-related deaths were the most frequent cause of mortality in the endarterectomy patients.23,34
European Carotid Surgery Trial
The European Carotid Surgery Trial (ECST) also reported on the risk of stroke in the distribution of the asymptomatic carotid artery in 2295 patients stratified into 4 categories of carotid stenosis: 0% to 29% (n=1270); 30% to 69% (n=843); 70% to 99% (n=127); and occluded (n=55). During a mean follow-up of 4.5 years, the 3-year Kaplan-Meier risks for ipsilateral stroke and fatal stroke were 2.1% and 0.3%, respectively. The 3-year risk of ipsilateral stroke for patients with an asymptomatic, severe (70% to 99%) carotid stenosis was 5.7%. This was significantly less than the 17.1%, 3-year ipsilateral stroke risk for ECST patients with a symptomatic, severe, carotid stenosis treated medically, and not significantly greater than the 3.1%, 3-year ipsilateral stroke risk for a severe, symptomatic, carotid stenosis after successful endarterectomy.
Given the modest benefit results of the asymptomatic endarterectomy trials and the low annual event rates associated with asymptomatic carotid stenosis, the cost-effectiveness of performing surgical endarterectomy for asymptomatic carotid stenosis has been questioned.37 The results of a second, large, multicenter, randomized trial examining endarterectomy in asymptomatic carotid stenosis, The Asymptomatic Carotid Surgery Trial (ACST), currently in progress, are awaited.38
Mayo Asymptomatic Carotid Endarterectomy Study
The Mayo Clinic undertook a randomized controlled trial to compare the effects of carotid endarterectomy with medical treatment. Over 30 months of recruitment, 71 patients were randomized and 87 patients who were eligible but unrandomized were included in the follow-up protocol. The total ipsilateral perioperative stroke and death rate was 0% in the randomized group and 3% in the nonrandomized group. The major stroke and death rate was 0% for both groups. Too few cerebral ischemic events occurred to compare the efficacy of endarterectomy with low-dose aspirin for asymptomatic carotid stenosis. However, the trial was prematurely terminated because there was a significantly high number of myocardial infarctions and transient ischemic events in the surgical group compared with the medical group.39
Nonrandomized Studies
Innumerable case series of carotid endarterectomy have been published. A systematic review of the risk of stroke and death caused by endarterectomy for symptomatic carotid stenosis was performed by Rothwell et al.40 The authors analyzed 51 studies since 1980, including the NASCET, and reported an overall perioperative risk of stroke and/or death of 5.64%. The overall death rate was 1.62%, with the risk of a fatal stroke (0.86%) slightly exceeding the risk of a nonstroke death (0.7%). The authors noted there was significant heterogeneity in the reported stroke and mortality rates between studies. Surgical series in which neurological outcome assessment was independently adjudicated by neurologists reported significantly higher risks of stroke and death.41
Rothwell et al performed a similar systematic review comparing the risk of stroke and death caused by carotid endarterectomy, performed by the same surgeons in the same institutions, for symptomatic versus asymptomatic stenosis.42 The authors analyzed 25 studies since 1980 and reported an overall perioperative risk of stroke and/or death for asymptomatic lesions of 3.35%. This risk estimate was significantly lower than for symptomatic lesions (5.18%) and consistent across virtually all studies.
Results from randomized trials may not be generalizable to the results of treatment in clinical practice. Wennberg et al assessed the perioperative mortality among 113 300 Medicare patients undergoing carotid endarterectomy during 1992 to 1993 in "trial hospitals" (those participating in NASCET and ACAS, n=86), and "nontrial hospitals" (nonfederal institutions performing endarterectomy n=2613), looking at all patients treated rather than those selected for a trial.43 The perioperative mortality rate was 1.4% at trial hospitals compared with 2.5% at low-volume (
6 procedures/year) nontrial hospitals.
High-Risk Patients
NASCET, ACAS, and the VA Cooperative studies excluded patients with significant comorbid illnesses such as lung, liver, or renal failure, unstable angina, and recent myocardial infarction. Therefore, the complication rates reported in these studies may be lower than the rates achievable when all patients are included. Wennberg et al,43 as noted, found that the perioperative mortality rate at NASCET trial hospitals was 1.4% when all patients were included, compared with 0.6% in NASCET patients. Similar findings were reported by Lepore et al,44 who found that NASCET/ACAS trial-eligible patients had a perioperative stroke and death rate of 1.5% compared with 3.6% for trial-ineligible patients.45 However, according to Dorros, these "high-risk" patients were excluded from the NASCET, not because the surgical outcomes may have been adversely influenced but primarily because attendant comorbidities could have potentially contaminated the outcome data.46 The ASA and carotid endarterectomy (ACE) trial was a randomized trial of high- versus low-dose aspirin at the time of endarterectomy.47 Patients were not excluded based on comorbidities; therefore, the data are likely to reflect the patient selection found in standard medical practice rather than selecting only the patients at lowest risk. Both symptomatic (n=1292) and asymptomatic (n=1512) patients were treated. Most patients had a carotid stenosis >70% diameter. Among symptomatic patients, there was a 6.4% rate of perioperative stroke (minor or major) or death but only 2.8% rate of perioperative major stroke or death.48 Among asymptomatic patients, the rate of any perioperative stroke or death was 4.6%.
