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Show The Management of Transient Monocular Visual Loss A60- year- old man develops sudden complete transient loss of vision OD three days ago lasting 30 seconds. It occurred while he was reading. He has a history of medication- controlled hypertension and has smoked 1/ 2 pack of cigarettes daily for many decades. His medical history is otherwise unremarkable. General physical, ophthalmological, and neurological examinations are normal. What is the probable cause of the deficit, and what is the next step in evaluation? Louis R. Caplan, MD: I would begin by ordering a complete blood count The most likely cause of his transient monocular vi- and sedimentation rate, an electrocardiogram ( EKG), a du-sual loss ( TMVL) is retinal ischemia ( 1- 3). Occasionally, plex ultrasound study of the neck arteries, and a transcranial transient optic nerve ischemia can present similar symp- Doppler ( TCD) exploration of the cranial arteries. The du-toms ( 3). Most ocular ischemia is caused by embolism to plex examination should detect significant ICA disease at the ophthalmic artery, and its branches that feed the retina the common carotid artery bifurcation. TCD can help detect and optic nerve. Sources of embolism to the eye include the disease of the carotid siphon proximal to the ophthalmic heart, aorta, ipsilateral extracranial and siphon portions of artery, disease of the ophthalmic artery itself, and help to the internal carotid artery, and the ophthalmic artery. quantify any reduction in blood flow related to ICA disease In this patient, a normal ophthalmologic examination in the neck ( 7). If the duplex findings in the neck are excludes impending central retinal vein occlusion ( 4), optic equivocal, 20- 30 minutes of TCD monitoring of the intra-disc drusen ( 5), and pre- retinal loops ( 6), which are occa- cranial middle cerebral arteries ( MCAs) might help identify sional causes of ocular ischemia. There were no Hollen- the presence and source of emboli ( 8,9). If the source is the horst plaques, white platelet- fibrin thrombi, or calcific ipsilateral ICA, embolic signals would be detected only in emboli within the retinal arteries- clues to the origin of the ipsilateral MCA; if the source is cardiac or aortic, em-emboli. The risk factors in this patient make internal carotid boli should be detected bilaterally. If a four- probe embolic artery ( ICA) disease the most likely source of TMVL. detection system is available, the ICAs can also be probe Atheromatous disease of the aorta or heart is another im- sites. Emboli from the heart or aorta would first be detected portant possibility. Patients with polycythemia and throm- in the ICA and shortly thereafter in the ipsilateral MCA. If bocytosis can occasionally develop TMVL. Temporal the emboli arise from the ICA, no embolic signals would be arteritis is an infrequent cause. heard in the neck. I usually order a brain and head- and- neck vascular absence of any atheromatous debris observed in the retina, imaging study ( computed tomography [ CTJ/ CT angiogra- Until proven otherwise, atherosclerotic stenosis or ulcer-phy [ CTA] or MRI/ MR angiography [ MRA]) along with ation in the ipsilateral carotid bifurcation represents the the ultrasound. Some patients have had unexpected brain most likely embolic source in this patient, especially con-infarcts; their distribution can give a clue as to their cause. sidering his long history of tobacco use. If cervical carotid Brain infarction ipsilateral to ICA disease also tells of the disease can be excluded by appropriate studies, however, biological activity of the lesion despite lack of symptoms then cardio- embolic and other less common etiologies ( 10,11). CTA and MRA examinations of the neck and head would have to be investigated ( 13). In an effort to prevent can show the presence, extent, and morphology of an ICA any further micro- embolic events while the diagnosis is lesion in the neck and provide images of occlusive disease being established, the patient should immediately be that might involve the pharyngeal portion of the ICA ( such instructed to begin taking aspirin at least 81 mg/ day ( 14). as fibromuscular dysplasia or dissection), the ICA siphon, The next step in the evaluation would be a carotid and its ophthalmic artery branch. duplex scan, preferably at a facility that has been certified An EKG should have detected atrial fibrillation and for accuracy by the Intersocietal Commission for the Ac-recent or past myocardial infarction. A transesophageal creditation of Vascular Laboratories ( www. iacvl. org). Pro-echocardiogram ( TEE), which searches for embolic sources