Published online before print August 14, 2003, doi: 10.1161/01.STR.0000087789.26400.A8
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(Stroke. 2003;34:2302.)
© 2003 American Heart Association, Inc.
Comments, Opinions, and Reviews |
Editorial Comment—Risk Stratification by Clinical Symptoms and Timing of Carotid Endarterectomy: How Could It Optimize Our Decision Making and Benefit Patients With Carotid Stenosis?
Neurotec Department, Karolinska Institute, Division of Geriatric Medicine, Stockholm, Sweden
Two roads diverged in a yellow wood,And sorry I could not travel both
And be one traveller, long I stood
And looked down one as far as I could
To where it bent in the undergrowth;
Then took the other, as just as fair,
And having perhaps the better claim ...
The prevention of stroke by surgical means originated half a century ago.1 In the early years, anecdotal criteria were used for the selection of patients with internal carotid artery stenosis for surgery. Within the last decade, the appropriateness of carotid endarterectomy (CEA) for the reduction of stroke risk has been demonstrated in a selected group of patients with symptomatic carotid artery stenosis. Analysis of pooled data from randomized control trials2 has confirmed the unequivocal results of the North American Symptomatic Carotid Endarterectomy Trial (NASCET),3 European Carotid Surgery Trial (ECST),4 and Veterans Affairs Trial (VA 309).5 CEA is highly beneficial in patients with transient ischemic attack (TIA) and nondisabling stroke (modified Rankin score <3) with high-grade stenosis (
70% diameter reduction). Within this group, CEA is most beneficial for the following patients: healthy elderly patients with hemispheric TIA, those with tandem extracranial and intracranial lesions, and those without evidence of collateral vessels. A moderate benefit has been reported in certain individuals with carotid stenosis caused by 50% to 69% diameter reduction. In the largest trial of asymptomatic subjects, the perioperative risk of stroke and death reported was very low, but results indicated that 83 subjects needed to be operated on to prevent 1 stroke in 2 years.
Because the rate of CEA is increasing in both Europe and the United States, the selection process of candidates for CEA needs to be according to the recommended guidelines to maintain the best results reported in the first publications. The benefit of CEA has been highly dependent on the operative risk. However, this benefit may not be solely dependent on the latter. The risk of stroke and death resulting from CEA has been shown to depend on a number of patient characteristics, particularly the presence and nature of recent cerebrovascular event. Yet, reliable data on parameters such as timing of surgery since the last event and benefit from CEA are still lacking. Asymptomatic patients with carotid stenosis are known to have a lower operative risk compared with symptomatic patients. For symptomatic patients, there is still uncertainty about the type of ischemic event and clinical decision making compared with the risk of operative stroke.
Therefore, classification of ischemic events into different categories such as ocular TIA, cerebral TIA, nonhemispheric events, cerebral infarction, or symptomatic restenosis after previous stroke may show differences in surgical operative risk and benefit. Furthermore, validated data on the risk of CEA for unstable patients with stroke in evolution or crescendo TIA or for early versus late surgery in stable patients are scarce. The risk of stroke is also dependent on whether the postoperative assessment was performed by a surgeon or a neurologist. Concomitant vascular risk factors such as diabetes mellitus are reported to worsen the outcome.
In this issue of Stroke, Bond et al6 present a systematic review of data from 383 potential reports on CEA. Pooled estimates of risk by type of clinical indication and timing of surgery since the last event are the focus of this review. The data reviewed from 60 studies (14 399 CEA cases) demonstrated an operative risk of stroke and death for asymptomatic stenosis of 2.8% (2.4% to 3.4%) versus 5.1% (4.6% to 5.6%) for symptomatic stenosis reported from 95 studies. Interestingly, the absolute risk of stroke and death for CEA was as low as 2.8% for ocular events and as high as 19.2% for patients with ongoing cerebral symptoms. This meta-analysis corroborated previous findings on the combined estimate of the relative odds of stroke and death for CEA in symptomatic patients versus asymptomatic patients. CEA for cerebral TIA was associated with a higher risk than surgery for ocular events only. This trend appeared to be consistent for patients with stable cerebral stroke versus ocular events only.
The indications for urgent CEA in a patient with acute ipsilateral ischemic stroke are controversial.7 A comparison of the risk of stroke and death in unstable and stable patients was performed. Unstable patients, defined as those with stroke in evolution and crescendo TIA, presented with the highest operative risk. Although only 13 studies, each with a low number of cases, reported outcome of CEA in unstable patients (all referred to as urgent), the results were consistent in all studies. However, no excess risk was associated with early versus late surgery in stable patients.
Optimization of management of stroke patients during recent years has resulted in an immense difference in outcome and survival for patients. CEA is a preventive measure for reduction of stroke risk. The ad hoc committees of the American Heart Association Stroke Council have established guidelines on the acceptable operative risk of CEA. These guidelines recommend that the combined risk of stroke and death resulting from CEA should not exceed 3% in asymptomatic patients, 5% in symptomatic patients with TIA, and 7% for those with stroke. Progress in therapeutic decision making for CEA is essential for minimizing the risk of stroke and death resulting from CEA.
The road we choose, ie, the decision we make when we refer subjects to CEA, has great implications for individual patients. As Robert Frost points out, taking the road less traveled has made all the difference. Clinical decision making for patient referral for CEA needs to follow the major guidelines, and audits of risk should be stratified accordingly.
Two roads diverged in a wood, and I–took the one less travelled by,
And that has made all the difference.
Robert Frost
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1. Fields WS, Maslenikov V, Meyer JS, Hass WK, Remington RD, MacDonald M. Joint study of extracranial occlusion, V: progress report of prognosis following surgery or nonsurgical treatment for transient cerebral ischemic attacks and cervical carotid artery lesions. JAMA. 1970; 211: 1993–2003.
2. Rothwell PM, Eliasziw M, Gutnikov SA, Fox AJ, Taylor DW, Mayberg MR, Warlow CP, Barnett HJ. Carotid Endarterectomy Trialists’ Collaboration. Analysis of pooled data from the randomised controlled trials of endarterectomy for symptomatic carotid stenosis. Lancet. 2003; 361: 107–116.[CrossRef][Medline] [Order article via Infotrieve]
3. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. N Engl J Med. 1991; 325: 445–453.[Abstract]
4. European Carotid Surgery Trialists’ Group. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet. 1998; 351: 1379–1387.[CrossRef][Medline] [Order article via Infotrieve]
5. Mayberg MR, Wilson SE, Yatsu F, Weiss DG, Messina L, Hershey LA, for the Veterans Affairs Cooperative Studies Program 309 Trialists Group. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. JAMA. 1991; 266: 3289–3294.
6. Bond R, Rerkasem K, Rothwell PM. Systematic review of the risks of carotid endarterectomy in relation to the clinical indication for and timing of surgery. Stroke. 2003; 34: 2290–2303.
7. Adams HP, Adams RJ, Brott T, et al. Guidelines for the early management of patients with ischemic stroke: a scientific statement from the Stroke Council of the American Stroke Association. Stroke. 2003; 34: 1056–1083.
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