A retrospective analysis by Sundt, in which 3111 consecutive endarterectomy patients were stratified into 6 risk classes according to neurological status, comorbid conditions, and angiographic variables, revealed a very low major complication rate (permanent stroke, myocardial infarction, or death) for class I and II patients, whereas class IV patients had an 8.1% risk and 2.9% mortality (Tables 1, 2
).49,50 Factors correlating with an increased surgical morbidity and mortality included unstable neurological status; the presence of comorbid conditions; age older than 70; and contralateral internal carotid artery occlusion.
|
|
Estes et al followed a random sample of 22 165 Medicare beneficiaries, who underwent carotid endarterectomy between 1988 to 1990, until the year 1992. They identified patients with acute myocardial infarction, congestive heart failure, diabetes mellitus, and age older than 80 years as having diminished perioperative and long-term survival rates after carotid endarterectomy. Recurrent carotid stenosis has also been felt to indicate a higher risk of complication from endarterectomy. Meyer et al reported a perioperative morbidity and mortality rate of 10.8% in their series of 82 patients undergoing carotid endarterectomy for recurrent stenosis; that was 5 times the risk of a routine endarterectomy at their institution.51 Cranial and cervical nerve injuries may occur in 21% of patients, although there are few permanent injuries.52
Radiation-induced carotid stenosis is more difficult to treat surgically because of long lesion length, periarterial scarring with ill-defined planes of resection, and a higher rate of wound complications.53–55
These categories of high risk for carotid endarterectomy are not uniformly accepted. In a recent study, age older than 80 was found not to be a significant risk.56 Hill et al and O’Hara et al found no increased morbidity or mortality for re-operation for carotid stenosis compared with primary carotid endarterectomy.57,58 Combined carotid endarterectomy and coronary artery bypass grafting has a high risk of stroke, but this risk may come almost completely from the coronary artery surgery rather than from the carotid procedure.59 Gasparis et al stratified endarterectomy patients into low- versus high-risk based on age older than 80 years, New York Heart Association class III/IV angina, Canadian class III/IV heart failure, myocardial infarct within 6 months, steroid- or oxygen-dependent pulmonary disease, creatinine level of 3, contralateral carotid occlusion, high carotid bifurcation, re-operation, or neck irradiation.60 The risk of perioperative stroke or death was 1.3% in the high-risk group and 1.1% in the low-risk group (not significant).
Carotid Endarterectomy
In summary, these trials have demonstrated that surgical carotid endarterectomy confers a significant benefit over best current medical management in patients with symptomatic carotid stenosis 70% with lesser, albeit significant, degrees of benefit in symptomatic lesions of 50% to 69% and asymptomatic lesions of 60%. However, important caveats apply. Patient selection criteria should be strictly adhered to.61 A recent, prospective, city-wide audit of 184 consecutive patients undergoing carotid endarterectomy reported that only 49% of these procedures were for appropriate indications.62 The surgeon should have a perioperative complication rate low enough to ensure the full (or any) benefit from the procedure. Some authors have even suggested that surgical teams provide data on their rates of stroke or death within 30 days of surgery, adjusted for the severity of carotid disease and coexisting conditions, to referring physicians and patients.63 Finally, there is ongoing debate as to the cost-effectiveness of surgery for asymptomatic carotid stenosis which, according to some authors, is not proven.37
|
Endovascular Treatment of Carotid Occlusive Disease |
|---|
|
TopIntroductionCarotid EndarterectomyEndovascular Treatment of...Summary: Carotid StentingComplicationsComparison Between Treatment...CostsConclusionGlossary of Terms:References |
|---|
Endovascular treatment (angioplasty and stenting) of carotid occlusive disease may offer the following advantages over endarterectomy: general anesthesia is usually not required, thus allowing the patient’s clinical status during the procedure to be monitored; increased patient comfort and significant cost savings because of shorter recuperation period; no cervical incision is made, thus eliminating the risk of cranial nerve palsies, wound infections, or neck hematomas; procedures can be performed simultaneously on carotid, vertebral, and coronary arteries; morbidity and mortality rates may be reduced in patients considered to be at higher risk for surgery (who have significant comorbidities, contralateral carotid occlusion, postendarterectomy restenosis, radiation-induced stenosis, previous radical neck dissection); and it provides an option for treatment of carotid stenosis in patients who are not suitable candidates for CEA (ie, patients with surgically inaccessible lesions).
Carotid Balloon Angioplasty
Percutaneous transluminal balloon angioplasty for carotid artery stenosis was first reported by Kerber et al in 1980.64 In 1987, Theron et al published the first large series of internal carotid angioplasty in 48 patients with de novo atherosclerosis or postsurgical restenosis. Technical success was achieved in 94% of cases, with a 4.1% rate of serious morbidity.65 In Kachel’s review of the literature through 1995, 523 carotid angioplasty procedures had subsequently been reported.66 The overall technical success rate was 96.2%, with a 2.1% rate of morbidity, 6.3% rate of transient minor complications, and no deaths. In one of the largest single-institution series, Gil-Peralta et al (1996) performed 85 balloon angioplasties in 82 patients with symptomatic carotid stenoses of >70% over a 4-year period.67 They reported a technical success rate of 92% (residual stenosis <50%), with 30-day mortality of 0% and a major morbidity rate of 4.9%, which compares very favorably to the ECST and NASCET results. The rate of recurrent stenosis (all of which were asymptomatic) was 6.7% at a mean follow-up of 18.7 months, with almost all of these occurring between months 3 and 6. Rates of restenosis (<2 years) reported in other large angioplasty series are between 0% and 16%;66,68–71 in carotid endarterectomy series, rate of restenosis was 10% in the first year.51,72–74