vided high- grade ( 70%- 99% or 80%- 99%) extracranial in the cardiac ventricles, atria, interatrial septum, cardiac carotid stenosis is identified on the basis of reliable duplex valves, and aorta, might be indicated depending on the scanning, carotid endarterectomy ( CE) could legitimately be results of the blood tests, EKG, neck ultrasound, TCD, and recommended without the small additional risk of a con-brain and vascular imaging ( 12). firmatory arteriogram ( 15). But if the duplex scan reveals only mild to moderate cervical carotid disease, MRA or Norman R. Hertzer, MD: even catheter arteriography may be required to exclude Despite its unusually brief duration, this episode of non- stenotic plaque ulceration, aortic arch lesions, or intra- TMVL almost certainly represents retinal microemboliza- cranial carotid siphon disease proximal to the origin of the tion, which, in this case, probably was related to platelet ophthalmic artery. An echocardiogram might be indicated if thrombi given the transitory nature of the event and the the underlying etiology still remains in doubt. The patient undergoes a duplex cervical carotid ultrasound that reveals 80% cross sectional stenosis on the right and 50% on the left. A brain MRI is negative. What do you advise as the next step? Louis R. Caplan, MD: ( 17- 20). ACE inhibitors and ACE receptor blockers have I would first review the results with the patient, indi- also been shown to have salutary effects on the endothelium eating that he has significant carotid artery disease and is at and could be prescribed ( 21,22). Some antiplatelet agents, risk for stroke. I would explain that the alternatives are maxi- especially an aspirin- dipyridamole combination or cilosta-mal medical therapy, CE, or carotid angioplasty/ stenting. zol, have effects on platelets and vascular endothelium and Maximal medical therapy, which consists of an antiplatelet may be more protective than aspirin alone or clopidogrel. agent, a statin in the appropriate dose, and an ACE inhibitor These medical prescriptions can be given while further or ACE receptor blocker, would be prescribed. Although investigations are performed and while the patient is the risk of stroke after a retinal transient ischemic attack deciding on a preferred strategy of treatment. ( TIA) is about one third the risk of stroke after a hemi- The nature of the carotid plaque might influence spheric TIA ( 16), it is likely to be more than 10% during the prognosis and treatment. The main features are plaque ensuing year or two ( 16). If he opted for medical treatment echogenicity, regularity, homogeneity, location, and the and was to have a hemispheric TIA or minor stroke, then thinness of the fibrous cap overlying the plaque ( 23- 25). the risk of major stroke would increase considerably, and Hypoechoic plaques contain more macrophages and lipid aggressive therapy would be mandated. materials and are more likely to become symptomatic ( and If medical treatment has not been optimal, consid- to be reducible by statins). Hyperechoic material indicates eration should be given to adding a statin or increasing the calcium and stability. Heterogeneity and irregularity of the dose of a statin if one is already being used. Studies have surface, especially with ulceration, carry a worse prognosis shown that large doses of statins can reduce plaques or for symptom development. These features can now be at least stabilize them and reduce the frequency of stroke detected by high- quality B- mode ultrasound and, in some centers, by modern CT and MRI imaging of plaques using The initial NASCET results were reported in 1991 for cross- sectional views of the artery. 70%- 99% stenosis ( 29) and demonstrated that CE signif- Brain imaging is also useful. The presence of brain in- icantly reduced the 2- year ipsilateral stroke rate as com-farcts on CT or MRI attributable to the stenotic artery gives pared with medical management alone ( 9% versus 26%; evidence of biological activity of the carotid disease despite P < 0.001). Interestingly, subset analysis later revealed that the absence of hemispheric symptoms and increases the risk patients in the medical cohort who originally presented of stroke ( 10). Embolic monitoring also provides prognostic with transient hemispheric TIA or stroke had a higher data. The number and frequency of microemboli ( high- 2- year stroke rate than did patients who presented with intensity transient signals on TCD) and their response to TMVL ( 43.5% ± 6.7% versus 16.6% ± 5.6%; P = 0.002), medical treatment is predictive of symptom development representing a relative risk ratio of 3.23 ( 95% confidence ( 26- 28). interval, 1.47- 