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Latest Evidence-base on Secondary Stroke Prevention Practices

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Description

This program is supported by an independent education grant from Bayer. This online education program has been designed solely for healthcare professionals in the USA. The content is not available for healthcare professionals in any other country.

This free, accredited, on demand teaching session presented by expert Professor Andrew Demchuk explores the latest evidence, trials and results relating to secondary prevention of stroke, including new insights on Factor XIa inhibition.

Accreditation: 0.5 AMA PRA Category 1 Credits™

Session Highlights:

  • Why Etiology Matters: Gain insights into the limitations of traditional antithrombotic treatments, including major bleeding risks, and also examine the latest evidence on the role of Factor XIa inhibition in this context.
  • Understanding the Global Stroke Burden: Explore the global and local impact of stroke on public health and healthcare systems. Discover the critical role of multidisciplinary teams (MDT) in reducing this burden and improving patient outcomes through coordinated, evidence-based approaches.

Presented by:

Professor Andrew Demchuk

Dr. Andrew Demchuk is a Professor in Clinical Neurosciences at the University of Calgary’s Cumming School of Medicine and a stroke neurologist with Alberta Health Services. He directs the Calgary Stroke Program and specializes in stroke research, particularly in vascular imaging to optimize patient selection for new treatments. Dr. Demchuk earned his medical degree from the University of Saskatchewan and completed a fellowship in cerebrovascular disease at the University of Texas-Houston. He has served on numerous stroke-related committees and received several prestigious awards.

Who is this course for

This online education program has been designed solely for healthcare professionals in the USA. The course provides continuing education for:

✅ Neurologists

✅ Critical care physicians

✅ Primary Care Physicians

✅ Nurses & Nurse Practitioners

✅ Pharmacists

✅ Other Health Professionals

Continuing Education Information

This continuing education activity is provided by AffinityCE and MedAll. This activity provides continuing education credit for physicians. A statement of participation is available to other attendees.

Faculty

Professor Andrew Demchuk

Disclosures

Andrew Demchuk

CME lectures for Bayer Pharmaceuticals, NovoNordisk & Astra Zeneca. Advisory board for Boehringer-Ingelheim/Roche, HLS Therapeutics/Pfizer & Servier. Research funding from Bayer Pharmaceuticals.

Intends to discuss non-FDA uses of drug products and/or devices and their unlabeled indications. This discussion relates to Factor XIa Inhibition in relation to stroke and will be disclosed to the audience when this discussion takes place.

AffinityCE staff, MedAll staff, as well as planners and reviewers, have no relevant financial relationships with ineligible companies to disclose.

Mitigation of Relevant Financial Relationships

AffinityCE adheres to the ACCME’s Standards for Integrity and Independence in Accredited Continuing Education. Any individuals in a position to control the content of a CME activity, including faculty, planners, reviewers, or others, are required to disclose all relevant financial relationships with ineligible companies. Relevant financial relationships were mitigated by the peer review of content by non-conflicted reviewers prior to the commencement of the program.

Activity Accreditation for Health Professions

UAN: 0829-9999-24-446-H01-P

Physicians

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and Medall. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring activity for a maximum of 0.5 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Physician Assistants

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring activity for a maximum of 0.5 AMA PRA Category 1 Credits™. Physician assistants should claim only the credit commensurate with the extent of their participation in the activity.

Nurse Practitioners

This activity has been planned and implemented in accordance with the accreditation requirements and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of AffinityCE and MedAll. AffinityCE is accredited by the ACCME to provide continuing medical education for physicians.

AffinityCE designates this enduring activity for a maximum of 0.5 AMA PRA Category 1 Credits™. Nurse practitioners should claim only the credit commensurate with the extent of their participation in the activity.

