Matthew Edwards, MD, professor of Vascular and Endovascular Surgery at Wake Forest School of Medicine, provides an overview of how significant the problem of stroke is, its epidemiology and risk factors, and how carotid disease fits into the development of stroke. He also discusses current evidence-based guidelines for stroke treatment.
DR. MATTHEW S. EDWARDS: Today we're going to talk about carotid disease. But I want to start by really-- we're going to start with a case, but I want to structure the talk around stroke. Because I think that a lot of times when we talk about carotid disease, we lose sight of the fact that the entire reason we're treating these people is to reduce the risk of stroke. And secondarily, as with any vascular disease and all the conditions I treat, trying to reduce the risk of a future heart attack or other adverse cardiovascular event. Because that's what kills these people. So I'm just going to put a quick clinical question up, and I would ask anybody who cares to, to just sort of think about the answer they would give, and see if it changes as we go through this. We usually run this through our fellows and almost none of them get it correct, which is a little bit troubling. But the case we're going to present, just to start with, is a 65-year-old recently retired mechanic, who presents to your office for his Welcome to Medicare physical. And because you're a great doctor and you examine everything, you pick up right carotid bruit, and you send him for a duplex. The duplex shows a complete occlusion of the right internal carotid artery, which is confirmed on a subsequent CTA after you call one of us and ask what to do with it. So which of the following should be a component of this gentleman's management? And the choices are there. Right carotid endarterectomy, right carotid angioplasty and stent, long term anticoagulation with a vitamin K antagonist. We could also say, or a Xa inhibitor. Intensive glucose control with A1c less than 7%, or administration of a statin with the goal to an LDL of less than 100. So just think about that, and I'll be interested to see how many of you have the correct answer, and then how many of you end up changing it after we run through this. So as I alluded to, we're going to start with just an overview and a significance of the problem, mainly around the real topic, which is stroke. And then we're going to shift into talking about how carotid disease fits into the genesis and occurrence of stroke. And then talk about the current guidelines for management, which are already several years old and will need updating soon. So why is this important? It's important because we like to operate on it. No, that's not the case. It's important because stroke is the number one cause of long term disability and loss of independence. And most of us in this room, we look like we're fairly close in age, meaning that our parents are right in the sweet spot for having these strokes and becoming incapacitated by them. And that doesn't just to incapacitate them, it incapacitates you, your sisters, your brothers, and other people who have to take time off from work to get them places to be cared for. And this is a really big deal, both in terms of direct resource consumption for the care of the patient, but also the indirect losses to the economy. It's also the third most common cause of death. And I think that combination makes this certainly a major public health issue, and certainly a major public health issue as this giant bolus of 65 year and older patients, our parents, and the products of all the soldiers coming home from World War II, works their way through their highest risk period. What are the big risk factors for stroke? The number one risk factor is not what I'm talking about today. The number one risk factor is high blood pressure, and we cannot stress that enough. We're going to talk about some guideline parameters for managing blood pressure. And I'll tell you now, and I'll tell you again then that I bet those are antiquated. How many people in here were aware of the recent early stoppage of the Sprint trial? Oh wow, so I actually can tell you something that's actually novel. There was a trial that was-- actually the coordinating center was at Wake Forest. And it was a major trial throughout the United States over 7,000 elderly patients, and elderly defined by age 65 or older, which that gets closer and closer every year. I don't like to call that elderly. But it was just a trial looking at more aggressive management of systolic hypertension to less than 120 millimeters of mercury, versus staying within the old guidelines. And there were dramatic reductions in all calls, cardiovascular death, sudden cardiac death, and a number of other end points so profound that the trial was stopped more than two years early, about six weeks ago. You'll be seeing that. That will be showing up, I'm sure in the New England Journal and/or JAMA within the next month or two. And I imagine that that's going to lead to a major change in the way in which we all try and control patient's blood pressure. And it was all done with generic medications, by the way. The other major risk factors are increasing age, the presence of cardiovascular disease, and especially the presence of rhythm abnormalities, and more specifically atrial fibrillation, cigarette smoking-- the great Satan-- and the presence of carotid stenosis, which is what we're going to mostly talk about today. So if you