7.12) ( 16). If the patient makes up his mind to undergo CE or It took substantially longer for the NASCET trialists to stenting, I would refer him to the appropriate specialist. If reach conclusions regarding the efficacy of CE in symptomatic he is opposed to a procedure, I would maximize medical patients who had only 50%- 69% carotid stenosis. Their 1998 treatment and instruct him about hemispheric attacks. If he report ( 30) showed that, whereas still statistically significant, is uncertain and believes that more data would help him the benefit of surgical treatment was much less convincing, decide, I would schedule further investigations such as The 5- year ipsilateral stroke rate for CE in these patients was cranial MRI, high- quality duplex ultrasound, and TCD of 15.7% versus 22.2% in medically treated patients ( P = 0.045). the intracranial arteries, along with embolic monitoring. CE provided no advantage in comparison to medical management for an exceedingly small group of only 36 patients who were randomized because of TMVL or retinal stroke. Norman R. Hertzer, MD: Provided the duplex scan was performed in a reliable For over a decade, the importance of identifying noninvasive vascular laboratory, I would recommend right symptomatic carotid disease primarily has been predicated CE by a qualified surgeon or participation in one of the cur-on the conclusions of the North American Symptomatic rent randomized trials comparing CE to percutaneous Carotid Endarterectomy Trial ( NASCET). In this pro- transluminal angioplasty ( PTA) and stenting with the use of spective, multicenter clinical trial, patients having a recent a cerebral protection device. The choice between these two history of TMVL, transient hemispheric ischemia, or non- options would depend in part on their availability at the center disabling stroke were randomized to receive CE plus where he receives his care. I should also add that obtaining " optimal" medical management ( predominantly anti- an MRI brain scan seems to have been an unnecessary ex-platelet therapy) or medical management alone for either travagance in our patient, especially after only a single 50%- 69% or 70%- 99% carotid stenosis documented on 30- second episode of TMVL. The chance that such a study the appropriate side of the neck by arteriography. would have revealed any useful information seems remote. In 2001, Benavente et al ( 31) finally reported the outcomes of the subgroup of TMVL patients from the NASCET trial who were randomized to CE versus best medical treatment. As you recall, they found that a meaningful benefit of CE was restricted to those who had at least three of the following characteristics: age > 75 years, male, history of hemispheric TIA or stroke, history of intermittent calf claudication, ipsilateral internal carotid stenosis > 80%, or no collaterals on angiography. Our patient meets only two of these criteria. Is CE indicated? Louis R. Caplan, MD: risk factors ( age, sex, and claudication) as surrogates for The cited NASCET data ( 31) must be put in the estimating the seriousness of vascular disease. The per-perspective of the study. The analysis was retrospective. It centage reduction of luminal size on catheter cerebral considered effectiveness as reducing strokes ( not just those angiograms and the presence of collateral circulation were related to the ipsilateral carotid artery). This means that the main direct measures of the nature and severity of the factors related to strokes and vascular disease in general, carotid artery disease. The details of the composition and such as hypertension, diabetes, hyperlipidemia, and smok- morphology of the stenosing plaques, as shown by high-ing, were heavily weighted. The data analyses used indirect quality ultrasound, were not included. Several factors were not included or sufficiently patient who has 80%- 99% carotid stenosis merely because emphasized, as is true in many large trials that must lump he is only 60 years old and does not claudicate. disparate patients. For example, the presence of brain Furthermore, it seems hard to know how the NASCET infarcts in the territory of the stenosed artery and other proportional hazards model applies to our patient because he medical therapies. Moreover, since the NASCET study was has not yet had an arteriogram to demonstrate the presence or planned, advances in technology and treatment have oc- absence of collateral circulation distal to his high- grade curred. There are new drugs and information about effec- cervical carotid lesion. An arteriogram presumably would tive dosages of statins, ACE inhibitors, ACE receptor have to be done in order to determine where he