Nurses

Continuing Nursing Education is provided for this program through the joint providership between MedAll and AffinityCE. AffinityCE is accredited as a provider of nursing continuing professional development by the American Nurses Credentialing Center’s Commission on Accreditation (ANCC). This enduring activity provides a maximum of 0.5 hours of continuing nursing education credit.

Criteria for Claiming CNE Credit: Participants must have registered and attended the entire program. Attendance is monitored online for participation in the entire activity.

Other Professionals

All other health care professionals completing this continuing education activity will be issued a statement of participation indicating the number of hours of continuing education credit. This may be used for professional education CE credit. Please consult your accrediting organization or licensing board for their acceptance of this CE activity.

Participation Costs

There is no cost to participate in this program.

CME Inquiries

For all CME policy-related inquiries, please contact us at ce@affinityced.com.

Learning objectives

Why Etiology Matters: Incorporate the latest evidence-base on secondary prevention practices into the management of stroke patients

  • Review tailored investigations on secondary stroke prevention, including the role of novel agents.
  • Identify challenges to implementing optimal secondary prevention strategies, including hemorrhage risk, adherence and follow-up care.
  • Develop evidence-based approaches to address these challenges and improve patient outcomes.

Quantify and articulate the global and local burden of stroke, emphasizing the importance of multidisciplinary teams (MDT) in managing this burden effectively.

  • Analyze the epidemiological trends of stroke to understand its impact on public health and the critical role of MDT in addressing this challenge.
  • Evaluate the economic and societal burden of stroke, and discuss how coordinated efforts by MDT can lead to more efficient use of resources and better patient outcomes.