take all strokes together, roughly 20% of these are caused by hemorrhage. We're not going to talk about that anymore after this slide. And the remainder are caused by ischemia, which is what we are going to talk about. And the image there just shows you a typical MCA distribution ischemic stroke, after it has matured. So because it's a CME event, and we want to give you the whole breadth and make you that much more glad you're out of nursing school or medical school, we'll just run through the anatomy real quick. The way blood gets to the brain is it's ejected from the heart, traverses the aortic arch, and then through a variety of vessels, finds its way to the brain. The major pathways of this would be innominate, which in most of us gives rise to the right common, and the right subclavian, and the right vertebral. And then separate origins of the left common, and left subclavian. And all four of the vessels, the carotid and vertebrals, as we all know interconnect in most people within the head and provide a robust circulation to the brain. So diseases, especially atherosclerosis, affecting these vessels can lead to stroke through a variety of causes. Once the carotid gets to the base of the skull, it traverses the skull, and importantly, it loses its external layers making it very fragile, which is important for those of us who do interventions in this area. And then that gives rise to the middle cerebral, and the anterior cerebral. And this slide just depicts the areas of the brain that can be affected by strokes. You'll see the middle cerebral is the light blue, or Carolina blue. And if you remember the picture the stroke we had, that's exactly where it was on that previous slide. The anterior cerebral more runs right along the division between the two hemispheres, affecting mostly the upper and lower extremity motor-- Upper motor neurons, or the central nervous system. So those are the most commonly affected areas for a stroke there. And this is just a lateral view of us imaging this when we're in the midst of an intervention. So how does vascular disease cause strokes? We all spend our lives talking about blood flow, we all remember that we all talk about ischemia. I've said ischemia, and we all think about coronary events, where it's usually caused by an abrupt plaque rupture and occlusion of the artery. And that is not how the majority of strokes are caused, by extra cranial vascular disease. And this was something that took me years to finally figure out, even though it was there for me to read. I just somehow didn't pick it up. But these strokes are typically cause, especially the carotid strokes, by little pieces of plaque or thrombus flicking off and moving up into the terminal circulation and causing a stroke. Also by small vessel occlusions from people who have remodeling of arteries within the head. But that is how these are caused. It's not usually a direct flow related phenomenon. Of the ischemic strokes, there's a roughly equal distribution of strokes caused by cardiac source embolization-- and the most common cause there would be atrial fibrillation. And you can see on this ECHO that we've pirated from one of our patients, you can see the thrombus sitting within the left atrium. And then a roughly equal distribution, or what we call atherothrombotic, with carotid stenosis being the greatest contributing factor. And that's where we're going to talk about for the remainder of today. So for the atherothrombotic strokes, the major causes of preventable stroke are, number one, carotid disease. And that is the vast majority of these strokes. And then there are these other issues, so-called vertebrobasilar disease, which is very complicated and could be its own two or three hour talk. Watershed events from hypotension, which can have a central cause from the dysrhythmia that I'm sure Dr. Whelan was talking about. In the setting of vascular disease, it can limit flow if the pressure head gets low. And then idiopathic and iatrogenic causes. The anatomy of these plaques is pretty much the same as every atherosclerotic plaque and the remainder of the artery. There's nothing special about the atherosclerosis that affects the carotid. The one point that comes up that I try to stress with the med students and our residents-- and when you call us, you'll hear us talk about how severe is the stenosis as we're trying to figure out what to do with the patient. And you're like, OK they're asking about how severe the stenosis is because they want to know how much flow is restricted. That's actually not the case, as I said, it's not a flow issue in the vast majority of patients. But the flow gets restricted as the plaque gets bulkier. As the plaque gets bulkier, the plaque becomes more unstable and more prone to plaque rupture and acute accumulation of thrombus, which can give you particulate matter for strokes. So we believe-- and there's pretty good data-- that the embolic risk is directly related to the plaque burden, which relates to stenosis, and also to the consistency of the plaque, with heterogeneous plaques with soft cores being the most high risk. This is a picture from a beautiful set of experiments done by Dr. Chris Zarins and Dr. Glagov. And this shows-- in that area where the two arrows are, you can see there's basically an absence of flow in the carotid bulb there. And that area where the friction and the stress is very low because you have recirculation and very little flow, that's where plaque