fits into the blockers, and non- aspirin platelet inhibitors, plaque mor- NASCET analysis, but findings from the Asymptomatic phology, as studied by modern ultrasound, the importance Carotid Atherosclerosis Study ( ACAS) indicate that an of brain infarcts seen on MRI, the ability to detect emboli arteriogram also would add a small but measurable risk to his by TCD, and the availability of carotid angioplasty/ stenting. management ( 32). Five ( 26%) of the 19 strokes or deaths contributing to the combined stroke and mortality rate of 2.3% in the surgical cohort of the ACAS were directly Norman R. Hertzer, MD: related to the preoperative arteriogram, an observation that So many subset analyses from the NASCET have undoubtedly has influenced a growing reliance on non-been published since the initial disclosures from this trial in invasive testing alone in the selection of patients for CE. At 1991 that it has become increasingly difficult to keep track the Massachusetts General Hospital, for example, only 10% of all of them. Now that I have read the article by Benavente of patients underwent preoperative arteriography before CE et al ( 31), I find that its data regarding the treatment of in 1998- 1999 compared with 87% in 1989- 1990 ( 33). TMVL are based on 107 patients having none of the five As a practical matter, two other large randomized stated risk factors, 150 patients having two of the risk trials- the ACAS and the more recent Asymptomatic Carotid factors, and 103 patients having three or more of the risk Surgery Trial- have shown that our patient already has factors. These sample sizes apparently do not detract from carotid stenosis of sufficient severity to justify prophylactic the statistical validity of the conclusions, but they do parse CE even if he had no symptoms whatsoever ( 32,34). For all of the total NASCET population ( n = 2,885) into some pretty these reasons, I believe that he is an appropriate candidate for small pieces. I personally would be very uncomfortable CE despite the fact that he has only two of the NASCET risk using this information to withhold CE from a symptomatic factors described by Benavente et al ( 31). Louis R. Caplan, MD: Norman R. Hertzer, MD: I would place some weight on the findings from First let me give a brief overview of catheter- based high quality ultrasound and vascular imaging. Since the intervention for carotid bifurcation disease. Isolated case re- NASCET study, there have been a number of studies of ports and experience with small series of patients suggested the risks and benefits of angioplasty/ stenting with and nearly two decades ago that angioplasty of the carotid without protective devices ( 35- 37). In a high carotid bi- artery might prove to be an appropriate alternative to tradi-furcation or very long smooth plaque, stenting is likely tional surgical treatment for high internal carotid lesions better. In a very focal ulcerated lesion, surgery is likely near the skull base, recurrent stenosis after previous CE, better. If there is a tandem lesion distal to the bifurcation, or a history of cervical irradiation ( 39). then angioplasty/ stenting might treat both lesions. The Intraluminal stenting was introduced in the early availability, experience, and complication rates of the sur- 1990s to reduce the incidence of peri- procedural embolic geons and interventionalists are also important in deciding events and recurrent stenosis that were associated with which treatment is preferable. angioplasty alone, and over- the- wire cerebral protection I would discuss the options with the patient, devices were later developed in a further attempt to prevent attempting to share the risks and benefits of each approach strokes caused by atheromatous emboli dislodged during in his individual case and in relation to the individuals stent deployment. These refinements have widened the available to provide the treatments. All things being equal, indications for catheter- based intervention, but as so often I usually favor stenting or entering the patient into a occurs with rapidly advancing technology, they also have randomized trial that compares stenting with surgery ( 38). turned outcome assessment into a moving target. The elusive nature ofthis target can be illustrated by two or CE ( n = 167) at 29 participating centers ( 35). Using relatively recent examples involving symptomatic patients. conventional end points consisting of the 30- day CSM plus In 2000, Golledge et al ( 40) conducted a meta- analysis of ipsilateral stroke or death within 1 year, the SAPPHIRE 33 single- center studies that had been reported from 1990 trial had equivalent outcomes for angioplasty/ stenting