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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Thank you very much. Uh, it's a pleasure to be here today and, and talk on this important topic. Yeah, I'm, uh, hoping to provide you with a bit of a strategy on how we work through, uh, our secondary prevention management. Uh, it's become much more, uh, complex and, uh, requires, uh, some, um, what I would call a multistep approach to investigations to really sort through. So, uh, let's get started. So these are my responsibilities, conflicts and disclosures. I have received honorary in the past for some secondary stroke prevention therapies. Uh, I'll start by just quickly, uh, discussing a stroke burden and cost. Um, obviously, uh, stroke is a serious problem. Uh, it's estimated that somewhere between seven and 13 million new stroke patients, uh, uh, uh, occur per year globally. Uh, this number is expected to double over the next 20 years with our aging demographic. The cost of stroke is substantial. The average cost being roughly $50,000 but this is of course much higher in severely disabled stroke patients with institutional costs and often doesn't account for lost wages and taxes that affect us economically. Uh, when someone suffers a stroke when we think about stroke care, uh we, we have to think on a continuum. Uh uh obviously primary prevention is important. This is done largely by general practitioners, uh far better to prevent the first stroke than to treat, to have to face it and, and deal with it. So, obviously, BP control, uh, diabetes, uh care, uh uh cholesterol lowering, et cetera, all important elements to that uh primary prevention. Uh Then of course, if a stroke does occur, there's a process uh uh that uh we go through in terms of uh evaluating and treating patients, there's a period of hospital admission. Uh the patients have significant deficits and then there's the rehabilitation and reintegration. Uh patients then come back to us uh for secondary prevention to prevent the recurrent stroke. Um for me, uh recurrent stroke, um risk is a serious matter. I'm always disappointed when my patients recur. I feel that, you know, um there's lots we can do to try to prevent recurrence. Obviously, it can still happen. But uh um and then this is really where getting the etiology correct and trying to optimize risk factor. Um uh ri risk factor control is so important but a 5% overall risk of recurrence at one year with about a 15% recurrence at 10 years. So, uh fairly common problem, stroke prevention clinics are a key facet to how we optimize stroke prevention. This is a multidisciplinary team, including nurses, stroke physicians uh therapists and pharmacy in some circumstances. Um One of the major things secondary stroke prevention clinics um do is triage and evaluate spells uh that in some cases are ti a s or minor strokes. And we try to do, we try to assess these patients on an urgent basis when they're high risk in some circumstances will involve uh the rehabilitation team. If the, if uh in the minor stroke patient seen in clinic, who happens to have a significant uh uh disabling element in, in their uh physical deficit uh that may warrant some therapy. Um So this is kind of the approach we call a minor stroke tia minor cerebrovascular syndrome. And there's a triaging element that occurs in these patients uh where we do a risk assessment. Uh when we hear about these uh events and if they're deemed lower intermediate risk, we'll, we'll refer them to the clinic and be seen within days or weeks if they're deemed high risk based on certain clinical features uh or have persistent deficits. We, we usually recommend that be sent to the emergency room for an initial assessment and then vascular imaging is performed in the Canadian context. Uh We um usually we'll send a patient home if the CTA is negative with an outpatient workup in our uh ti rapid assessment clinic. If the ti is significantly abnormal, we'll often admit the patient as there's a certain additional workup and uh different strategies uh in that regard. Um the CD negative group uh uh is important from the perspective of uh of the, the ti Rapid Assessment clinic, we call Tia A uh where we've actually uh adopted a strategy where we can we have uh certain MRI slots in our hospital uh daily. So that when you see these patients in the clinic uh with negative CT S, we can arrange a fast MRI protocol which is diffusion flare in SW I uh which will help detect the the stroke and the pattern of infarction, which will help us with understanding etiology. We'll often follow up also with uh urgent uh cardiac investigations like echo and holter in terms of the initial management of of ischemic strokes and the mild cerebrovascular syndrome space. So these are mild strokes and tias. Uh there's now evidence for dual antiplatelet therapy in the form of aspirin and clopidogrel. Uh The best evidence appears to suggest based on multiple trials of uh at least a 3 to 4 week course of therapy followed by long term aspirin. Uh This is uh further um uh evolved uh in uh based on the recent chance two trial, which looked specifically in a Chinese population of patients who have loss of function uh for an important uh metabolic uh enzymes in the uh liver that are important to convert the prodrug of clopidogrel