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Show Carotid Endarterectomy for Transient Monocular Visual Loss and Other Ocular Ischemic Conditions Jonathan D. Trobe, MD Evidence from randomized clinical trials ( RCTs) is a rare and prized commodity in medicine. When it does come along, as in the case of carotid endarterectomy ( CE) for stroke prevention, it evokes an amazing variety of responses ( 1- 5). The evidence may be rejected because it does not conform to preconceptions. It may be dismissed as out of date, especially when techniques have improved. The fine print or follow- up reports may be ignored and the evidence misapplied to subgroups that differ substantially from the general cohort. It may be applied to types of patients who were not even in the original cohort, and, most often, " statistically significant" benefits may be surmised as " clinically meaningful" without any consideration of cost. In this issue of the Journal ofNeuro- Ophthalmology, three articles ( 6- 8) deal with the use of CE for transient monocular visual loss ( TMVL) and other ophthalmic indications. It is astounding how differently the same evidence is interpreted and applied. In a Viewpoint article, Wolintz ( 6) finds little robust evidence to support a meaningful benefit of CE in TMVL. The basis of her argument is an after- the- fact subset North American Symptomatic Carotid Endarterectomy Trial ( NASCET) analysis by Benavente et al ( 9) who found that TMVL patients required at least three of the following features to benefit from CE: 1) male sex, 2) age of 75 years or older, 3) history of hemispheric transient ischemic attack ( TLA) or stroke, 4) history of intermittent claudication, 5) ipsilateral internal carotid artery stenosis of 80%- 94%, and 6) absence of collateral vessels on angiography. Only 20% of the NASCET cohort met those criteria. Yet, in another Viewpoint article, Nicolle and Hachinski ( 7) report that at the University of Western Ontario, the home of the authoritative NASCET study, CE is offered to patients of either sex and of any age if the ipsilateral cervical carotid stenosis is high grade (> 70%) without consideration of how many of the above risk factors are present in the patients. In a Point Counter Point debate on CE for TMVL, Caplan and Hertzer ( 8) both support the use of CE for TMVL, dismissing the findings of Benavente et al ( 9) for different reasons. Caplan argues that, as a large study, the NASCET could not consider individual patient characteristics such as the echographic features of the plaque, now believed to refine stroke risk. Hertzer rejects the subgroup analysis of TMVL in the NASCET report as being statistically flawed. There is no doubt that RCT data support CE for stroke prevention in patients with transient hemispheric TIA and stroke ( 2,3). But do patients with clinical manifestations of ocular ischemia belong in that group? In its abstract summarizing a review of articles on CE and stroke prevention published between 1990 and 2002, the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology ( 10) affirms that " evidence supports carotid endarterectomy for severe ( 70 to 99%) symptomatic stenosis" but makes no exception for patients with TMVL or retinal stroke. Yet, deep within the text of the article, the authors acknowledge that " patients with hemispheric TIA/ stroke had Departments of Ophthalmology and Neurology, University of Michigan, Ann Arbor. J Neuro- Ophthalmol, Vol. 25, No. 4, 2005 259 greater benefit from CE than patients with retinal ischemic and the benefit from CE is not established; 2) CRAO should events" ( 10). This difference in benefit is based on the fact not be lumped with a hemispheric TIA or stroke; carotid that medically managed patients with retinal ischemic events stenosis is often mild, suggesting a non- embolic mecha-clearly have a much lower risk of major hemispheric stroke nism; and 3) asymptomatic patients with Hollenhorst plaques than do