and through 1999 and calculated that the risks for any related CE ( 5.5% versus 8.4%; P = 0.36). When increased peri-stroke ( 7.1% versus 3.3%; P < 0.001) or stroke or death procedural cardiac enzyme levels also were considered, the ( 7.8% versus 4.0%; P < 0.001) were significantly higher for CSM/ MI plus 1- year event rates were lower for angio-angioplasty than for CE. In 2001, the results of a multicenter, plasty/ stenting than for CE ( 12% versus 20%; P = 0.05). prospective randomized trial ( CAVATAS) conducted in Europe The ongoing Carotid Revascularization Endarterec-from 1992 to 1997 indicated that, whereas the 30- day tomy versus Stent Trial ( CREST) is a multicenter, prospec-combined stroke and mortality rates ( CSM) of angioplasty tive, randomized investigation that is supported by the National and CE were uniformly poor ( 10% versus 9.9%), the 1- year Institutes of Health with plans to recruit 1,200 to 1,600 symp-incidence of recurrent 70% stenosis was significantly higher tomatic patients ( 43). No outcome data have been disclosed ( 14% versus 4.0%, P < 0.001) for angioplasty ( 41). However, for approximately 650 randomizations, but information has the conclusions of both of these investigations became obso- been reported for 749 non- randomized patients who were lete nearly as soon as they were published for two reasons: 1) treated by angioplasty/ stenting with adjunctive cerebral pro-stenting had been done in only 44% of the angioplasty cases tection during a lead- in phase used for credentialing catheter-reviewed in the meta- analysis and in just 26% of the angio- based interventionalists at 51 sites ( 44). These results sub-plasty cohort of the CAVATAS; and 2) cerebral protection stantiate that the CSM for angioplasty/ stenting is correlated devices were not yet available during either of the two study with advancing age, ranging from 1.4% in 349 patients periods. Therefore, the evidence base for contemporary aged less than 70 years to 7.0% in 400 patients aged 70 angioplasty/ stenting with intra- procedural cerebral pro- years or older ( P = 0.0006). Others ( 45) have made similar tection is limited to the past five years and still is evolving. observations regarding age and the early risk of angio- Two industry- funded trials now have shown out- plasty/ stenting, despite the use of anti- embolic devices, comes for angioplasty/ stenting with cerebral protection Now, which option would I choose for this patient? that are equivalent to CE in a mix of symptomatic and He does not represent a predictable early risk for either asymptomatic patients drawn from the United States. The approach at only 60 years of age, and therefore, he should CARESS study ( Boston Scientific, Natick, MA; Medtronic be given the opportunity to enroll in the CREST if a trial AVE, Santa Rosa CA) is a Phase I clinical trial in which center is nearby. If not, his anticipated life expectancy 397 typical patients were treated at 14 sites by angio- becomes a consideration with respect to the risk for recur-plasty/ stenting ( n = 143) or CE ( n = 254) ( 42). In that rent stenosis, which may be greater for angioplasty/ stenting study, there were no significant differences in the 30- day although this has not been rigorously verified for con- CSM ( 2.1% versus 2.4%) or the CSM- plus- myocardial temporary angioplasty/ stenting techniques. In the absence infarction ( MI) rates ( 2.1% versus 3.1%). The other study of further data, I favor CE with carotid patching on the basis is the Stenting and Angioplasty with Protection in Patients of my own experience. But the key point is: what are the at High Risk for Endarterectomy ( SAPPHIRE) trial ( Cordis comparative results of CE and angioplasty/ stenting at the Corporation, Warren, NJ), in which 3 34 patients with medical hospital where the patient will be treated? A decision con-comorbidities or anatomic features considered unfavorable cerning management options cannot be made objectively for CE were randomized to angioplasty/ stenting ( n - 167) without this information. Would your management differ if, instead of transient visual loss, this patient had presented with acute persistent unilateral visual loss owing to a central retinal artery occlusion ( CRAO)? Would management differ if the patient had presented without visual symptoms but had been found to have a Hollenhorst plaque in one eye? Louis R. Caplan, MD: incidentally, I would be heavily guided by the nature and My suggestions for management would not be differ- extent of the carotid artery lesion. I would also lean more ent had the patient presented with a CRAO. If he was toward surgery if brain imaging disclosed a brain infarct