Despite these favorable results, balloon angioplasty has a number of potential limitations, including vessel wall recoil, angiographically evident intimal dissection, and plaque dislodgement with particulate embolization. Angioplasty of atherosclerotic lesions has been reported to generate emboli composed of atheroma, cholesterol crystals, thrombus, and platelet aggregates.75–78 Embolization of microparticles has also been demonstrated during and after carotid endarterectomy and has been shown to correlate with complex plaque morphology79 and with clinical postoperative cerebral ischemia.80–83 However, studies examining the frequency of emboli during carotid balloon angioplasty using transcranial Doppler (TCD) have failed to show a clear-cut correlation between embolism frequency and neurological sequelae.76–78 Crawley et al, in an analysis of 14 patients undergoing carotid balloon angioplasty versus 14 endarterectomy patients with shunt placement, reported an average of 202 embolic signals during carotid balloon angioplasty compared with 52 during carotid endarterectomy. However, during the recovery period of 20 minutes, the average number of embolic signals was 5 for balloon angioplasty versus 19 for endarterectomy. There was no correlation between the number of TCD-detected emboli and the periprocedural stroke rate.77
The risk of cerebral damage is thought to depend on the size and composition of the embolic material as well as the extent and location of brain involvement. Because it is difficult to accurately distinguish between air and particulate emboli using TCD,84 the lack of correlation between emboli and clinical sequelae has led to the suggestion that the majority of emboli detected during balloon angioplasty are either gaseous or small platelet aggregates <200 µm in diameter, both of which correlate with a more benign outcome.75–77 This underscores the importance of premedication with antiplatelet agents to prevent larger platelet aggregates.85
Endovascular revascularization of carotid occlusive disease may result in cerebral hypoperfusion from luminal compromise by catheters and guidewires crossing the stenotic lesion and/or during balloon inflation. This is of even greater relevance in the presence of contralateral carotid artery occlusion or stenosis. Eckert et al monitored 22 patients undergoing carotid balloon angioplasty using TCD, noting that a >50% reduction of middle cerebral artery mean blood flow velocity compared with baseline values represented a critical threshold for the development of ischemic symptoms in conscious patients even with short occlusion times of 10 to 40 seconds.86 However, Crawley et al reported hemodynamic ischemia was significantly greater with endarterectomy than balloon angioplasty and was not predictive of adverse neurological outcome.77 It is recommended to keep balloon inflation and occlusion times <30 seconds to avoid potential cerebral ischemia. If there is attendant compromise of the contralateral carotid artery, then establishing the adequacy of the cerebral collateral circulation becomes even more important and the procedure should be performed with as little sedation as possible to facilitate neurological monitoring. Tsurutani et al described the successful use of a continuous-perfusion dilatation catheter for high-risk patients with poor collateral circulation.87
Carotid Stenting
The impetus for carotid stenting has arisen principally from trials of stenting with balloon angioplasty versus simple balloon angioplasty in the coronary arteries, which have consistently demonstrated a persistent benefit in event-free survival at 1 year and a lower rate of repeat angioplasty.88–90 The purported advantages of stent placement over simple angioplasty include avoiding plaque dislodgment, intimal dissection, elastic vessel recoil, and late restenosis. Despite the fact that it is unknown whether these benefits apply to the carotid circulation, endovascular carotid revascularization is now most commonly performed with stents.
Since 1996, there have been 11 large carotid stent series published in which the total number of patients is 131171,91–101 (Table 3). Comparative analysis of these reports is made difficult by inconsistencies in the sample populations, lesion characteristics, endovascular techniques, and outcome data. However, the overall reported rate of technical success is >95%; procedure-related mortality rates (including cardiac deaths) are 0.6% to 4.5%; major stroke rates are 0% to 4.5%; minor stroke rates are 0% to 6.5%; and a 6-month restenosis rate is <5%. This excludes the other studies that represented very-high-risk cohorts.98,99,102–105 Similar favorable results were reported by Al-Mubarak et al, who reported on 51 consecutive patients undergoing simultaneous or staged carotid artery stenting and percutaneous coronary intervention. Technical success was achieved in all carotid arteries, with a minor stroke rate of 4% and no major strokes, myocardial infarctions, or deaths.106 In the NASCET, the perioperative stroke and death rate was 5.8%, with 0.6% mortality rate mostly caused by myocardial infarction.23
|
Vitek et al presented their experience in treating 404 patients with carotid angioplasty and stenting.107 They report a technical success rate of 98%, 30-day morbidity/mortality rate of 1.9%, major stroke rate of 0.7%, minor stroke rate of 5.8%, and a 5% rate of restenosis (>50% narrowing). The authors report a lower complication rate in the last 122 patients (with increased procedure-related clinical experience): minor stroke rate of 2.5% with no major strokes or deaths. Wholey et al have published the results of a worldwide stent survey in which 3047 endovascular cervical carotid artery stent procedures are reported from 24 centers in North America, Europe, Asia, and South America.108 They reported a 30-day procedure-related mortality rate of 0.98%, major stroke rate of 1.35%, minor stroke rate of 2.53%, and a restenosis rate at 6 and 12 months of 2.23% and 2.48%, respectively. Centers having worked with <50 cases had a 6.4% rate of major stroke and death compared with 2.3% for centers having worked with between 50 and 100 cases. The authors thus suggest a 50-case learning curve for carotid stenting.