tends to accumulate. And for those of us who do carotid endarterectomy, that's always where you start to endarterectomy because it's easiest to find the correct plane where the plaque's the heaviest. And I just think that's a beautiful graphic demonstration of why it forms there. So of the carotid lesions we treat, the vast majority are atherosclerotic. There are other causes, however, and that would include fibromuscular dysplasia. If you have young patients, particularly women who you know have that, that's something you need to keep an eye out for. You can see this in arteritis, patients with giant cell arteritis and Takayasu's. And you occasionally see it as a result of dissection, either aortic or isolated carotid. And in this area, we see a lot of them from radiation, which is usually a combination of radiation and atherosclerosis. Because the patients were seeing it in are head and neck cancer patients, which are probably the closest analog to my patients because they tend to be so self abusive with alcohol and tobacco. And then you radiate them and that's a perfect mix to create very complex plaques in the carotid. So epidemiologically, the big epidemiologic factors that would predict having a carotid stenosis are mainly advanced age, and the presence of cigarette smoking. And then a mishmash of other typical atherosclerotic risk factors. The most common presentation-- and the vast majority of these you will see in your practice-- are going to be patients who have no symptoms. And this is an area of great controversy now, as we'll come back to. Occasionally you'll find it by finding a bruit on someone, and again, it's an asymptomatic bruit in most cases, like the individual we presented at the start of the talk. Occasionally you'll find these on evaluations for other problems. Somebody gets CT of their head and neck for a bad headache, they give them contrast, you find it. Occasionally people will just get screened because they're going to have major surgeries-- we'll talk about in a minute. But these patients tend to come in asymptomatic. And this is now I think, in the era of people being more savvy about getting patients on statins and antiplatelet therapy, this is probably become the most common mode of presentation to the tune of nine or 10 to one. You can have patients who present with symptomatic disease, and the things that we would consider symptomatic disease from a carotid lesion are really transient ischemic attack, which are symptoms identical to a stroke but that don't last very long, and they resolve. You can have patients who present with amaurosis fugax, which is a single eye blindness. So it's one eye, it's usually the entire eye being blacked out. Or occasionally you'll have patients tell you that they just lose all the visual acuity and it becomes gray. Or it's like a shade of that, half like the shade being pulled halfway down over their eye, or halfway up over their eye. If you ever anybody describes those symptoms, you can call us, we'll see them straight away. Most of the ophthalmology faculty will see them straight away as well. But those would be the biggest symptomatic non-stroke presentations. We also consider patients who have had a completed stroke that did not take out the entire hemisphere as symptomatic. And we endeavor to get those patients treated within two weeks when they present with their symptoms. So what is a TIA. As we said, a TIA is the same symptoms as a stroke. And by that we mean contralateral paresis, or weakness contralateral to the affected carotid artery and hemisphere, contralateral numbness or loss of coordination, and you can have patients who have expressive aphasia. And we see that usually in lesions that are left sided, because speech centers are on the left side in over 99% percent of patients. And in right handers, it's probably almost universal, in left handers it's probably over 90%. Amaurosis, we've already run through what amaurosis entails. And this is just a beautiful picture from Dr. Kurup in our ophthalmology department who sent this to me. This is a retinal photograph of a patient he sent down to see me. You can actually see the plaque sitting within one of the branches of the retinal artery, and those are called Hollenhorst plaques. But it's important to remember that floaters, squiggly lines, blurred vision, double vision, those are not TI-- those are not amaurosis. Amaurosis is a visual field defect, a loss of vision in that area from temporary ischemia of the retina. So how do you diagnose it if you've got a symptomatic patient, or if you have an asymptomatic patient that you're concerned about. I think the test that almost everyone should rely on is duplex ultrasound. Number one because it's cheap, but number two because it's effectively completely safe for the patient, as long as they don't have an event getting to or from the table falling. Because ultrasound, really, does not have any risks that we know of in 2015. There are other tests that can be used, and I would say the most commonly used in 2015 are CT arteriography and MR arteriography. And we'll talk more about those in a bit. The natural history of these lesions largely depends upon the mode in which the patient presents to you. If they're asymptomatic-- the number we all carry around in our head and tell them is drawn from the asymptomatic carotid atherosclerosis study, which tied up in the early '90s. So that data is now 25 years old, and it is probably an overestimation