in asymptomatic and had a Hollenhorst plaque discovered the carotid artery territory. Norman R. Hertzer, MD: Asymptomatic Hollenhorst plaques can originate None of the prospectively randomized trials of CE from the heart or the aortic arch as well as from the carotid or angioplasty/ stenting has generated data specifically bifurcation, in which case additional retinal emboli and/ or concerning either CRAO or incidental Hollenhorst plaques, neurologic events may still occur even if CE already has but independent case series suggest that these findings are been performed for what was thought to be the responsible much less likely than TMVL to be associated with serious lesion ( 50). This emphasizes the importance of a thorough underlying carotid stenosis. For example, three studies ( 46- 48) ophthalmologic evaluation, because the presence of bi-have collectively reported at least 60% ipsilateral carotid lateral retinal atheroemboli would clearly imply that they stenosis by duplex scanning in 31 ( 37%) of 84 patients with share a common proximal source in the chest. Another TMVL, compared to just seven ( 11%) of 63 patients with dilemma in the management of Hollenhorst plaques is the Hollenhorst plaques and two ( 7.4%) of 27 patients with CRAO. fact that they may persist for as long as three years ( 51). The observation that CRAO is a poor predictor of Therefore, unless serial ophthalmologic examinations have carotid artery disease is not surprising because it often is documented that a Hollenhorst plaque is recent, it could merely an ophthalmic manifestation of systemic illness, have originated in an atheromatous ulcer in the ipsilateral such as uncontrolled diabetes, arteritis, or a variety of carotid artery or elsewhere that has healed and is no longer coagulation disorders ( 49). For this reason, medical consul- a threat for further embolization. tation probably should be obtained as one of the first steps Despite all of these uncertainties, a unilateral in the evaluation of CRAO. If another plausible etiology Hollenhorst plaque remains an appropriate indication for is discovered, investigation of the carotid arteries may carotid duplex scanning if only because one does not want not be required provided, of course, that the onset of to overlook an easily accessible lesion for which anti- platelet sudden monocular blindness had not been preceded by therapy alone would offer no guarantee against future athero-earlier episodes of classic TMVL in the same eye. With embolic complications. It seems prudent, however, to limit a history of previous TMVL, one might be more likely to CE or angioplasty/ stenting strictly to patients who, like our suspect ipsilateral carotid emboli and proceed with own, have such severe carotid stenosis that they would be a duplex scan. candidates for carotid intervention anyway. If you were this patient, with the same scenario, what would you wish to have done? Louis R. Caplan, MD: current stenosis, and re- operations as compared with Stenting with a competent experienced intervention- primary arteriotomy closure. In general, CE/ patching is alist using a protective device. associated with a CSM less than 2%, a 5% incidence of recurrent stenosis, and a re- intervention rate of 3% or less Norman R. Hertzer, MD: ( 33, 52- 56). I would first seek out a qualified surgeon, preferably It may be that angioplasty/ stenting will someday one who holds the Certificate of Special or Added Quali- match these results and, at certain centers of excellence, fications in Vascular Surgery issued by the American perhaps it already does. At the present time, however, the Board of Surgery and who practices in a hospital at which technology of catheter- based carotid intervention and the the outcome of CE is continuously audited for quality learning curve of its practitioners are in their maturation assessment. I would then opt for CE with a patch because phases. For this reason, I believe that CE with patching so many randomized and non- randomized studies now currently represents the best available approach throughout have shown that patching reduces the risks for post- the countless communities, large and small, where most operative death, postoperative stroke, late stroke, re- patients receive their care. Louis R. Caplan, MD: over the less familiar. No doubt Dr. Hertzer would have It comes as no surprise that Dr. Hertzer, a renowned access to a very capable, experienced vascular surgeon with vascular surgeon, would choose vascular surgery over a superb track record for CE, a luxury our patient may not angioplasty/ stenting. We tend to choose the more familiar have. Dr. Hertzer's discussion and some of the