Many of these case series also analyzed outcomes for patients considered at higher risk for surgery (ie, NASCET-ineligible). In the NASCET, the perioperative stroke and death rate was 5.8%, with 0.6% mortality rate mostly caused by myocardial infarction.23 NASCET criteria were applied to the patient cohorts in 5 of these carotid stenting series, demonstrating that 79% of these 574 patients would have failed eligibility because of comorbidities.91,95,96,99 Despite this, morbidity rates of 2.0% to 7.9% and mortality rates of 0.6% to 2.0% for these early carotid stenting reports compare favorably to those in the NASCET and the ECST. However, 41% (n=233) of these patients had asymptomatic carotid stenosis for which lower endarterectomy morbidity and mortality rates would be expected. Similarly, Yadav et al reported on 22 patients with angioplasty and stenting for postendarterectomy carotid stenosis with no major and only 1 minor stroke (4.5%).109 Lanzino et al also reported favorable results in 18 patients undergoing angioplasty and stenting for recurrent carotid stenosis after endarterectomy, with no periprocedural strokes and 1 transient ischemic attack.110 Mericle et al also reported on 23 patients with high-grade carotid stenosis and a contralateral carotid occlusion undergoing elective carotid stenting.111 The 30-day perioperative stroke and death rate was 0%. This is in contrast to the NASCET, which reported a perioperative stroke/death rate for contralateral occlusions of 14.3%.23
Mathur et al retrospectively analyzed the risk factors for stroke in 231 patients undergoing elective stenting of the extracranial carotid arteries; 14% of which were NASCET-eligible.112 The overall 30-day stroke rate was 6.9%; however, by stratifying for the NASCET-eligible group, the stroke rate decreased to 2.7%. Advanced age (older than 80 years) and long or multiple stenoses were found to be independent predictors of periprocedural strokes. However, contralateral carotid occlusion, previous carotid endarterectomy, and combined carotid and coronary procedures, all of which are associated with a higher incidence of complications in carotid endarterectomy, were not found to have an increased risk of adverse outcome in stented patients.51,112–115 Increasing age was also identified as a predictor of increased risk for carotid stenting procedures by Chastain et al. The authors stratified 182 patients undergoing elective carotid artery stenting into 3 age groups: older than 80 years, 75 to 79 years, 74 years or younger. The overall rate of major stroke and death (0.5%) was 1.6%, with a 0.5% rate of myocardial infarction. Neurological complications (mostly minor strokes) were significantly more frequent in patients older than age 80 years than for those 74 years or younger (25% versus 8.6%, respectively).116
There are few published studies directly comparing carotid endarterectomy with carotid stenting. Jordan et al retrospectively compared 107 endarterectomy patients with 166 prospectively followed-up patients undergoing carotid stenting and reported a higher early minor stroke rate in the stent group (6.6% versus 0.6%) but a higher rate of major stroke/death in the surgical cohort (4.2% versus 2.8%).117 Jordan also analyzed outcomes from a subset of 109 patients undergoing endarterectomy under regional anesthesia and compared these results to 268 patients undergoing carotid stenting in the same institution. The total early stroke and death rates for stent versus endarterectomy were 9.7% versus 0.9%. Most of these strokes were minor; the major stroke rates for stent versus endarterectomy were 1.5% versus 0%. There is one report of an early prospective randomized study in 17 patients treated for symptomatic stenoses of >70%.118 The authors reported no complications in 10 patients undergoing endarterectomy; however, 5 of 7 stent patients had strokes, 3 of which were disabling at 30 days. This prompted early stoppage of the trial in favor of endarterectomy. However, this trial had methodological problems that may explain these poor results.
In reviewing the current literature on carotid artery stenting, the technical success rate, procedure-related morbidity and mortality rates, and restenosis rates seem to compare favorably to carotid endarterectomy.119–121 However, inconsistencies in the trial design, reporting criteria, and follow-up render comparison of endarterectomy with endovascular revascularization most challenging (Table 4). The validity of comparisons between such disparate clinical data is unsound. In the case of carotid endarterectomy, there exists class I evidence of efficacy, whereas the bulk of the endovascular data are derived from nonrandomized uncontrolled studies, usually from single institutions.122,123 Class I evidence is that which is proven by a prospective randomized trial with a small chance of false-negative or false-positive values. Therefore, 5 prospective, randomized, multicenter trials comparing carotid endarterectomy to carotid angioplasty or stenting have been undertaken, the results of which are included in Table 4.
|
The Carotid and Vertebral Transluminal Angioplasty Study (CAVATAS), a large, prospective, randomized, multicenter trial comparing carotid endarterectomy to carotid angioplasty was recently completed. In the CAVATAS, patients with symptomatic stenoses (at least 30% luminal diameter reduction) suitable for surgery were randomized to either angioplasty or surgery.124 Patients unsuitable for endarterectomy were randomized to percutaneous transluminal techniques or medical treatment alone. The CAVATAS randomized 504 patients to surgery and angioplasty over 5 years. There was no significant difference in the risk of stroke or death related to the procedure between carotid endarterectomy and angioplasty. The rate of any stroke lasting >7 days or death within 30 days of first treatment was 10% in the surgery or angioplasty groups. The rate of disabling stroke or death within 30 days of first treatment was 6% in both groups. Preliminary analysis of long-term survival showed no difference in the rate of ipsilateral stroke or any disabling stroke in patients up to 3 years after randomization. The rates of stroke or death within 30 days in CAVATAS in both groups are higher than those of many previous reports but not significantly different to the ECST rate of 7%. Cranial nerve injury and myocardial ischemia were only reported at the time of treatment in the surgical group. Long-term follow-up is not yet available.125
The Wallstent Trial was an industry-supported, prospective, randomized trial comparing endarterectomy and carotid stenting for symptomatic stenosis 60%.126 The results have been published in abstract.127 In this study, 219 patients with symptomatic carotid stenosis of 60% to 90% diameter were randomized to endarterectomy or stenting. The risk of any perioperative stroke or death was 4.5% for surgery and 12.1% for stenting. At 1 year, the risk of a major stroke was 0.9% for surgery versus 3.7% for stenting. This trial was stopped early because of poor results from stenting.
A single-center community hospital study randomized 104 symptomatic patients to either carotid endarterectomy or stenting without distal protection.128 Perioperative stroke or death rate was 2% for surgery and 0% for stenting. Other complications for the surgery group totaled 16% and included hematoma (requiring treatment), cranial/cervical nerve injury, and hypotension (requiring treatment). Other complications for the stent group totaled 45% and included transient cerebral ischemia, leg amputation, retroperitoneal hemorrhage, bradycardia (requiring temporary pacing), and hypotension (requiring treatment).