to the active metabolite. So if you don't have those uh those key enzymes, you're not able to uh actually have active clopidogrel and therefore, the effect is lessened. And in that scenario, with that loss of function, uh aspirin tag was superior. And so this is uh open the door to that combination therapy in some settings. Uh It's important to know that particularly in South Asians and East Asians, there's a very high incidence of a loss of allele function uh and risk of claver resistance, three-month followup, post stroke admission is another important element in the care of patients. It's uh after patients are discharged, either home or to rehabilitation, we we will reach back at the three-month mark to reassess the patient, get a sense of the disability and look at uh uh uh anything else we can do both from a risk factor modification perspective, but also to dot the I's and cross the Ts around uh the work up of the patients to ensure we've looked far and wide uh to determine the etiology of that ischemic stroke. So those are the overall key features of the stroke prevention clinic for us. So if we now move on to sort of long term stroke prevention management, it's really about getting the etiology correct through a thorough what I would call multistep workup. Uh and a careful interpretation of such workup with a tailored management approach based on that etiology of both drugs and even procedures. So this is kind of how uh I break it down. I've put in read here what I uh what are the various investigations that can be performed uh in this setting? Um uh in particular, um we start with uh what is the CTA of the head and neck that we perform acutely in all our patients? This has implications for both acute management such as thrombolysis and, and particularly with thrombectomy, large vessel occlusion detection for instance, but also it helps with etiology. Uh And so the, the two major classes or causes the large groups are the arteriopathy and the large artra patients that are picked up quite well by act angiogram. There, there are several different arteriopathy, dissections, fibromuscular dysplasia, webs, moyamoya or C vs. And then for large arteries disease, obviously, we're looking at any uh outro throughout the vasculature from the arch to the vertex. Um So obviously, the most common location that's certainly well known in the literature to look for is uh carotid stenosis in the neck. And we know that with uh uh for sure, 70% stenosis and in some cases, even 50% stenosis patients will benefit from early revascularization. Uh if they have a symptomatic carotid stenosis. So, getting making that detection early in our setting, we do it right in the emergency room allows for an expedited uh plan and uh subsequent uh carotid revascularization procedure when appropriate. But there are other locations that we see around this uh such as, you know, bows or stenosis, MCA stenosis, uh siphon stenosis, um carotid uh common carotid origin or origin stenosis or arch disease that uh can uh can play a AAA significant role in terms of cost. So the CTA offers a very good look at the entire vasculature and I think is far superior to performing. For example, a car Doppler study which is gonna be focused only on a small region of the neck uh to evaluate things. Why does this become important from tailoring therapy? Well, we have the growing literature now, particularly around cholesterol lowering. This is the recent uh target trial, um stroke stroke to target trial that doctor Aino and colleagues performed focusing in on the patients who had atherosclerotic related stroke or a history of coronary disease and stroke. They uh targeted a lower LDL range of 1.8 millimoles per liter or that's around 70 mg per deciliter um versus the sort of more standard 100 deciliters. Uh the um deciliters per or um and or a millimoles per liter of about 2.4. And uh when they went to this lower target, uh um they were able to show a statistically significant reduction in ischemic stroke events. And so this has led to pretty much practice changes uh and recommendations uh across multiple guidelines to target an LDL below 1.8 especially in patients with atherosclerotic related uh uh ischemic stroke. Uh We, we are um anxiously awaiting the results of uh two major studies of add on therapy factor 11 inhibitor add on therapy to antiplatelets that will include a, a large population of a large r afroc stroke patients. The idea here is that uh these drugs work on the intrinsic path path pathway to prevent thrombosis, but don't impact hemostasis and therefore the, the safety profile is quite positive. So, uh perhaps ideal drugs to test is add on therapies. We'll see. Um, but I think uh encouraging, uh um, to know uh that, uh we'll, we'll have more data uh therapeutically in in this area, moving on to uh postadmission investigations. The uh the fast uh MRI is, is to us a very important part of the decision making process. And again, we're looking at the presence and pattern of infarcts uh and trying to get an idea based on that pattern, what the underlying etiology is, right. And, and so if we look at the large artery aro patients, they typically have multiple diffusion hits in one vascular territory in the carotid territory, MCA or sometimes MC and AC A and usually it's small and scattered in that