patients with hemispheric TIA or minor stroke ( 11). and high- grade carotid stenosis may have a stroke risk equal What about the value of CE for other ophthalmic to that of patients without such plaques; if so, they should indications? Nicolle and Hachinski ( 7), Caplan ( 8), and not undergo CE because the reduction in future stroke is too Hertzer ( 8) consider central retinal artery occlusion ( CRAO) low, even if the peri- operative complications are minimal. as much of an indication for CE as TMVL. Yet CRAO need Two other facts ought to caution the use of CE in not be the result of an embolic event; it often appears patho- ocular ischemia. First, patients probably are at just as high logically as thrombosis within a retrolaminar atheroscle- a risk of myocardial infarction and cardiac death as are rotic plaque ( 12). In one study of 34 patients with CRAO, those with hemispheric TIA and stroke ( 14- 16), which is only 12% had ipsilateral carotid stenosis of 80% or more a risk that cannot possibly be made better by CE. Second, ( 13); in another study of 77 patients, only 20% had stenosis the benefit of CE, even in symptomatic patients, depends on of 50% or more ( 14). Moreover, although the risk of hemi- a peri- operative stroke and death rate less than 5% ( 2). In spheric stroke in patients with CRAO has not been rig- most hospitals, this rate is not tallied or made known to orously documented, it seems to be lower than in patients non- surgeons ( 22); when it is tallied, it is often more than an with recent hemispheric TIA or stroke ( 15). acceptable level ( 23). For all these reasons, it is time to Finally, what about CE for patients with asymptom- remove ophthalmic ischemic conditions from the indica-atic Hollenhorst plaque? Nicolle and Hachinski ( 7) do not tions for CE. offer CE to such patients, but Hertzer ( 8) does, and Caplan ( 8) might. Is there a compelling reason to believe that the asymptomatic patient with high- grade carotid stenosis and a Hollenhorst plaque should be managed differently from L R° thwell PM. why do clinicians sometimes find it difficult to use the ,. , ,. ,• , -, i 1 • 1 1 ,• 1 , • results of systemic reviews in routine clinical practice? EvalHealth the asymptomatic patient with high- grade carotid stenosis Pm,' 2002- 25- 200- 9 but no Such plaque? An older Study ( 16) pointed OUt that 2. Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid early death from myocardial infarction is the major risk in endarterectomy in patients with symptomatic moderate or severe . , , _ T , , ,• , , stenosis. N EnglJ Med 1998: 339: 1415- 25. patients with retinal plaque. No study has directly ad- 3 Farrell B Fraser A> Sandercock R et al. Randomized trial of dressed the value of CE in such patients. But the American endarterectomy for recently symptomatic carotid stenosis: final Academy of Neurology report of 2005 ( 10) finds that for results of the MRC Eu ™ Pean Carotid Surgery Trial ( ECST). Lancet 1998- 3511379- 87 " asymptomatic patients with 60 to 99% stenosis, the bene- 4 wins'low CM> Solomon DH chassin MR> et al The appr0priateness fit/ risk ratio is smaller compared to symptomatic patients," of carotid endarterectomy. N Engl J Med 1988; 318: 721- 7. suggesting that in this group, " individual decisions must be 5- Rothwe11 P M > W a r i o w C R ° n behalf of the European Carotid Surgery ^ l " TU tu + tu f 11 u f t ' Trialists' Collaborative Group. Prediction of benefit from carotid made. the authors Cite the tollOWing sobering tacts in endarterectomy in individual patients: a risk- modelling study. Lancet relation to CE in asymptomatic high- grade carotid stenosis: 1999; 353: 2105- 1. 