The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial randomized 307 high-risk patients to endarterectomy or carotid stenting using a distal protection device. Perioperative (30-day) results have been presented in abstract.129 High risk was defined as congestive heart failure (class III/IV) or ejection fraction <30%, open heart surgery needed within 6 weeks, recent myocardial infarction (24 hours to 4 weeks), or unstable angina (CCS class III/IV). Perioperative stroke and death rates were 7.3% for surgery versus 4.4% for stenting. Rates of myocardial infarction were 7.3% for surgery versus 2.6% for stenting.
The Carotid Revascularization Endarterectomy versus Stent Trial (CREST), a North American, multicenter, randomized, controlled trial comparing the efficacy of surgical endarterectomy with carotid stenting, is currently in progress.130,131 In the CREST, patients with symptomatic extracranial carotid stenosis of 50% are randomized between stent-supported angioplasty and endarterectomy. To demonstrate a clinically significant difference between the 2 treatments, CREST will require at least 2500 patients, excluding comparison between various clinical subgroups (eg, recurrent stenosis), for which an even greater number will be required.
Adjuncts to Stenting
Potential areas of innovation include methods of providing cerebral protection using intravascular filters or balloons; smaller-diameter, more flexible, and hence less traumatic delivery systems; lowering rates of restenosis secondary to intimal hyperplasia by using local catheter brachytherapy; radiation-emitting stents;132–134 or biologically active coatings135 and improved adjuvant pharmacological regimes using antiplatelet agents such as the glycoprotein IIb/IIIa inhibitors, which could potentially reduce the incidence of acute thromboembolism and improve long-term patency.136 This genuine potential for future improvement has prompted some authors to suggest a direct comparison with carotid endarterectomy may be premature.46,137–139
It remains unclear whether carotid artery stent placement helps reduce the number of particulate emboli by trapping them beneath the metallic meshwork. Current stent designs may trap larger fragments but not efficiently prevent microemboli because the interstices size is too large.140 A recent prospective study, in which patients undergoing carotid artery stenting were examined preprocedurally and postprocedurally with MRI, failed to show evidence of brain signal abnormality referable to emboli. However, a similar prospective study examining 17 patients with diffusion-weighted MRI showed new (clinically silent) lesions in 3 cases.141,142
The problem of distal embolization during balloon angioplasty and carotid stenting has increased interest in providing methods of cerebral protection. A triple-coaxial catheter system, designed to provide cerebral protection, has been described by Theron et al.143 Theron et al reported distal embolic complications in 3 of 38 patients (8%) undergoing internal carotid artery balloon angioplasty without distal protection versus 0 of 43 patients (0%) undergoing the same procedure using distal balloon protection.71,140 Henry et al used Theron’s distal occlusion balloon technique in 32 of 163 carotid stenting cases.144 However, 2 of the 3 major strokes that occurred in this series were in conjunction with this device. The authors cited prolonged procedure time and increased embolism risk when traversing ulcerated lesions as potential problems associated with its use.
A number of commercial devices aimed at reducing the microembolic burden associated with carotid angioplasty and/or stenting, using filters or guide wire attached balloons, are currently undergoing development. These include a low-profile embolic filter deployed and retrieved on a 0.014-inch or 0.018-inch shaft that serves as the guidewire for balloon and stent delivery catheters. Studies in ex vivo models have shown >90% capture of particles >200 µm and 100% capture of particles >500 µm.145 Alternatively, a 0.014-inch guidewire with a protection balloon incorporated into the tip has been used. After angioplasty and stenting with the protection balloon inflated, an over-the-wire aspiration catheter is passed through the dilated area to clear debris.146 This balloon-protection method has the disadvantage of temporary occlusion of carotid flow, whereas filter devices allow constant cerebral perfusion.
|
Summary: Carotid Stenting |
|---|
|
TopIntroductionCarotid EndarterectomyEndovascular Treatment of...Summary: Carotid StentingComplicationsComparison Between Treatment...CostsConclusionGlossary of Terms:References |
|---|
The results of carotid angioplasty and stenting vary. Case series show results comparable to endarterectomy, particularly in NASCET-ineligible patients. However, 2 large, prospective, randomized trials have given discordant results, with CAVATAS showing carotid angioplasty and/or stenting to have comparable outcomes to surgery and the WALLSTENT trial showing carotid stenting to have significantly inferior outcomes compared with surgery. Given these discordant results and inconsistencies in patient selection and in definitions used to report outcomes, uniform reporting standards are needed, along with guidance for study design. This will allow creation of reliable trials to study the safety and effectiveness of carotid endovascular revascularization using current and future technology.
Patient Selection
Discussion
Patients can be selected according to multiple factors such as degree of stenosis, presence of symptoms, and presence of factors that place the patient at high risk for endarterectomy. Degree of stenosis is first measured with noninvasive studies such as carotid duplex sonography, MRA, or CTA. Various endarterectomy and stent trials (Tables 3, 4
) have defined symptomatic patients as those with symptoms within 90 to 180 days of trial entry. For purposes of consistency, it is recommended that symptomatic patients be defined as those with neurological symptoms or neurological changes within 6 months (180 days) of treatment, consistent with NASCET entry criteria. Symptoms may be before stroke or transient neurologic event. Transient events may be hemispheric or retinal (amaurosis). The patient population can be classified as either "low-risk cohort" or "high-risk cohort" of patients with respect to endarterectomy. It is unknown if such patients are also at higher risk if treated with carotid stenting. Although it is generally accepted that some patients can be categorized as high risk, as noted earlier this is not uniformly accepted.60 The low-risk cohort is those patients with similar risk factors who were enrolled into the NASCET and ACAS study. The definition of the high-risk cohort is more controversial. Suggestions for categorizing high-risk patients are listed in Table 5, based on criteria used in previous stent trials and from the criteria of Sundt (Table 2). The high-risk cohort can be defined as having 1 anatomical risk factors or 2 group A comorbidity risk factors or 1 group B comorbidity risk factors as defined in Table 5.
|
To avoid confounding the effects of other procedures with the effect of elective carotid revascularization, the selected patients should not undergo any interventional carotid, coronary, or peripheral treatment within 30 days before enrollment or after procedure unless this is part of the study protocol.