queries Norman R. Hertzer, MD: emphasize trial data. Caring for individual patients is dif- Aside from our personal preferences for CE or per-ferent from trials. The CREST and other trials pit CE cutaneous angioplasty/ stenting, the main areas in which I against angioplasty/ stenting with the naive idea that one disagree with Dr. Caplan regarding the management of this approach is always superior to the other. Actually, one patient involve the extent of his initial work- up and his will-approach may be better for some lesions and some patients ingness to continue medical management even after severe with coexisting conditions and risks. The location, content, carotid stenosis has been documented by noninvasive extent, and morphology of the occlusive plaque are impor- imaging. tant determinants for the choice of treatments. The carotid Dr. Caplan apparently would obtain a lot more tests artery investigations reported on this patient do not suffi- than I feel are necessary for the evaluation of an otherwise ciently detail this information. Also, trials assume equi- healthy 60- year- old smoker who has had a single brief poise between the surgeon and the interventionalist. As episode of TMVL. It would not cross my mind to order Dr. Hertzer notes, this is not always the case at the a sedimentation rate, a TCD examination, a head- and- neck institution where the patient will be treated and heavily CT/ CTA, or an MRI/ MRA for this patient before the duplex influences selection of strategy. scan had even been performed. Once a reliable duplex scan Most important, and again not included in trials, is has shown 80%- 99% stenosis in the ipsilateral carotid the preference of the patient and the referring physician. bifurcation, the cost effectiveness of the other studies be- General anesthesia poses a very definite risk and many comes very questionable. I believe they should be reserved doctors and patients would avoid it. CE is customarily per- for patients who have less than severe carotid stenosis by formed under general anesthesia; angioplasty/ stenting is not. duplex scanning or some other specific reason for addi- Patients live in different socioeconomic- psychological tional testing, milieus. Given the same information, they make different Dr. Caplan considers " maximal medical therapy" decisions. Some find the knowledge of a severe carotid to be a reasonable alternative to CE or angioplasty/ stent-lesion very difficult to live with. Told that they are at ing in this patient. He then states that " if medical imminent risk of having a disabling stroke, they feel that treatment has not been optimal" ( that more symptoms a sword ( the stenotic artery) is hovering over them. Some have occurred), " consideration should be given to adding will gamble on removal of the sword. Others fear the knife a statin" or some other refinements in medical man-and opt for no incision and remaining awake. Still others agement " while further investigations are performed and have heard of risk to their health from these interventions while the patient is deciding on a preferred strategy of and will not let knowledge of their carotid artery disease treatment." Assuming for a moment that this patient, like interfere with their lives; they are content to pursue medical most others, is content to follow whatever evidence-therapy and clinical monitoring. They may have decided based advice is given to him, I think this is all a waste of that a stroke during surgery or stenting would affect them time and merely places the patient at risk to have the now, whereas the risk of stroke without aggressive inter- stroke for which his TMVL was a warning event. His vention is spaced over the years ahead. original symptom and the severity of his carotid stenosis Patients should be provided with information and the already satisfy the criteria for intervention that have been pros and cons of each alternative. Doctors should convey established by several major randomized trials ( NASCET their own advice and opinion, but ultimately, the patient has ( 29), ACAS ( 32), and ACST ( 34)) comparing CE to best the right to choose. Trial data that average out results may medical management. In my opinion, the patient should not heavily influence some individuals. get on with it. These two eminent physicians- a neurologist spe- patient's welfare. Dr. Caplan, the neurologist, cites the 1995 cializing in stroke and an experienced vascular surgeon- report ( 16) in which follow- up data from the NASCET appear to agree on one fundamental point: that under the study showed that patients with TMVL had a 16.6% 2- year right circumstances, CE or angioplasty/ stenting is indicated