setting for small vessel disease. Uh However, the pattern of course is different. It is a deep lacunar infarction usually less than two centimeters in maximum diameter due to an art uh a small artery or arterial occlusion. Uh from this small vessel disease. We have some evidence from the SPS three trial suggesting that lowering BP to a lower target below 130 millimoles per liter. Uh M millimoles per uh mmhg S uh that uh the patients will do uh uh better um in uh the lower target range, um particularly preventing intracerebral hemorrhages. Interestingly enough, the ischemic stroke prevention is borderline. Uh and overall all stroke was borderline in this uh in this data. But uh there's a general feeling we should pushing BP to a lower target in this setting. Diabetes. Uh Type two, of course, is also very strongly linked to a small vessel disease, uh etiology of stroke. Uh And uh we now have uh growing literature with uh uh agents such such as second line agents like the GLP one receptor agonists demonstrating an effect on preventing stroke. And so the general recommendation now is to, to move to work considering G LP ones uh um um uh in a second line setting and this would make the most sense uh particularly in small vessel stroke. But also I think arguably in large artery out for patients which can be due to diabetes as well, cardio embolic mechanisms of stroke. Uh Again, the pattern there uh in in some cases is gonna be multi territory, bilateral, suggesting proximal source. Uh um And um uh other tests include the halter monitor. Uh which of course is there to d to detect uh atrial fibrillation primarily. And of course, the therapy there is do ax uh we know from uh uh the last 10 years, there's been a AAA shift fairly aggressively to Dox over Warfarin in this setting, largely driven from the data and atrial fibrillation trials. Uh where you can see the uh the, the, the, the, the, the blue solid line there, which is the Warfarin line falling quite rapidly and being replaced by the uh dash line, which is the Dox. Uh Obviously the DOAC we're talking about are doin Roman, Epix and dabigatran and they work of course, at different levels of the coagulation cascade. Uh Overall, there's a trend toward less stroke and systemic embolism in afib patients with these drugs. And importantly, uh uh a clear reduction in intracranial bleeding overall, although that's offset at least in part by a numerical or slight increase in gastrointestinal bleeding uh in the setting of patients who require stenting either coronary or even carotid stenting. Uh in the setting of atrial fibrillation, we now have evidence for combining Doac with clopidogrel. And this is based on the Augustus trial showing the uh a clear uh uh uh advantage uh of uh these are all patients where all these groups were taking clopidogrel and then either a Apixaban um or Vitamin K was added and either placebo or aspirin was added. Well, the group that did the best was the Apixaban group and the placebo group, meaning that aspirin was not necessary and Apixaban was superior to Warfarin. So, Apixaban clopidogrel is generally the preferred approach. Um in most cases to these patients, rheumatic atrial fibrillation. Um um uh uh is also uh another condition. Uh Warfarin is generally recommended in this setting. And this was based on a randomized trial comparing Rivaroxaban to Warfarin in this setting. Um So, uh we do still have a role for, for warfarin in, in, in, in such a situation. Transthoracic echocardiography is another test we tend to do on day two. Again, we're looking there for things like an LV thrombus major wall motion abnormalities. Um uh There's still some controversy as what uh as to what the best therapy is in this setting. Um But um um it does at least suggest so far in uh uh some of the Rando early randomized data that, that uh the DOAC are uh at least a safe and may be more efficacious uh than warfarin in this setting. So, my personal practice, I, I'm comfortable using do AX in the setting of an LV. Thrombus and stroke, transesophageal echo does have its place in some settings. Usually. Um ideally transesophageal echo really looks well at the valves and sometimes uh can identify masses. Uh And so, uh you know, it's important if you're, if you've got somebody uh who you're worried about with a mechanical valve or, or could have a, a mass or infective endocarditis. And that's really where te comes in in terms of helping to better identify the underlying problem. And of course, the management there is quite different and unique cancer thrombosis syndrome is something I think that's completely underappreciated in the field. Uh very good literature on this. Now, this is the so called three territory classic pattern of cancer, multiple hits in multiple territories, usually small and scattered. Um The DDIMER is a critical second test. Uh This is our review in International Journal of stroke where we workout, which show basically uh how D dimer uh should be. Uh uh uh you looked at uh you know, low normal D dimer levels and mildly abnormal D dier levels are very nonspecific and not helpful. However, when D dimer levels, you know, are, are above two or three or five, they're very helpful in terms of uh differentiating a very small group of patients. The only things that can cause D levels above three are