Chapters Transcript Video Updates in Stroke Prevention: What Every PCP Needs to Know Anirudh Sreekrishnan, MD, presents on the diagnostic criteria and etiologies of storke as well as medication management for stroke preventions. It's very a pleasure to be here today. I'm, I'm very excited to talk to you about this topic, stroke prevention. Um, this is something that I do day to day talking to patients about, and I love any opportunity to speak to others about, um, stroke prevention. Um, a little, just a little background about our stroke clinic here at UCSF. Um, this is kind of what we do day in and day out. We have a number of providers that kind of focus on cerebrovascular disease. Our main site is over at 400 Parnassus in San Francisco, but we do have satellite locations in both San Mateo and Mission Bay, and we've been. Rapidly growing our telemedicine outreach in the past couple of years, with about half of our patients being seen virtually these days. So distance is no longer an issue for kind of good secondary prevention. We obviously see and treat patients with an ischemic stroke. We also see hemorrhagic strokes, microbleeds, concerns for cerebral amyloid angiopathy. Various vascular malformations, aneurysms, as well as intracranial disease. Um, and then we very closely work with our cardiology colleagues, um, with patients who have cardiac, um, issues or require, uh, conjunction, um, help with both cardiac and stroke risk, um, and work closely with our neurosurgery, neuro-interventional colleagues, um, for management of things like the. Carotid stenosis, aneurysms, uh, AV fistulas, and other vascular malformations. Um, we've worked to expand our referral process and make availability for patients in the community. That's been a big thing that we've focused on, um, and these days we are able to fit patients in in about a 2 to 3 week time frame, um, for kind of secondary stroke prevention care. Um, there's a lot to talk about in the world of stroke. We'll only be covering a little bit about this today. Um, but, uh, formally, the kind of main things that I'd like to make sure we highlight and review together are kind of our diagnostic criteria and etiologies for stroke, really kind of a focus on what we think about as a high yield workup for diagnostic testing for ischemic stroke patients. Um, really talking about the fundamentals of medication management for both primary and secondary stroke prevention. And then I have a variety of common clinical dilemmas that we deal with in practice for ischemic stroke patients, um, and we can kind of review those together depending on time. I also want to make sure we have time at the end to answer any questions people have. Throughout this talk, I'll be referencing. Um, multiple pivotal landmark clinical trials, um, as well as, uh, kind of class one AHA recommendations. So I'll include the Cigna, um, throughout our presentation today so that you have a sense of where, where some of this guidance is coming from. With all that being said, we have to start with some of the basics. What is a stroke? You know, a stroke is fundamentally a clinical diagnosis, which we defined as a fixed neurological deficit of the central nervous system due to a pathological process of the blood vessels. You know, I tell patients, basically I'm the, I'm a plumber of the brain. I just deal with the issues with plumbing in the brain. The most common question I get from patients alike is what is the difference between a TIA and a stroke? I've been diagnosed with one, but then they've been told I have another. You know, what I tell people is, you know, TIA and stroke kind of fit on a spectrum, a spectrum of time, with the longer time indicating a concern for actual neurological injury to the brain. Um, we now formally use our MRI technology to best sense of having the highest sensitivity, um, for picking up ischemic damage in the brain and use that to formally define when a stroke has occurred. So, you know, TIA traditionally would defined as a transient neurological symptoms that go away completely. However, if on MRI imaging we see evidence of of Actual ischemic damage, then we will still classify that as a stroke. Ultimately, at the end of the day, a clinical diagnosis of a TIA versus a stroke is treated the same way. We treat it the same way in terms of kind of the workup and management of it. We take these events seriously, and everything that we talk about when we think about secondary prevention is the same no matter that, that, uh, diagnosis. You know, uh, taking a hundred-step view, you know, we broadly define strokes as either hemorrhagic or ischemic, with 20% of, uh, strokes being hemorrhagic stroke, where the pathological blood vessel of the, uh, sorry, the pathological process is an injury to the blood vessel resulting in bleeding in the brain, um. We're not going to be spending too much time talking about this today. There are a variety of different etiologies for bleeding in the brain, most commonly hypertension, especially in our older patients. But we also see amyloid angiopathy, especially if there's a concurrent dementia diagnosis. We see bleeds associated with tumors, as well as vascular malformations. The large bulk of what we do see, 80%, are ischemic strokes. Pathologically this can occur in two primary ways. One is a thrombotic process in which plaque builds up in the blood vessel over time, and then there's some form of plaque rupture or a development of plaque. Back to the point where there's a limitation in blood flow causing the ischemic damage. The other is an embolic process where a clot forms either within the blood vessel or from somewhere else in the body, then travels and occludes the blood