risk of ipsilateral hemispheric stroke if they were managed in this typical case of TMVL. They differ in other critical medically. But he does not mention that not one of the aspects. TMVL patients in this study had a major stroke in the Both experts accept the idea that surgical opening follow- up period! When confronted with the evidence from of the ipsilateral cervical carotid artery will improve the the 2001 NASCET report by Benavente et al ( 31) suggesting that this patient would probably not meet criteria for " no other plausible cause" were found, particularly if the definite benefit of CE, Dr. Caplan points out that the study patient had had a recent flurry of TMVL episodes. For does not incorporate the new and improved methods of asymptomatic Hollenhorst plaque, Dr. Caplan would be predicting stroke risk from carotid artery disease. cautious, being " heavily guided by the nature and extent of Dr. Hertzer, the surgeon, acknowledges the better out- the carotid artery lesion" and more inclined to favor come of medically treated TMVL patients with high- grade surgery if " brain imaging disclosed a brain infarct in the carotid stenosis. But to perform this analysis, he believes carotid artery territory." Dr. Hertzer apparently considers that the NASCET cohort was excessively " parsed." As asymptomatic Hollenhorst plaque a perfectly good in-a result, he " would be very uncomfortable using this in- dication for a carotid procedure provided the plaque is new. formation to withhold endarterectomy" The problem: there is usually no way to know if the plaque After agreeing on that fundamental issue, the experts is new. diverge. Given the finding of hemodynamically significant Finally, in choosing between CE and angioplasty/ stent-ipsilateral carotid stenosis, Dr. Caplan does not want to ing, the experts acknowledge that there is not yet enough make a recommendation until he knows more about the information to make a meaningful decision. Both doctors patient's medical risk factors and how they are being suggest enrolling the patient in a randomized trial compar-managed, the nature of the arterial lesion, heart, intracranial ing the two approaches but acknowledge that this choice is circulation, and brain parenchyma. In asking for this infor- often not convenient. Without that option, Dr. Caplan favors mation, he seems to be saying that: 1) he is not utterly angioplasty/ stenting for distal, long smooth, or tandem convinced that the impressive carotid stenosis is the cause plaques, and CE for very focal ulcerated lesions, but he of the TMVL; 2) he wants to fractionate the risk of stroke emphasizes the importance of " the availability, experience, better; and 3) he needs to know if there is room to improve and complication rates of the surgeons and intervention-medical management. Dr. Hertzer, on the other hand, says alists." In providing a comprehensive review of the trials of that if you find convincing carotid stenosis with ultrasound, CE and angioplasty, Dr. Hertzer points out that the risk of stop fussing and get on with the procedure. Only if carotid recurrent stenosis, originally a concern in angioplasty, may echography is equivocal would he extend the work- up. not apply for angioplasty plus stenting. Also, the older data In considering other ophthalmic indications for ca- on the higher peri- operative rate of stroke and other rotid intervention, the debaters also seem to differ. Dr. mortality after angioplasty may be obsolete if brain protec- Caplan approaches a patient with new CRAO exactly as he tive devices are used in the procedure. For this patient, he does a patient with new TMVL. Dr. Hertzer points out that favors CE. data show that CRAO patients are much less likely to have For other opinions on this topic in this issue of the high- grade ipsilateral carotid stenosis than are TMVL pa- journal, see the editorial on page 259 and the viewpoints tients, but he would still recommend a carotid procedure if starting on page 295. 1. Caplan LR. Transient ischemia and brain and ocular infarction. and Technology Assessment Subcommittee of the American In: Albert DM, Jakobiec FA, eds. Principles and Practice Academy of Neurology. Neurology 2004; 62: 1468- 81. of Ophthalmology. Vol 4. Philadelphia: WB Saunders; 1994: 8. Sitzer M, Siebler M, Steinmetz H. Silent emboli and their relation to 2653- 69. clinical symptoms in extracranial carotid artery disease. Cerebro- 2. Wray SH. Visual symptoms ( eye). In: Bogousslavsky J, Caplan LR, vase Dis 1995; 5: 121- 3. eds. Stroke Syndromes. 2nd ed. Cambridge, UK: Cambridge University 9. Droste DW, Dittrich R, Kemeny V, et al. 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