Recommendation for Reporting
Inclusion and exclusion criteria must be reported. These include age, categorization of patients as symptomatic or asymptomatic, type of symptoms, degree of stenosis, technique for measuring the degree of stenosis, and presence and type of high-risk comorbidities.
Define Outcome of Therapy
Discussion
The primary objective of any study involving the carotid artery should be to evaluate the safety and long-term efficacy of the stenting device versus either surgical or medical control population or historical controls for atherosclerosis in preventing ipsilateral stroke and/or death. As noted in Table 4, various studies have used perioperative (within 30 days) events of minor stroke, major stroke, myocardial infarction, and death as outcomes. Long-term events used as outcomes include ipsilateral stroke, ipsilateral disabling stroke, any stroke, and death. These long-term events can be measured as a 1-year risk or an annualized risk over longer time periods. To assess long-term efficacy, patients should continue to be followed up annually for at least 2 to 5 years.
Recommendations for Reporting
It is recommended that the primary endpoint for any study should be the occurrence of major adverse events, defined as death or ipsilateral stroke at 6 months and 1 year after procedure or myocardial infarction (Q-wave and non–Q-wave) 30 days after procedure.
The secondary safety endpoint should be freedom from any stroke, myocardial infarction (Q-wave and non–Q-wave) or death at 30 days and freedom from target lesion revascularization at 1 year. The secondary efficacy endpoint is acute success defined by lesion, device (stent delivery system and distal protection device), and procedural success.
Pretreatment Evaluation
Discussion and Recommendations for Reporting
Pretreatment evaluation should include assessment of degree of stenosis using noninvasive imaging, neurological assessment (NIH stroke scale, Barthel index, and Rankin scale) performed by a neurologist, preprocedural laboratory results such as hematocrit, hemoglobin, platelet count, white blood cell count with differential, serum creatinine, pregnancy test (for women of childbearing potential), CK, CK-MB, or troponin-I, prothrombin time, and activated partial thromboplastin time. These laboratory results should be obtained within 72 hours of the procedure. A 12-lead ECG should be performed and documented for all patients before the procedure. A baseline brain CT or MRI scan should be obtained to document any preexistent infarction and exclude nonvascular neuropathology such as tumor that may mimic transient ischemic attacks. Evaluation of severity of underlying chronic obstructive lung disease may require pulmonary function tests. Evaluation of cardiac function may require measurement of cardiac output or severity of underlying coronary artery disease. Not all of this information needs to be reported in the published data, but it should be collected for patient stratification and assessment of outcomes and complications. The tests used for pretreatment evaluation should be reported. Training of the person performing the neurological assessment (ie, neurologist or non-neurologist) should be reported.
Treatment Description
The results of carotid revascularization will vary depending on operator and institutional experience.43,56,147–151 Previous operator experience should, therefore, be reported.
Medical therapy may need to be adjusted for arteriography. Patients using long-term anticoagulation may need to have their treatment converted to heparin. Patients with preexisting renal disease may be admitted 1 day early for intravenous hydration or monitored vasodilator therapy.152 Oral enteric-coated aspirin and clopidogrel (Plavix) have been recommended at least 3 days before the procedure to reduce periprocedural platelet emboli. Experimental data suggest that aspirin and clopidogrel have a synergistic effect on platelet anti-aggregation, antithrombotic activity and in preventing myointimal proliferation (restenosis).153,154 After the procedure, oral antiplatelet agents are usually continued.
The procedure may be performed under general anesthesia but is more commonly performed under local anesthesia at the puncture site along with conscious sedation, which allows continuous monitoring of the patient’s neurological status.155 Although patients may have been included in the study based on previous noninvasive imaging or arteriography, the final determination of stenosis severity is made from the arteriogram at the time of intervention (Figure). Because the carotid stenosis may be eccentric, the optimal projection to demonstrate the stenosis should be found, which may require multiple projections or rotational angiography.156 In the case of presumed ICA occlusion, prolonged filming is necessary, because otherwise delayed, faint, antegrade opacification of the cervical ICA may be missed ("string sign" of critical ICA stenosis).157 Standard AP and lateral intracranial views should be obtained in all cases to establish the adequacy of the intracranial collateral circulation via the external carotid and anterior communicating arteries and also to document any intracranial stenotic lesions. Many experienced operators also advocate routine vertebral angiography to assess collateral flow via the posterior communicating arteries and document any extracranial or intracranial vertebrobasilar stenoses. Certainly, in cases of contralateral carotid occlusion, bilateral severe stenosis, or deficient anterior collateral pathways, evaluation of the adequacy of collateral flow via the posterior circulation becomes even more important.
|
The use of systemic heparin is standard. Glycoprotein IIb/IIIa inhibitors such as abciximab have been shown to decrease mortality and morbidity in a number of coronary stent studies and also potentially improve long-term patency rates, but their role remains undefined in carotid artery stenting.158–160 These agents may have a potential role in the uncommon event of acute stent thrombosis because platelet aggregation (white thrombus) represents the primary mechanism.161
The decision to predilate the lesion using balloon angioplasty depends on the type and size of stent being used, the narrowest lumen diameter, and the morphological configuration of the stenotic segment. Many operators perform routine predilatation to 4.0 mm diameter. However, others suggest that the risk of embolism is high during this part of the procedure, and if atraumatic crossing of the lesion with the stent-delivery catheter is possible without predilatation, then it may be attempted.
