(Circulation. 1997;95:303-305.)
© 1997 American Heart Association, Inc.
Articles |
Elective Stenting of Extracranial Carotid Arteries
the University of Texas Houston Medical School.
Correspondence to James Grotta, MD, Professor of Neurology and Director, Stroke Program, University of Texas Houston Medical School, Houston, TX 77030.
Key Words: Editorials • stroke • stents • arteries
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Introduction |
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The efficacy of surgical carotid endarterectomy (CEA) for extracranial carotid stenosis has now been unequivocally demonstrated. The publication of several large worldwide trials1 2 3 4 has finally provided clinicians with critically important data for practical management of a group of patients at particularly high risk of stroke: those with transient ischemic attacks (TIAs) or minor strokes referable to a high-grade stenosis at the carotid bifurcation. These data come after more than 20 years of inconclusive, noncontrol case studies and are the result of cooperative efforts of neurologists, neurosurgeons, and vascular surgeons to address the question of the efficacy of CEA in proper prospective randomized trials. The field of angioplasty/stenting (AS) for carotid disease has much to learn from the CEA experience.
In patients with TIAs or minor stroke, the CEA trials have shown the following: (1) if the symptoms are referable to a >70% diameter stenosis at the carotid bifurcation, CEA reduces the risk of subsequent ipsilateral stroke from 26% during the first 2 years with optimal medical management to 9% if CEA is added; (2) the risk of stroke without surgery is greater with increasing degrees of stenosis, reaching >30% during the first year for 90% to 95% stenosis; (3) surgery is not of benefit for <50% stenosis; (4) the risk/benefit of CEA for 50% to 70% stenosis remains unknown and is still under investigation; (5) although the best way to measure stenosis is debated, these degrees of stenosis assume a standard method of measurement comparing the narrowest lumen diameter at the bifurcation to the normal diameter of the internal carotid in a vertical distal segment; (6) benefit occurs with CEA with either hemispheric or retinal symptoms and in all relevant demographic subgroups; and (7) the benefit assumes a perioperative risk of stroke or death of 
5% to 6%. Data supporting surgery for patients with asymptomatic carotid stenosis >60% have also been reported,5 6 7 although the magnitude of effect is smaller (
1% per year reduction in stroke) and is further qualified by the low risk of major stroke with either surgery or medical treatment and a possible lack of benefit in women. The benefits of CEA are critically dependent on the rate of perioperative complications. If the complication rate goes up, the benefit of surgery is quickly lost, and if it can be reduced, the benefit would be even greater.
In this context, the work of Yadav and colleagues8 provides a possible alternative to CEA. This noncontrol study demonstrates what appears to be an acceptably low rate of complications and restenosis after carotid AS in a relatively large, well-described patient cohort followed up for 6 months. Several other case series9 10 11 12 13 have also reported short-term success with angioplasty alone, although restenosis has been a problem. The encouraging feasibility and safety reported by Yadav et al may be related in particular to the addition of stenting to the angioplasty procedure.
In understanding the possible future role of AS vis-a-vis CEA, it is important to recognize that patients in whom CEA has proved beneficial have been carefully selected: they had disease at the carotid bifurcation, which is relatively easily approached surgically; the surgeons had to have a proven track record of expertise; and patients had to be free of major potential cardiac causes of stroke or other serious medical illnesses. Finally, the CEA studies have not addressed the vexing problem of patients with simultaneous cardiac and cerebrovascular disease and the safety of serial or combined CEA with coronary artery bypass grafting. Therefore, there are substantial clinical scenarios in which the benefit of CEA is not yet proven and may be obviated by heightened surgical risk. AS has potential advantages, even in the best candidates for CEA, by lowering perioperative risk, costs, and patient inconvenience or discomfort. The demonstration by Yadav and colleagues8 is indeed encouraging in that in a series of 107 high-risk patients (mean preoperative minimal lumenal diameter of 1.3 mm, 45% referred by surgeons, and 77% who did not meet criteria for CEA), AS can be carried out relatively simply from the patient's standpoint (mean length of stay after the procedure was 1.9 days), with low risk (30-day risk of stroke or death was 9.3% of patients and 7.9% of arteries) and with only a 4.9% incidence of asymptomatic restenosis by 6 months.