of stroke risk with contemporary medical management. But it is the best data we have right now. And we would estimate that stroke risk is about 2% a year, if you're asymptomatic. The risk does appear to increase with lesion severity, for the reasons we alluded to earlier, as far as lesion severity affecting plaque burden. And lesion progression is common and that-- I should put an asterisk there. Because with the advent of everyone understanding to get patients on statins, there is a lot of undercurrent and institutional data, but not large scale epidemiologic data, that we're seeing a slowing of lesion progression with more and more patients on statin. The symptomatic data again likely represents an over estimation, but I don't think that-- I think that it's still a very significant risk. And every symptomatic patient needs to be seen immediately if they have symptoms. And there we estimate their two year stroke risk at 15% to 30%. We generally tell people, you got roughly 15% annual risk. And most of that risk is font-loaded in the first 60 days after they have their symptomatic event, underscoring why it's so important to get them seen quickly and treated if you can. What is the treatment for carotid disease? For asymptomatic patients and symptomatic patients, the real cornerstone is secondary prevention and medical management. Doing all of the things that we know reduces the risk of stroke, and secondarily the risk of other adverse cardiovascular events. And we're going to talk about each of these categories as we go through. But its management of all the things we know are bad. Manage their high blood pressure, get them off the cigarettes, make sure their diabetes is controlled, manage their lipids, probably get everybody on the statin-- even if they're lipids aren't bad-- and get them on some variety of antiplatlet agent. This is just the title slide. If anybody ever wants this reference, just email me or Meghan and we can get this to you. But we're going to summarize now the basic medical management guidelines put forth by a number of societies, including the American Heart Association and the Society for Vascular Surgery and the Society for Vascular Medicine, and a number of neurologic societies on the way that we should manage these patients with extracranial carotid disease. Most of you are probably familiar with the levels of evidence, and this will be summarized in each of the recommendations that we run through. And basically grade A evidence is stuff that's been supported by a number of large randomized prospective clinical trials. And as you progress through the alphabet, they are less and less rigorous degrees of evidence supporting the recommendation. So as far as imaging, what you'll see here is-- as we discussed previously-- duplex ultrasound is the recommended mode of initial detection if you suspect someone has a carotid stenosis. It is recommended in the evaluation of an asymptomatic carotid bruit. And it is recommended in the surveillance of patients with a significant stenosis over time, and patients who've undergone prior interventions. It is also reasonable to get a carotid duplex in a patient who has a condition that has a strong association with carotid stenosis, including aortic aneurysms, symptomatic peripheral arterial disease, coronary disease, or patients who have two or more of the typical atherosclerotic risk factors. MRA and CTA, we see a lot of patients who are screened with that. That's a very expensive way to get at it, and it's also-- there is some implied risk because you're giving patients contrast agents. And in the case of CTA, using ionized radiation. But if you don't have access to duplex in your community, this is considered to be a reasonable test. I would priority-- you ought to send them to a community that has duplex, it's just a better way to get at it. And when the demonstrated lesions that you find are not severe enough to account for symptoms, echocardiography is recommended to look for cardiac source of embolization. So as far as medical treatment, the major recommendations are summarized here. First is, antihypertensive treatment recommended to keep the pressure under 140 over 90. And I guarantee you, that number is going to come down in the aftermath of the Sprint trial. Patient should be advised to quit smoking, and offered smoking cessation interventions. And these should be offered, and smoking cessation discussed at every visit with any patient with peripheral arterial disease, coronary disease, or carotid disease. Treatment with a statin medication is recommended to reduce their LDL to level below 100 milligrams per deciliter, unless they have an indication to push it to less than 70, and then you need to do that. And that would include patients who have had a stroke, and you all are well aware of the other indications from a cardiac perspective. We all know that the goal management for diabetics now is to get their A1C less than seven, but that has not been proven to reduce the risk of stroke in diabetics. And actually there is some data that getting control too tight can lead to more strokes. Those are likely hypoglycemic strokes, but we don't tend to recommend that people really push the glycemic envelope in these patients for stroke prevention by itself. Antiplatelet therapy is very important in the management of these patients. And aspirin is considered a level A evidence, sort of a class one drug for the antiplatelet administration for these