The currently used stents are either balloon-expandable or self-expandable, with the self-expandable stents made of either stainless steel or Nitinol. Early reports of carotid stenting mainly used balloon-expandable stents such as the Palmaz stent (Johnson & Johnson Interventional Systems), which can usually be positioned with greater precision than self-expandable types.91–94,96,162 However, reports of a 2% to 16% rate of Palmaz stent collapse on follow-up imaging has led to increased use of self-expandable types.91,108,163 Mathur et al reported Palmaz stent collapse in 11 of 70 patients (16%) at 6-month angiographic follow-up, attributing this to probable external compression. Furthermore, carotid Doppler ultrasound performed retrospectively in 7 patients with stent compression was only 29% sensitive.163 Compression of balloon-expandable stents has been found to be a significant cause of restenosis in the superficial femoral arteries and hemodialysis grafts.164 The 1999 global survey of 3047 carotid stenting procedures by Wholey et al reported 3033 endovascular carotid stents placed. Balloon-expandable Palmaz stents were used in 47% of cases; self-expandable Wall stents in 46%; and other stents including Strecker (Medi-tech), Integra (Medi-tech), Symphony (Medi-tech), and SMART stents (Cordis) in the remaining 7% of cases.108 In this series, 28 stent deformations occurred exclusively with the Palmaz stent (2%). However, Bergeron et al reported no instances of compression at a mean 13-month follow-up among 96 patients with carotid stenosis, all treated with Palmaz stents.100 Nevertheless, the balloon-expandable stent may not be an ideal choice for superficially exposed arteries such as the internal carotid. However in nonexposed locations such as the vertebral artery or great vessel origins, the superior positional accuracy of deployment may be advantageous. Self-expanding Nitinol stents offer the purported advantage of crush recoverability or "spring-like" behavior. If an external force compresses or deforms a Nitinol stent, then it will reassume its expanded shape on removal of the external stress.
In terms of stent sizing, based on current techniques, the stent margins should optimally extend 1 cm beyond the proximal and distal margins of the stenotic plaque. This may necessitate crossing the external carotid artery origin, which does not usually result in significant clinical sequelae. The stent diameter should be 1 to 2 mm larger than the largest vessel diameter that the stent will need to appose. Stent oversizing leads to a greater metallic coverage of the lesion per unit area, which is theoretically advantageous in preventing distal embolism, reducing tissue prolapse, and is not necessarily associated with a higher rate of restenosis.165,166
Postdeployment angioplasty using a high-pressure (12- to 20-atm), semicompliant balloon may then be performed to closely appose the stent and intima and, moreover, expand regions of residual stent narrowing. This may require the use of varying diameter balloons, particularly if the stent extends into the common carotid artery. Obvious gaps between the stent circumference and endoluminal surface potentially increases the risk of acute or delayed thromboembolism.140 Angioplasty beyond the stent margins is not recommended because it may result in acute vessel dissection, symptomatic vasospasm, or subsequent restenosis. Some operators do not advocate routine postdeployment angioplasty of the stent other than for obvious gaps between the stent and vessel wall and regions of residual stenosis, suggesting that this reduces the risk of embolic complications and improves restenosis rates because of reduced intimal injury.
There is insufficient information to define technical success scientifically. For extremity and renal angioplasty, technical success requires <30% diameter residual stenosis by angiography and may require improvement in trans-stenotic pressure gradient.167,168 In the coronary literature, technical success for balloon angioplasty and stenting had originally been defined as at least 20% relative improvement with a decrease in stenosis to <50% but has recently been revised to a decrease in stenosis to <20% diameter.169,170 However, unlike extremity, renal, or coronary stenoses, carotid stenoses are very rarely symptomatic because of hemodynamic compromise. Rather, symptoms arise because of thromboembolism formation on the carotid plaque. It is unknown what degree of correction of carotid stenosis is necessary to reduce the risk of embolization, but removal of the embolic source is fundamental. It is possible that in the attempt to more completely eliminate residual stenosis by full balloon dilation, additional emboli may be produced during the procedure that could cause a higher risk of procedural complications. Alternatively, leaving a higher degree of residual stenosis may lead to a higher rate of late restenosis, which at this time is of uncertain clinical significance. Some carotid stenting trials have defined technical success as residual stenosis <30%.171 Others have used a definition of residual stenosis <50%.172 In the absence of definitive scientific evidence, technical success in this document is arbitrarily defined as stent placement resulting in improvement of the stenosis by >20%, with a final residual stenosis <50% using NASCET measurement criteria. Some practices may prefer to use a lesser degree of residual stenosis as their desired endpoint for technical success.
Iatrogenic vasospasm may occur during the procedure but usually resolves soon after removal of the guidewire from the internal carotid artery. Some investigators describe the use of injectable nimodipine (200 µg diluted in 10 mL injected slowly as a 2 mL to 3 mL bolus)140 or nitroglycerin (100 µg)96 into the carotid artery to treat mechanically induced vasospasm. Recalcitrant iatrogenic vasospasm usually responds well to low-pressure balloon angioplasty (<3 atm).
AP and lateral cerebral angiograms are obtained after stenting to exclude any embolic branch occlusion and to document new patterns of flow. Heparinization is generally allowed to taper physiologically rather than reverse using protamine sulfate. Alternatively, the femoral sheath may be removed immediately after the procedure without the need for heparin reversal using percutaneous closure devices. The patient is usually monitored in the intensive care unit for 12 to 24 hours after treatment. Antiplatelet agents are frequently administered after procedure, such as Clopidogrel for 4 to 6 weeks and enteric-coated aspirin indefinitely.