vessel, blocking blood flow and causing the ischemic damage. Back in the 1990s, we described, uh, different various etiologies of stroke using a toast criteria. Um, I still like talking about this criteria because it highlights the three most common causes of stroke that we see, um, especially in our adult population. The first being small vessel disease, which references the tiniest arteries deep within the artery, um, deep within the brain that get occluded off. Um, these are usually due to a constellation of risk factors, things like hypertension, hyperlipidemia, and diabetes. Large artery atherosclerosis. This is the development of plaque on more larger proximal arteries, including things like the carotid arteries in which plaque will then break off. There will be plaque rupture traveling downstream to cause a stroke. And then cardioembolic, referring to clots that are generated through or via the heart, and then travel to the brain to cause a stroke, with atrial fibrillation being the most common, um, cause in this category, um, for a cardioembolic stroke. Um, and then there are a variety of other etiologies that we see, um, things like dissections. Vasculitities, all sorts of rare, um, infectious presentations of stroke, and then there is a category of cryptogenic stroke, um, about 10% of the strokes we see in which we can't really determine the inherent cause. There might be multiple different reasons why the patient may have had a stroke, or no clearly identifiable reason. Um, you know, the, the ways I like to think about stroke, especially if we're thinking about, um, the workup and kind of management, um, is really trying to understand if the strokes are happening deep within the brain or on the cortical surface. So when we see patients who've had, um, strokes deep within the brain, they tend to have presentations where the strokes are tiny. They're deep within the brain, as you can see from these pictures here. Um, but despite their small size, they can have devastating symptoms because this tends to be the areas in which major fibers pass through. So these patients can present with unilateral weakness, um, a loss of sensation on one side of the body, um, and it's all due to these tiny blood vessels that are occluded deep within the brain. Um, these, these are kind of formally what we call lacunar disease or small vessel disease. Disease and these are most attributable to risk factors like diabetes, hypertension, hyperlipidemia. And so when we think about the workup and management of these patients, it's really through the identification of those risk factors and real risk optimization of those risk factors. These are patients. If we don't get their risk factors well controlled, they're, they're highly likely to represent with other lacunar strokes. And I have some areas of the brain in which we see lacunar injury, including the areas of the internal capsule, areas of the thalamus, or the areas of the brain stem. Conversely, we'll sometimes see these larger territory cortical strokes. They tend to be these wedge-shaped infarcts that happen on the cortical surface of the brain. I have some pictures here of what these patients' MRIs of what these strokes look like. Um, these tend to be due to a more proximal occlusion. So you can imagine a more proximal artery to this area that's occluded by a clot that blocks blood supply to the cortical surface. Um, cortical strokes like these are either due to things like cardioembolism, clot generation from the heart, or due to more proximal artery to artery disease. And so for patients with stroke presentations like this, our focus is really on trying to identify if there is evidence of large artery atherosclerosis through a good examination of both their head and neck vessels, as well as a good cardiac workup to look at their cardiac rhythm, as well as the cardiac squeeze, the valves, and evaluate for signs of atrial fibrillation. So, um, a little bit on the high yield diagnostic workup for an ischemic stroke. Preliminary imaging, um, with, uh, patients who we are concerned of a stroke usually incorporate either a head CT or an MRI, really just to highlight a couple of things. The sensitivity of a head CT, as we're all aware of, is not as sensitive very early on, within the 1st 24 hours. It usually takes Um, uh, either a day or longer for there to actually be, uh, a head CT to be sensitive enough to pick up on a, uh, uh, pick up a stroke. Um, conversely, an MRI is going to be the most sensitive to assess for a stroke. Um, so especially for patients presenting acutely, um, and who are hospitalized, we're usually getting an MRI in order to help with that diagnosis. Um, brain tissue imaging is one thing, but as a vascular neurologist, I, I always care about the vessels, and, you know, broadly, we care about not only the intracranial brain vessels, um, but also the neck vessels. This is commonly an area I see often missed as part of a stroke evaluation, a real good evaluation of the neck vessel. Vessels, specifically the carotid arteries, and the reason we highlight the carotid arteries so much is because when we see evidence of severe disease in the carotid arteries, that is, um, there are secondary considerations in terms of management beyond just medication management, but, but considering potential surgical management for certain cases. You know, I want to spend a moment to think about or just discuss and review the various ways in which we can evaluate neck vessels, um, because this comes up. Um, the most common modalities are going to be a CTA neck, um, which is an iodinated scan, so contrast is injected, gives you a good lumen, uh, a good characterization of the lumen of the blood vessel, as well as the