The role of CEA or AS must be evaluated in the context of other major advances in stroke prevention learned from clinical research in the past decade, in particular the contribution of modifiable risk factors (especially hypertension and smoking), the recognition of the importance of anticoagulation for atrial fibrillation,14 15 16 17 and the efficacy of antiplatelet drugs in high-risk patients.18 19 20 The recent approval of recombinant tissue plasminogen activator for acute stroke treatment21 not only represents the first step toward effective stroke therapy but has also fostered the development of a new breed of "stroke neurologists" who are rapidly changing the face of acute stroke management, including providing public education about stroke warning symptoms; reprioritizing prehospital, emergency room, and critical care of stroke; and applying the results of basic investigations of the pathobiology of cerebral ischemia to neuroprotective therapies. The field of endovascular neuroradiology has made innovative strides in the approach to both stroke prevention and treatment, including angioplasty, local thrombolysis into occluded cerebral arteries and venous sinuses, and embolization of cerebral aneurysms and arteriovenous malformations. There is truly a renaissance occurring in the field of stroke therapy, and interested cardiologists should be able to find enthusiastic partners in the stroke community. The evaluation of AS for stroke prevention must be orchestrated by those who understand all the complexities of preventing and treating brain ischemia.
Interventional neurologists are indebted to their cardiological colleagues for demonstrating the efficacy of interventional therapies and how they can be implemented in practice. The similarities between approaches to the cerebral and coronary circulations are too numerous to repeat here, but it is particularly critical to recognize some important differences. First is the nature of the atherosclerotic plaque and the mechanisms by which it results in symptoms. In the coronary arteries, the plaque typically is associated with in situ thrombosis. When a carotid plaque causes symptoms, they are usually due to distal embolization, and this danger must be kept in mind when designing and assessing any approach to carotid artery disease. Second, the carotid plaque is only one source of stroke, no more than 20% in most series, and is clearly dependent on patient demographics. Much more frequently, infarcts are caused by emboli from the heart or, particularly in blacks, Hispanics, and Asians, obstruction of deep penetrating vessels supplying critical white-matter tracts in the subcortical regions or brain stem. Furthermore, the brain has a propensity to hemorrhage, which is responsible for 15% to 20% of all strokes and the narrow benefit/risk ratio for anticoagulant and thrombolytic therapies for stroke prevention or treatment. Third, although both myocardial and cerebral damage result in loss of function, even a small strategically placed lesion in the brain can have devastating consequences, and multiple "silent" emboli can cause cumulative damage; therapeutic complications or failures, therefore, are particularly dreaded by the neurologist, leading to very careful scrutiny of new invasive procedures. Thus, AS has some theoretical limitations: it does not address the cause of most strokes; potential embolic sources may be left behind even after successful reduction of stenosis; the need for potentially dangerous associated antithrombotic therapy must be evaluated; and the possibility of relatively subtle short-term and long-term embolic complications must be evaluated carefully.
Given the converging nature of cardiology and vascular neurology, it was just a matter of time before these disciplines would join forces in a therapeutic effort. This has already occurred in the atrial fibrillation trials. Yadav and his colleagues in neurology, radiology, vascular surgery, and neurosurgery provide us with a model for collaboration in demonstrating the feasibility, apparent safety, and possible cost savings of angioplasty coupled with stenting of the extracranial carotid arteries. But, as always, important questions remain. The first is whether the procedure is needed in patients in whom CEA has not been proven unequivocally useful, such as symptomatic patients with <70% stenosis and most asymptomatic patients. Patients with carotid disease at locations other than the bifurcation may have a lower natural risk of stroke, and those with other medical problems or coexisting coronary disease may die or become disabled from these other conditions before the benefits of CEA or AS can be seen. The 6-month follow-up in the study by Yadav et al8 is obviously too brief to address this question. In addition to patient selection, there are other details that make it difficult to compare the results from Yadav et al with the surgical CEA trials. One of the most intriguing is the choice of antiplatelet agent. Only aspirin was used in the CEA trials, and retrospective evidence suggests that perioperative morbidity could have been reduced if high-dose aspirin (650 mg twice daily) had been used in all surgical patients. In the study by Yadav et al, a combination of aspirin and ticlopidine was used that was recently shown to be even more effective than a combination of aspirin plus anticoagulation in coronary AS.22
Of course, the relative merits of AS can only be assessed in an adequately powered (and therefore multicentered) prospective randomized trial comparing long-term outcome and costs of AS versus CEA in those patients in whom the latter has proved effective, and AS versus best medical management in others. Such trials are now being organized. Standardization of clinical and radiographic inclusion and exclusion criteria, AS procedure, assessment of radiographic and clinical outcome, and cost and quality-of-life analyses will be major challenges in these trials. In the meantime, it must be emphasized that the use of stenting above the aortic arch is neither approved nor proven effective and should not be performed outside the context of clinical trials. However, the study by Yadav et al8 should serve as a stimulus to develop teams of stroke neurologists, cardiologists, neurosurgeons, vascular surgeons, and endovascular neuroradiologists with the expertise to carry out such work.
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Footnotes |
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The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
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References |
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TopIntroductionReferences |
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1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445-452.[Abstract]
2.