patients. There is no clear indication that an 81 milligram-- or they have 75 milligrams available in Europe-- 81, 325, whatever you want to give the patient, whatever you think they'll take and tolerate. In patients who had an ischemic stroke, antiplatelet therapy with aspirin, alone Clopidogrel alone, or the combination of aspirin plus dipyridamole is recommended, and preferred over the combination of aspirin and Clopidogrel. Antiplatelet medications are preferred rather than oral anticoagulation with vitamin K antagonists, or Xa antagonists, unless there's an indication for those, such as atrial fibrillation. And if aspirin is contraindicated, Clopidogrel or Ticlopidine or Ticlid are reasonable alternatives. Combination aspirin and Clopidogrel is not recommended within the first three months following stroke, even if the patient has another indication for it and it can be avoided. So having run through those medical management guidelines, we're going to run quickly through the most robust investigation of interventional therapies, which was the Crest trail, which tied up three or four years ago. And this was a comparison of carotid endarterectomy and carotid angioplasty and stenting, in the treatment of patients with asymptomatic lesions, 70% or greater and symptomatic lesions 50% or greater. This was a randomized trial, and we can go through this slide real quickly if you'll just trust me that the randomization did its job. And we had a nice even distribution of all the major demographics and co-morbidities between the endarterectomy any angioplasty. And this is just another slide showing these patients had similar prevalence of cardiovascular disease, similar degrees of stenosis, and similar blood pressures. And interestingly, we thought there'd be quite a lag in getting some patients treated with angioplasty and stenting, and there wasn't. We had a nice even distribution of the time of treatment between the two arms as well. The primary endpoint for the trial was any stroke, heart attack, or death within the peri-procedural period plus any ipsilateral stroke in follow up. And between carotid stenting and endarterectomy we had essentially equal occurrences of these, showing absolutely no statistically significant difference. Recommending that these were fairly equivalent therapies considering that endpoint. And this slide just shows the life tables for the occurrence of that endpiont. Subsequent sub-analysis showed that there was no effect detected for symptomatic status or gender in terms of the occurrence of that primary endpoint. But when women were looked at alone, it was clear that they were much more likely to suffer adverse events after carotid artery stent placement, and that's a basic, generalizable truism for any catheter based intervention for women. They tend to not do as well as men after endovascular aneurysm repairs, after endovascular treatment of lower extremity disease, or after endovascular treatment of carotid disease. So this is just something we know. The common wisdom is that it just has to do with the fact that women are smaller than men, and their arteries are smaller. And we all know that smaller arteries don't do as well with endovascular interventions, but that's not all completely clear that that's all there is. There was an interaction suggested for age, and we'll come back to that for a minute. And there was a small short term benefit in the health related quality of life for carotid stenting immediately after the procedure, but this effect was completely gone after one year. So far as the age interaction, there wasn't really an age interaction suggested, as much as there was a clear age interaction that we mitigated early in the trial and so it wasn't conclusive at the end. When the trial started, it was clear that the older patients-- and specifically patients over the age of 80-- were having strokes at a tenfold clip to younger patients when you stented them. And that led to us all receiving an advisory from Bob Hobson, who was the principal investigator, about not enrolling those patients anymore in Crest, because they didn't want them randomized. And that deleted the effect in the ultimate publication, but it was very clear. And the reason for that-- we are relatively sure-- is the fact that as we all get older, our aortic arch changes in its configuration, and it's much more apt to be calcified. And traversing the aortic arch to get into position to put carotid stents in, you're doing a lot of manipulation, rubbing, a lot of catheters and [INAUDIBLE] in that area, and likely given patients lots of strokes. We're probably giving patients more strokes than we realize, and there is research going on about that because the strokes can be bi-hemispheric because you're in the arch. And there's concern that we may actually be exacerbating cognitive decline and a number of other adverse psychiatric and behavioral issues in older patients, who we spent as well. But that data is still relatively immature. When the primary endpoint was pared down to just the peri-procedural components of any death, stroke, or MI within the procedural period, there still was no difference. But when we started to look at just peri-procedural stroke and death-- which is what we used to look at-- some fairly strong differences started to arise and that really weighs on how most people recommend, or what most people recommend to their patients now. As far as the occurrence of stroke, at the time of