aortic syndromes, active cancer D IC, uh and venous thromboembolism essentially. And so, um it's a matter of then just working out which of these, it could be if you've got small multi territory, uh scattered infarcts and UD dimer above three, there's a high likelihood that a cancer coagulopathy is responsible for uh your patient's uh stroke. And we also know now that uh these patients are at a very high risk of recurrence, the highest risk of recurrence of really any of the, the allergies of stroke. This can be as high as 40% at 30 days if the patients have a high D dier and multi territory infarcts, Doac um and lo heparin um both uh are potential options in this setting. There remains some debate as to which to use in which setting. And I think that will be soon sorted out in uh in randomized clinical trials. Uh certainly some concern for Doac particularly in the setting of an, of an unresected GI or GU cancer where the risk of bleeding is higher and where usually no me heparin is preferred. But I think this remains controversial as to which therapy is more appropriate in this setting. P fo related uh ideology of stroke is another important uh ll um uh ideology and I think deserves its own attention. And this is best detected actually with a TCD bubble study. Uh transthoracic echo is being used in most places, but in fact, um uh is actually an inferior task to detect right to left shunt. The reason why we look for PF OS is that we now have very clear evidence for P FO closure under age 60. The bubble study is very good at uh detecting things. We're, we're dealing with a very straightforward uh s situation, not a grainy image. Uh And we can inject bubbles in the arm and um we'll immediately see uh significant microbubble signals on the TCD. This is the five point grading system that's used in a head to head study. Uh The yield uh was three times higher for a large shunt uh using uh in this case, robotic assisted TCD uh versus transthoracic echo. And this is a very consistent literature that uh that uh uh TT TCD bubble studies, far outperform transthoracic echo and the detection of a right to left shunt and particularly the all important large right to left shunt. Similarly, it has some advantages over te uh sometimes TE is very difficult to, to detect right to left shunt when patients are quite sedated and when they have a tube down, their ability to sava is compromised. So, um uh transthoracic uh TCD has some advantages in that setting. The last group uh falls into what we call the uncertain or embolic stroke of uncertain source population. And this is uh the trials uh for um embolic stroke of uncertain sort have been disappointing for anticoagulation. So the current practice is still aspirin as a default. But that's not to say we can, you know, we stopped there. I will often take uh patients to those last stages of work up when they're in a stroke, considering a cardiac MRI in some settings, hemophilia screening and uh prolonged ecg monitoring. I only do these additional tests when I haven't identified a clear cause from some of the previous multistep investigations I've already done. So this is really at a later stage of investigation several days in hospitalization or in some cases even after discharge. Uh um um cardiac MRI is particularly useful uh in picking up an apical thrombus in patients with an a apical wall motion abnormality. So if you see some sort of apical wall motion abnormality on your echo. Then that's a very important clue to consider uh a cardiac MRI study as uh the de detection of an al thrombus would of course change management. The role of long term monitoring for AFIB is, is a challenging one. certainly in a Canadian context. Uh If you look at the randomized trials of implantable loop recorders, um their overall stroke prevention effect is about 1% absolute reduction and that's nonsignificant. Um So, and, and so you, you have a number needed to screen of around 100. So if your implantable loop recording technology is expensive, this, you know, really uh results in a very large cost per stroke saved. So you really have to consider it in the context of your health system. I do think that there are uh going to be solutions particularly around smartwatches, et cetera that are going to be more cost effective, you know, screen 100 to screen screen 100 to identify one isn't bad if the cost of that screening isn't high. So I think our it really behooves us to identify ways to screen for atrial fibrillation in a in a less expensive um uh way uh the current phase three trials of the factor inhibitors are including these ESIs patients where uh aspirin remains the standard of care. And the hope is that maybe in addition of an anticoagulant plus an antiplatelet might be the best uh approach to ESIs uh uh ESIs population. We'll, we'll soon find out in the next uh about the next two years. So I'm gonna end off quickly with a case. Um uh Just to put things into perspective. Uh This is a, a patient, this is actually a published case uh uh of a 54 year old male. Um oh was first seen back in 2006 in our institution has slumped over uh on their sofa with a left hemiparesis. Uh And exam revealed a moderate left hemi pleach and sensory loss. Um The um the, the CTA was performed here. There was some sort of vague area of big out poaching in the carotid