Mayberg MR, Wilson SE, Yatsu F, Weiss DG, Messina L, Hershey LA, Colling C, Eskridge J, Deykin D, Winn HR, for the Veterans Affairs Cooperative Studies Program 309 Trialist Group. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. JAMA. 1991;266:3289-3294.
3. European Carotid Surgery Trialists' Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet. 1991;337:1235-1243.[Medline] [Order article via Infotrieve]
4. European Carotid Surgery Trialists' Collaborative Group. Endarterectomy for moderate symptomatic carotid stenosis: interim results from the MRC European Carotid Surgery Trial. Lancet. 1996;347:1591-1593.[Medline] [Order article via Infotrieve]
5. Hobson RW II, Weiss DG, Fields WS, Goldstone J, Moore WS, Towne JB, Wright CB, and the Veterans Affairs Cooperative Study Group. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. N Engl J Med. 1993;328:223-227.
6.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421-1428.
7.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1459-1461. Comment.
8.
Yadav JS, Roubin GS, Iyer S, Vitek J, King P, Jordan WD, Fisher WS. Elective stenting of the extracranial carotid arteries. Circulation. 1997;95:376-381.
9. Kerer CW, Cromwell LD, Leohden OL. Catheter dilation of proximal stenosis during distal bifurcation endarterectomy. AJNR Am J Neuroradiol. 1980;1:348-349.[Medline] [Order article via Infotrieve]
10. Mullan S, Duda EE, Patro NAS. Some examples of balloon technology in neurosurgery. J Neurosurg. 1980;52:321-329.[Medline] [Order article via Infotrieve]
11. Higashida RT, Tsai FY, Halbach V, Dowd C, Smith T, Fraser K, Hieshima G. Transluminal angioplasty for atherosclerotic disease of the vertebral and basilar arteries. J Neurosurg. 1993;78:192-198.[Medline] [Order article via Infotrieve]
12. Ferguson R, for the NACPTAR Investigators. Vascular determinants of successful cerebral percutaneous transluminal angioplasty (CPTA). Neurology. 1995;45:A375. Abstract.
13. Hacein-Bey L, Pile-Spellman J, Koennecke C, Moohan N, Marshall RS, Sacco RL, Mayer SA, Young WL, Mohr JP. Balloon angioplasty of supra-aortic and cerebral arteries: what are the indications? Stroke. 1996;27:167. Abstract.
14.
Stroke Prevention in Atrial Fibrillation Investigators. Stroke Prevention in Atrial Fibrillation Study: final results. Circulation. 1991;84:527-539.
15. Boston Area Anticoagulation Trial for Atrial Fibrillation Investigators. The effect of low-dose warfarin on the risk of stroke in patients with nonrheumatic atrial fibrillation. N Engl J Med. 1990;323:1505-1511.[Abstract]
16. Ezekowitz MD, Bridgers SL, James KL, Carliner N, Colling C, Gornick C, Krausse-Steinrauf H, Kurtze J, Nazarian S, Radford M, Rickles F, Shabetai R, Deykin D. Warfarin in the prevention of stroke associated with nonrheumatic atrial fibrillation. N Engl J Med. 1992;327:1406-1412.[Abstract]
17.
The European Atrial Fibrillation Trial Study Group. Optimal oral anticoagulant therapy in patients with nonrheumatic atrial fibrillation and recent cerebral ischemia. N Engl J Med. 1995;333:5-10.
18. Hass WK, Easton JD, Adams HP Jr, Pryse-Phillips W, Molony BA, Anderson S, Kamm B, for the Ticlopidine Aspirin Stroke Study Group. A randomized trial comparing ticlopidine hydrochloride with aspirin for the prevention of stroke in high-risk patients. N Engl J Med. 1989;321:501-507.[Abstract]
19. Gent M, Easton JD, Hachinski VC, Panak E, Sicurella J, Blakely JA, Ellis DJ, Harbison JW, Roberts RS, Turpie AGG, and the CATS group. The Canadian American Ticlopidine Study (CATS) in thromboembolic stroke (see comments). Lancet. June 3, 1989;1215-1220.
20.
Antiplatelet Trialists' Collaboration. Collaborative overview of randomized trials of antiplatelet therapy, I: prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ. 1994;308:81-106.
21.
The NINDS rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995;333:1581-1633.
22.
Schomig A, Neumann FJ, Kastrati A, Schuhlen H, Blasini R, Hadamitzky M, Walter H, Zitzmann-Roth EM, Richardt G, Alt E, Schmitt C, Ulm K. A randomized comparison of antiplatelet and anticoagulant therapy after the placement of coronary-artery stents. N Engl J Med. 1996;334:1084-1089.
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