The patient should be carefully examined neurologically after the procedure. Neurological deficits may be caused by intracranial embolism, hemorrhage, or reperfusion injury.173,174 After successful revascularization, lowering of the mean arterial pressure to 10% to 20% below baseline may be desirable to prevent cerebral reperfusion injury. Intravenous diltiazem may be used postprocedurally to control elevated blood pressure, particularly if associated with headache or neurological sequelae, because it has minimal cerebral vasodilatory effects.175
Postprocedural prolonged bradycardia or hypotension, or both may occur as a result of carotid sinus dysfunction, necessitating the use of intravenous vasopressors or inotropic agents.176
Recommendations for Reporting
Previous operator and institutional experience should be described. This includes the number of previous carotid revascularization procedures, preferably with at least 30-day outcomes for technical success and 30-day periprocedural complications of stroke, myocardial infarction, or death. The procedure should be described in sufficient detail that it could be reproduced accurately by others. Reporting requirements include use of adjunct antiplatelet agents before and during the procedure, use of anticoagulation during the procedure, type of anesthesia (general or conscious sedation), and techniques of neurological and physiological monitoring during the procedure. The technique of cerebral angiography should be reported (ie, AP and lateral cerebral views, other vessels evaluated such as vertebral and contralateral carotid to look for collateral vessels). Final determination of the severity of the carotid stenosis to be treated and a description of the stenotic plaque (ie, ulceration, overhanging margins, circumferential narrowing) is made from the angiogram at the time of the intervention. The technique of carotid stenting must be reported, including use of guide catheter, technique of crossing the lesion, use of predilation and diameter of predilation before stenting, type of stent used, stent diameter and length selection, and poststent deployment balloon dilation. Posttreatment degree of residual stenosis should be reported. Use of medications to prevent bradycardia, treat vasospasm, and control blood pressure should be reported. The use of postprocedural antiplatelet or anticoagulant medications should be reported.
Evaluation
Discussion
Posttreatment evaluation should include the information necessary to evaluate for study endpoints: stroke, death, myocardial infarction, restenosis, and complications. The major morbidity of carotid revascularization, whether from stenting or endarterectomy, is perioperative (within the first 30 days). Therefore, patients must be evaluated in this time period for major and minor strokes using the NIHSS and myocardial infarction using ECG and cardiac enzymes. Stroke definitions listed should be used.
Carotid revascularization is intended to reduce the long-term risk of stroke from the carotid stenosis; therefore, long-term evaluation of treated patients for 2 to 5 years is necessary to determine the incidence of ipsilateral stroke that can be attributed to the treated vessel. Neurologic assessment including the NIH Stroke Scale, Barthel index, and modified Rankin scale for all subjects should be performed by a neurologist at 6 months and 12 months after procedure and yearly thereafter for 2 to 5 years. The NIH Stroke Scale is a somatically oriented measure of neurological function. Its limitations are relatively reduced weighting of neuropsychological measures. For instance, a patient with global aphasia receives 2 points on the NIH Stroke Scale, the same number of points received by a patient with hemianopsia but with significantly different implications for functional recovery. The Barthel Index is a measure of functional dependency that has implications for rehabilitative needs and long-term cost of chronic care for the neurologically disabled. The modified Rankin Scale is a rather crude measure of social recovery that has not been validated in patient care before 3 months. Consequently, the modified Rankin Scale should be recorded but has clinical significance only at 90 days and beyond.
Assessment of long-term mortality is also important, but will be markedly affected by patient selection—high-risk patients with multiple medical comorbidities are likely to die sooner regardless of carotid revascularization—and is best assessed in randomized trials.
Posttreatment evaluation should also include evaluation for recurrent carotid stenosis. Recurrent carotid stenosis after endarterectomy is usually asymptomatic, but repeat revascularization is necessary in 5% of patients who receive endarterectomy.58,177 Similarly, repeat endovascular revascularization for restenosis has been reported in 8% of patients undergoing carotid stenting,178 although the rate may be higher in patients in whom the original carotid stent was placed to treat a recurrent stenosis caused by endarterectomy.179 Follow-up evaluation is easily performed with carotid duplex ultrasound and should be obtained at least 2 to 4 weeks after procedure, 10 to 12 months after procedure, and if ischemic symptoms recur. More frequent surveillance intervals may be desirable.177
Recommendations for Reporting
In the perioperative (30-day) period, patients should be evaluated for stroke, myocardial infarction, and death. Stroke is defined as per this document. Beyond the perioperative period, patients should be evaluated for stroke, death, and restenosis. Degree and length of residual stenosis or restenosis should be reported at least once during the 30 days after treatment, preferably before discharge, at 10 to 12 months after procedure, and if ischemic symptoms recur.
|
Complications |
|---|
|
TopIntroductionCarotid EndarterectomyEndovascular Treatment of...Summary: Carotid StentingComplicationsComparison Between Treatment...CostsConclusionGlossary of Terms:References |
|---|
Discussion
Stroke is a complication of carotid revascularization and an outcome measure of the effectiveness of the revascularization. The stroke may be ipsilateral or contralateral to the treated vessel. Neurological deficits as a complication of the procedure may be caused by intracranial embolism, hemorrhage, or reperfusion injury.174 The phenomenon of reperfusion hemorrhage after surgical endarterectomy is well described. Ouriel et al in a review of 1471 patients undergoing surgical endarterectomy reported a 0.75% incidence of intracerebral hemorrhage. Hemorrhage occurred at a median of 3 days postoperatively and accounted for 35% of the total perioperative neurological events. Death from massive hemorrhage and herniation occurred in 36% of cases. Factors correlating with an increased hemorrhage risk were hypertension, high-grade ipsilateral stenosis, high-grade contralateral stenosis or occlusion, and younger age.180 This complication has also been reported with carotid angioplasty. Schoser et al reported 2 patients with reperfusion hemorrhage, 1 intraparenchymal hemorrhage and 1 subarachnoid hemorrhage after balloon angioplasty for carotid and vertebral artery stenosis.