1) the Mayo Study ( 17) was terminated early because of 6- Wolintz RI Carotid Endarterectomy for Ophthalmic Manifestations: . . . r . . . . . . . /„„„/.. • , • , Is It Ever Indicated? J Neuroopthalmol 2005: 25: 299- 302. a high rate of myocardial infarction ( 22%) in the Surgical 7 M c o l l e D Hachinski V Carotid Endarterectomy for Ophthalmic group; 2) the Veterans Administration Study ( 18) found no Manifestations: What Do We Do? J Neuroopthalmol 2005; 25: 303. Significant benefit of CE; 3) the Asymptomatic Carotid 8- Caplan LR, Hertzer NR. The Management of Transient Monocular » o 1 / tn\ r- 11 ^ T, 1 11 1 • • 1 r- Visual Loss. J Neuroopthalmol 2005: 25: 304- 312. Artery Study ( 19) found that CE reduced the relative risk of 9 Benavente O, Eliasziw M, Steifler JY, et al. Prognosis after transient ipsilateral hemispheric Stroke by 53%, but the five- year risk monocular blindness associated with carotid artery stenosis. N EnglJ was only 11% in the medically treated group. The small Aferf200i; 345: i084- 90. , „ ... .. 1 •,- 1 • • 1 10. Chaturvedi S, Bruno A, Feasby T, et al. Carotid endarterectomy: an benefit would have disappeared it the pen- operative stroke evidence- based review: report of the Therapeutics and Technology rate had been more than 2.3%, a rate much lower than has Assessment Subcommittee of the American Academy of Neurology. been found in other studies ( 20); and 4) the Asymptomatic Neurology 2005; 65: 794- 801. _ - io m • i / VM\ r 11 • 1 • ll- Streifler JY, Eliasziw M, Benavente O, et al. The risk of stroke in Carotid Surgery Trial ( 21) found that patients undergoing patients wiih fcst. ever retinal vs hemispheric tmni. isnt ischemic early CE had a five- year Stroke risk of 6.4%, whereas attacks and high- grade carotid stenosis. Arch Neurol 1995; 52: 246- 9. patients undergoing delayed CE had a five- year stroke risk 12- Green WR- Retinal ischemia: vascular and circulatory conditions _ . . _ „ , _ , . . 1 1 11 1 - 1 1 - 1 and diseases. In: Spencer WH, ed. Ophthalmic Pathology. 3rd ed. Of 11.8%. But these data totaled all Strokes, including those Philadelphia- Saunders- 1985- 685 in the Contralateral carotid and vertebrobasilar distributions. 13. Merchut MP, Gupta SR, Naheedy MH. The relation of retinal artery This information leads to Some inescapable COn- occlusion and carotid artery stenosis. Stroke 1988; 19: 1239^ 3. 1 • 1 \ ™ , x rr 1 11 , 1 i - i i • 1 • 14. Babikian V, Wiiman CA, Koleini B, et al. Retinal ischemia and elusions: 1) TMVL should not be lumped With hemispheric embolism: etiologies and outcomes based on a prospective study. TIA or stroke; the stroke risk without CE is relatively small, Cerebwvasc Dis 2001; 12: 108- 13. 15. Savino PJ, Glaser JS, Cassady J. Retinal stroke: is the patient at risk? 20. Taylor DW, Barnett HJM, Haynes RB, et al. Low- dose and high- dose Arch Ophthalmol 1977; 95: 1185- 9. acetylsalicylic acid for patients undergoing carotid endarterectomy: 16. Pfaffenbach DD, Hollenhorst RW. Morbidity and survivorship of a randomized controlled trial. Lancet 1999; 353: 2179- 84. patients with embolic cholesterol crystals in the ocular fundus. Am J 21. MRS Asymptomatic Carotid Surgery Trial ( ACST) Collaborative Ophthalmol 1973; 75: 66- 72. Group. Prevention of disabling and fatal strokes by successful carotid 17. Mayo Asymptomatic Carotid Endarterectomy Study Group. Effec- endarterectomy in patients without recent neurological symptoms: tivenessof carotid endarterectomy for asymptomatic carotid stenosis: randomized controlled trial. Lancet 2004; 363: 1491- 502. design of a clinical trial. Mayo Clin Proc 1992; 64: 897- 904. 22. Goldstein LB, Bonito AJ, Atchar DB, et al. US national survey of 18. Hobson RW, Weiss DG, Fields WS, et al. Efficacy of carotid end- physician practices for the secondary and tertiary prevention of arterectomy for asymptomatic carotid stenosis. N Engl J Med 1993; ischemic stroke: design, service availability, and common practices. 328: 221- 7. Stroke 1995; 26: 1607- 15. 19. Toole JF, Adams HP, Chambless LE, et al. Endarterectomy 23. Tu j y Hannan EL, Anderson GM, et al. The fall and rise of carotid for asymptomatic carotid artery stenosis. JAMA 1995; 273: endarterectomy in the United States and Canada. N Engl J Med 1421- 28. 1998; 339: 1441- 7. |