that we didn't really appreciate at that time in 2006 is significant. Uh The patient had an M one occlusion. Uh This was a patient who was treated pretty aggressively at a time where we didn't have evidence, in fact, for uh thrombectomy yet. Uh and uh did achieve a, a good outcome. Fortunately, we're able to apply some at the time. Uh uh um limited therapies. Uh patient did quite well. Investigations otherwise were unremarkable. The patient was placed on du platelet therapy for three months. Uh and then long term aspirin and, and simvastatin. I think we interpreted that out poaching as atherosclerotic at the time, the patient then returned seven years later, having stopped their aspirin for a few days due to an excision. Uh uh uh of the left ear uh uh for a little basal cell carcinoma. Um And then a day before presenting presentation, we started the Aspirin. So it just really gotten back on it, presented with a mild deficit at that time, but also had a, a large vessel occlusion. Uh This out poaching was a little more prominent actually than uh before. Uh And I think uh better appreciated this time. Uh He presented a bit late and was quite mild. So we treated him conservatively put him on duo therapy. Uh And um um watched him, uh I think we, he, he was getting a bit of rehab and uh um essentially uh repeated the vascular imaging and much to our surprise, the out poaching had changed in its appearance uh which we interpreted as some thrombus formation behind the pouch. Um And we're very concerned about this uh morphological change in a short period of time while on doing on platelet therapy. Um So, uh uh at that time, um we um began to sort of appreciate this condition of carotid web, uh which is a one, a form of arteriopathy detected quite well on CTA. Uh we switched the patient over to IV Heparin uh thinking that it's probably a slow flow situation, of course, that's not an evidence base of the decision, but we felt that the patient was failing to any platelet therapy. Uh We then went on and actually uh performed enterectomy. Uh which would be a controversial sort of management decision with the fact that we thought that this man had had actually suffered two strokes related to his web. Uh And the pathology uh clearly shows this uh in intimal variant FMD uh and not atherosclerosis uh since uh this has been removed. Um He's had no recurrent events now for 11 years. So that's certainly somewhat reassuring and uh um we continue to follow him closely with no recurrence of uh his web. Um uh TCD was performed on two separate occasions during the, the um uh the management of this patient. Um uh um And uh but no emboli were seen. So, um and he did have repeat cta imaging at day 10 which showed a complete resolution of the thrombus and IV Heparin. So, you know, in this particular case, the, the heparin seemed to, to help the anti actually occur on day 12. But of course, we really don't have randomized evidence uh for what the best management of webs are. There's certainly a, a growing literature to suggest that revascularization is an important option. And hopefully someday we see a small randomized trial to confirm that so that uh we can further raise awareness about carotid webs and uh their importance as an etiology of stroke as an arteriopathy. So, in summary, uh stroke burden is rising, uh the cost of stroke is high uh and will get higher in a setting in a, in a in a world where, uh, we're having a great difficulty, uh, reining in healthcare costs with, uh, and, uh, whether they're not keeping, uh, that they're exceeding the growth in our GDP. Uh, stroke prevention clinics are important, uh, particularly in minor stroke and ti triage investigations as well as poststroke. Follow up. The long term ster secondary prevention management really is about getting the etiology correct through a multistep workup. Sometimes patients have more than one etiology. So you end up having to treat two, which is uh it generally uh a fine option, large artery ather has the additional consideration of a lower LDL target small vessel disease. Do think about uh diabetes control. Uh in addition to hypertension control, cardiac uh sources, um the the management can be source specific. Uh So tests like uh uh trans vasic echo culture, transesophageal echo uh are all important to uh sort that out. Cancer is your classic multi territory, small scattered emboli stroke with a high D dimer or doac or with heparin. Are are the appropriate options. TCD. Bubble studies are much better for detecting right to left shunt than transthoracic echo. So if you have the capability of a TCD service in your area, do consider this test is a stroke. Uh you know, is really where we get into some of the more advanced investigations like cardiac MRI and prolonged AFIB monitoring factor. 11 inhibitors uh are are currently in add-on therapy trials with results. Uh pending and likely available in an 18 month to three year time frame. And then don't forget the unusual causes like carotids which can be detected uh fairly easily on CTA. And may I think we're gonna get more data around this and, and the likely uh um uh potential of uh revascularizing these webs removing them essentially to remove the stagnant flow, um any currents that occur behind them. So I will stop there. and uh thank you for your attention.