the intervention and in the immediate post-operative period, carotid endarterectomy appears to be significantly safer than carotid stenting. Probably for the reasons we just discussed, as far as the aortic arch. However, for the occurrence of an MI in the peri-procedural period, stenting appears to be, to roughly the same degree, safer than carotid endarterectomy. I would add that the bulk of the carotid endarterectomies in Crest were done under general anesthesia, which is not represent most practice patterns around the country. There's been a lot of debate about that, but still we factor these into our decisions. Patient with very high cardiac risk, we may favor stenting. Patients who are really good risk candidates, we tend to take them to surgery because they've got a higher risk of stroke with the stent procedure. When we looked at it from a peri-procedural stroke standpoint, the one good thing was the majority of strokes that you were seeing in excess with the carotid stents tended to be minor and major strokes. But that's somewhat of a small consolation, and we'll come back to why that is in just a second. As far as cranial nerve palsies, as one would expect, carotid endarterectomy had a much higher occurrence of cranial nerve palsies, because you're actually cutting into the area where a lot of the cranial nerves traverse the neck. But the good news is the bulk of these resolve on their own within four to six weeks. As far as follow up events, much to our surprise stenting was just as good as endarterectomy at preventing future ipsilateral stroke, which was a very pleasant surprise. Because everyone thought these stents would re-narrow and people would return back to a higher stroke risk, but that has not been the case. Stents in the carotid tend to perform much better in terms of re-stenosis, than stents in the coronaries, and renals, and the femoral arteries. So just to summarize the results of Crest, there was a complete similarity in the primary endpoint, but we believe that was driven by differences in perioperative stroke and heart attack. With stroke being more apt to occur in stent patients, MI being more apt to occur in patients after stenting-- I mean after endarterectomy. Excuse me. That's important both because no one wants to have a stroke or an MI, but also there's been subsequent secondary analysis of those patients showing that there are significant increases in mortality associated with MIs, even though the patients did not notice a long term decrement in their health related quality of life. So those MIs do portend a worst prognosis for those patients in the future. What we don't know is, is that problem with their increased mortality secondary to the small MI they had, or was the MI just indicator that those patients were at higher risk to have subsequent problems? As far as the strokes, those patients noted significant long term changes in the quality of life. No surprise, a stroke really affects one's quality of life. And it was associated with a significant increase in mortality. The bottom line from this is, I think, is everyone just needs to view these two tools as just tools in a toolbox to treat these patients. And as with all medicine, we should try and tailor it around the needs, the desires, and the anticipated outcomes for each individual patient. This is just another one of these slides showing the increase in mortality with the patients with MI for those who would be interested. This slide just shows the quality of life scatter plot showing that patients you had strokes-- if you look at those vertical blue lines-- if your confidence interval spanned those blue lines, you did not have a significant decrement or increase in your health related quality of life. And as you can see for major stroke versus none and minor stroke versus none, there were clear problems with the physical functioning of patients as noted by their own reports on the SF-36. And actually the minor stroke patients noted decrements in their mental functioning, major stroke patients curiously did not. This is just another scatter plot showing where we think stenting is superior, and where we think endarterectomy a superior based on a variety of endpoints. Really the only place you see stenting superior is in not having a heart attack around the time of treatment, and not producing a cranial nerve palsy. And endarterectomy appears to be superior in the prevention of all of the stroke endpoints. This is just a slide that summarizes the advisory that we were all sent in 2004. Unfortunately right before Doctor Hudson died-- he was real gentleman-- telling us to stop enrolling the patients over the age of 80. And I want to bring your attention to the bottom where they put in a couple of other criteria, where they told us to be very circumspect about putting patients in the trial. Age was the number one thing they wanted us to be careful of, but also patients who had extreme tortuosity, which you would define as two or more 90 degree turns, which you can see this individual did. And the presence of severe calcification, which if you look right at the ball, right below that piece oxygen tubing that's laying across the image, you can see the outline of the calcium in that plaque. This individual had that. And in patients with limited cerebral reserves, which we all joke about because we have no idea what in God's name is meant by that. But the sad thing was that picture that you see was one of our Crest enrollees, who