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Stroke. 2005;36:257-258
Published online before print January 13, 2005, doi: 10.1161/01.STR.0000152956.81155.af
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(Stroke. 2005;36:257.)
© 2005 American Heart Association, Inc.


Original Contributions

Editorial Comment—Plaque Pathology and Patient Selection for Carotid Endarterectomy

J. Max Findlay, MD, PhD, FRCSC

Department of Surgery, Division of Neurosurgery, University of Alberta Hospital, Edmonton, Alberta

Experienced carotid surgeons know that when performing a carotid endarterectomy, it is important to avoid excessive manipulation of the carotid bifurcation during dissection, especially when the patient has had recent symptoms from an "active" plaque. This study by Fisher et al comparing the pathology of carotid plaques obtained from the asymptomatic carotid endarterectomy trial, ACAS, to those taken from the symptomatic trial, NASCET, helps explain the danger. Plaques resected from symptomatic patients are more frequently ulcerated and have attached thrombus compared with asymptomatic plaques and, therefore, are at greater risk to embolize clot and atherosclerotic debris into the cerebral circulation during surgical mobilization. During carotid endarterectomy, the tube-like carotid plaque is cut length-wise and not infrequently torn, preventing a highly accurate gross or microscopic assessment. This might explain why the associations between ulcers, thrombus, and ipsilateral symptoms were not found to be even stronger. In the study reported here, ulceration has a similar frequency in either carotid of a patient with unilateral symptoms, and thrombus was relatively common in plaques not causing symptoms, being present in 21% of plaques in which the symptoms were from the contralateral carotid and 18% of asymptomatic patients. Trends detected in this study (not reaching statistical significance) included the greater prevalence of plaque thrombus when symptoms were closer to the time of surgery (29% for symptoms ≤30 days versus 19% for symptoms >30 days from surgery) and the greater prevalence of thrombus in those symptomatic patients with stroke (35%) than those with transient ischemic attack (18%).

Is there anything in this study we can apply to patients in the clinic? As suggested, it might partly explain the frequent observation that carotid endarterectomy seems safer in asymptomatic than symptomatic patients.1 Does it in any way help us to better-select patients for carotid endarterectomy? The authors suggest that asymptomatic plaques found opposite to symptomatic plaques in the same patients are more commonly ulcerated with attached thrombus and, therefore, perhaps more dangerous. But they remind us also that ulceration and intraluminal thrombus are sometimes difficult to detect with carotid imaging, and this is particularly true with carotid ultrasound and contrast magnetic resonance angiography. So, I am not sure how further ahead we are with the information provided in this report.

Is it in fact possible to determine which asymptomatic carotid plaques have the greatest risk of causing future stroke, therefore justifying consideration of prophylactic repair? Suggested risk factors include male sex,2 ipsilateral brain infarction on brain imaging,3 plaque ulceration detectable on angiography,4–8 the presence of an occluded contralateral carotid artery,9 a stenosis that worsens over time,10 a partly echolucent or heterogenous ("soft") plaque or evidence of intraplaque hemorrhage on ultrasound,10–14 carotid wall "stiffness" or distensibility during the cardiac cycle,15 and the presence of microemboli detected distal to the plaque on transcranial Doppler.16 Of course, younger patients stand to benefit more from carotid endarterectomy than an elderly person with asymptomatic stenosis. Interestingly, higher degrees of arterial narrowing caused by plaque, an important risk factor for symptomatic stenosis17 and an intuitive and commonly considered risk factor for asymptomatic patients, was not found to correlate with surgical benefit in either ACAS18 or the recently published Asymptomatic Carotid Surgery Trial (ACST).19 Perhaps in the future, chemical composition of carotid plaques as determined by magnetic resonance spectroscopy or molecular markers in either the plaque or serum will be found to correlate with stroke risk,20 but a powerful relationship would be required for a significant correlation to exist, given the overall relatively benign natural history of asymptomatic plaques.

We continue to consider asymptomatic carotid stenosis to be an "uncertain" indication for carotid endarterectomy under any circumstance, requiring individual patient assessment and selection, and surgery should be offered only by expert surgeons with low complication rates.21


*    References
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*References
 

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  2. Rothwell PM, Eliasziw M, Gutnikov SA, Warlow CP, Barnett HJ; Carotid Endarterectomy Trialists Collaboration. Effect of endarterectomy for symptomatic carotid stenosis in relation to clinical subgroups and to the timing of surgery. Lancet. 2004; 363: 915–924.[CrossRef][Medline] [Order article via Infotrieve]
  3. Hougaku H, Matsumoto M. Handa N, Maeda H, Itoh T, Tsukamoto Y, Kamada T. Asymptomatic carotid lesions and silent cerebral infarction. Stroke. 1994; 25: 566–570.[Abstract]
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  6. Dixon S, Pais SO, Raivola C, Gomes A, Machleder HI, Baker JD, Busuttil RW, Barker WF, Moore WS. Natural history of nonstenotic asymptomatic ulcerative lesions of the carotid artery: a further analysis. Arch Surg. 1982; 117: 1493–1498.[Abstract]
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  8. Weschler LR. Ulceration and carotid artery disease. Stroke. 1988; 19: 650–653.[Free Full Text]
  9. Rutgers DR, Klijn CJM, Kappelle LJ, Eikelboom BC, van Huffelen AC, van der Grond J. Sustained bilateral hemodynamic benefit of contralateral carotid endarterectomy in patients with symptomatic internal carotid artery occlusion. Stroke. 2001; 32: 728–734.[Abstract/Free Full Text]
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  13. Reilly LM, Lusby RJ, Hughes L, Ferrell LD, Stoney RJ, Ehrenfeld WK. Carotid plaque histology using real-time ultrasonography. Clinical and therapeutic implications. Am J Surg. 1983; 146: 188–193.[CrossRef][Medline] [Order article via Infotrieve]
  14. AbuRahma AF, Wulu JT, Crotty B. Carotid plaque ultrasonic heterogeneity and severity of stenosis. Stroke. 2002; 33: 1772–1775.[Abstract/Free Full Text]
  15. Dijk JM, van der Graaf Y, Grobbee DE, Bots ML; SMART Study Group. Carotid stiffness indicates risk of ischemic stroke and TIA in patients with internal carotid artery stenosis. The SMART Study. Stroke. 2004; 35: 2258–2262.[Abstract/Free Full Text]
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  17. 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 randomized controlled trials of endarterectomy for symptomatic carotid stenosis. Lancet. 2003; 361: 107–116.[CrossRef][Medline] [Order article via Infotrieve]
  18. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995; 273: 1421–1428.[Abstract]
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  20. Cipollone F, Fazia M, Mincione G, Iezzi A, Pini B, Cuccurullo C, Ucchino S, Spigonardo F, Di Nisio M, Cuccurullo F, Mezzetti A, Porreca E. Increased expression of transforming growth factor-ß1 as a stabilizing factor in human atherosclerotic plaques. Stroke. 2004; 35: 2253–2257.[Abstract/Free Full Text]
  21. Findlay JM, Marchak BE, Pelz DM, Feasby TE. Carotid Endarterectomy: a Review. Can J Neurol Sci. 2004; 31: 22–36.[Medline] [Order article via Infotrieve]

Related Article:

Carotid Plaque Pathology: Thrombosis, Ulceration, and Stroke Pathogenesis
Mark Fisher, Annlia Paganini-Hill, Aldana Martin, Michele Cosgrove, James F. Toole, Henry J.M. Barnett, and John Norris
Stroke 2005 36: 253-257. [Abstract] [Full Text] [PDF]




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