was done literally eight days before the advisory came out. And was the only major fatal stroke we had in that trial with a patient. This guy had a huge stroke and he met every single one of these criteria, and I wish we'd gotten that letter eight days earlier. Because this guy, unfortunately, did not do well and now we know better. Restenosis, as we said, remarkably uncommon. Very common in endovascular interventions, remarkably uncommon in endovascular interventions of the carotid. The things they do impart a greater risk of restenosis are female gender, an abnormal lipid panel, the presence of diabetes, and the presence of smoking. And those are all things we-- other than the female gender, we can't change that-- but we can work on everything else with these patients as we go through their secondary prevention. So this is the slide that summarizes the recommendations from that joint professional society paper that I showed you the cover page for earlier. And this says for patients at low or average surgical risk with symptoms within the preceding six months should undergo carotid endarterectomy if their stenosis is a greater than 50% diameter reducing stenosis. And you can anticipate a stroke or death rate less than 6%. That's based on your institutional data. Carotid stent placement is considered to be an acceptable alternative to endarterectomy in symptomatic patients at low or average risk with 50% or greater stenosis, and again, an anticipated stroke and death rate less than 6%. They summarize that it is reasonable to perform a carotid in asymptomatic patients with stenosis exceeding 70% if you can keep your risk there. I will tell you that I think this is going to be a moving target. In most of Western Europe people were not operating on asymptomatic carotids anymore, based on some European trial data that we've not yet accepted in the US, for reasons that are unclear to me. But we are re-initiating a study called Crest 2 looking at medical therapy verses endarterctomy and medical therapy versus stents. And it will not surprise me if we come to the conclusion that we shouldn't be treating any asymptomatic patients, or if we are treating them we're going to narrow the range a little bit more. They also summarized as we discussed, that it's reasonable to choose endarterectomy over stenting in patients who are of advanced age. And it's reasonable to choose carotid stenting over endarterectomy in patients with unfavorable arterial pathology or anatomy. And what we mean by that are patients who have things like radiated necks and tracheostomies, very high lesions up, where you'd have to dividers-- or dislocate the jaw to get to it. And that really summarizes, I think, the practice for all people who operate in this area around the country right now. When revascularization is indicated for TIA or stroke and there's not contraindications, the current recommendation is to try and get to these patients within two weeks. And I would just like to stress to everyone here who may be a hospitalist, a neurologist, or a general practitioner who sees patients who may have had a completed stroke, or may see patients who have TIA to understand this is something we want to get treated urgently. If you ever have a problem, you should be able to get the patient seen by our group, if you want to send them to us within 24 hours with this diagnosis. If you have any problem with that call Meghan or me, because we have open spots everyday held for patients with symptomatic carotid disease or any other thing that a practitioner would want seen urgently. We will see these patients same day as well, if the patient can get there before the clinic closes. In symptomatic or asymptomatic patients at high risk for complications, the effectiveness of revascularization versus medical therapy is not well established. And again I can't stress this enough. I got a recent call from a very well meaning surgeon out at the coast, wanting me to take an 87-year-old gentleman and put him under circ arrest to do is carotid because he-- that was the only vessel he had feeding his brain and he was completely asymptomatic. I do think that we overestimate the risk of stroke in these asymptomatic lesions. And if a patient has a lot of the risk factors, we probably need to really rein the horses in on doing stuff to these people, because we can hurt them. Carotid revascularization is not recommended for patients with chronic total occlusions of the targeted carotid artery. We may have talked about someone like that earlier. And carotid revascularization is not recommended for patients with severe disability caused by their stroke that precludes preservation of usual function. So going back to this question, does anybody want to raise your hand and tell me what you think the answer would be after we've run through this? Yes ma'am. Which one? It's actually the statin. Because in the chronic total occlusion, we think we can hurt these patients worse. And a lot of our residents want to do an endarterectomy on this person. But as we said, for these patients with asymptomatic carotid lesions, no anticoagulation with warfarin. We don't know about the high intensity glucose management. This patient has a chronic total occlusion, so you don't want to intervene on it. That rules out A and B and that leaves us with the statins. And if you got it wrong, don't feel bad. Most of our trainees get it wrong too.
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