evaluation of any plaque present. Um, in those vessels. Similarly, we can get an MRA of the neck. Um, this is also a contrast scan with gadolinium, can also give good resolution of the lumen, um, and, uh, give good characterization of the carotid bifurcation. Um, uh, with patients who are unable to get contrast or have an allergy to contrast, there are ways of getting a non-contrasted MRA of the neck. This is called a time of flight scan. Um, however, uh, this scan is not as accurate. Um, there can be a lot of artifacts with this imaging, especially, uh, when. It's imaging of the neck, specifically, this artifact is actually due to a person's heartbeat. It creates an artifact that disrupts the flow, so that imaging is obstructed, as you can see here. So in most patients, an MRI time of flight is not a good enough scan to examine the neck vessels. And then there is also a handy dandy. Carotid ultrasound. Um, this is quite useful, especially in the outpatient setting, to get a sense of the baseline of, uh, of, uh, if there is any evidence of carotid disease. Um, obtaining a baseline carotid ultrasound is useful to compare, um, if you're following carotid disease over time. Um, and so this is something I often We'll obtain and, um, get in our outpatient clinic setting, um, as well. Um, though there are, uh, limiting features to, uh, carotid ultrasound, um, compared to the contrasted scans, because we don't get as much characterization of the lumen itself. Um, but a carotid ultrasound is still quite useful if you're following carotid disease over time. I mentioned earlier in patients that were concerned for clot generation in the heart that we perform a standard set of cardiac testing that most commonly involves an echo. Specific things that we think about with an echo are going to be things like the ejection fraction, looking for signs of left atrial dilation, which can be a marker of potentially paroxysmal atrial fibrillation. Um, any sort of valvular dysfunction or vegetation on a valve that can be a predisposing source of an embolus, um, as evidence of a frank ventricular thrombus in the heart, which is a rare, but, uh, a condition we sometimes see. And in young patients without traditional. cardiovascular risk factors. Um, we use an echo as a first-line test to evaluate for a PFO, um, uh, in the heart to see if there are signs of, uh, an intraattrial septal, um, uh, hole that, that could be an explanation for a clot generation. Um, and then in terms of cardiac rhythm monitoring, there are multiple modalities in which we can look at rhythm monitoring. Um, a very common and very low-risk device is a Zopatch. It's very small, so it's Very easy to, um, um, place on the chest. Uh, this is useful, especially in our patients, um, who may have cognitive impairment or have significant disability after their stroke, just given the ease of use. There are mobile cardiac telemetry monitors that tend to be slightly bulkier. However, the advantage of these monitors is that they can be kept up to 30 days, so you can get a much longer monitoring window. And then there implantable loop recorders. These are devices that are implanted with the help of cardiology here at UCSF implanted under the skin that can stay in place up to 3 years performing monitoring and giving a sense of the heart rhythm. In general, when it comes to heart rhythm monitoring, you know, the AHA talks about at least 24 hours of monitoring. However, most providers, um, after a patient has had a stroke, will do a minimum of 2 weeks of monitoring. We do have clinical trials and clinical evidence that longer monitoring. is associated with a higher likelihood of capturing atrial fibrillation. So specifically in our patients in which we are concerned, have a what we call a cardioembolic reason or an embolic reason for their stroke, we will usually advocate for longer monitoring, including thinking about implantable loop recorder. Um, to kind of ensure that we are not missing atrial fibrillation as a cause. Um, the, the, the biggest thing with identification of atrial fibrillation is going to be a fundamental change in our management with anticoagulation. So there is utility in, in being proactive about monitoring in that regard. Um, now let's transition to some of the basic fundamental managements of ischemic stroke. Um, you know, when we think about the fundamental managements of ischemic stroke, um, the good news is stroke prevention, cardiac protection, most of the principles go hand in hand. I tell patients all the time that what's good for the heart is good for the brain. Um, and so a lot of these fundamentals are crossed. Applicable. Um, you know, at the base, we always talk about antithrombotic therapy, um, and then we also think about cholesterol modification, um, blood pressure control, diabetes, as well as lifestyle changes. These are the central tenets, and they've been the central tenets for a long period of time. As it pertains to antiplatelet therapy, you know, aspirin 81 mg is still the mainstay for kind of secondary stroke prevention. So for patients who've had a stroke, this is our usual go to for um patients, um, to help prevent stroke. As it pertains to primary prevention, so preventing a stroke, their first ever stroke, there isn't any clear clinical evidence for an indication for aspirin in the primary prevention setting. And as I'm sure everyone on the call is familiar with, there is now newer evidence suggesting or limiting the widespread use of aspirin. For primary prevention for heart disease. Um, so we aren't routinely starting patients on aspirin for primary prevention of stroke and really are thinking about their overall cardiovascular risk profile as well as using emerging, um, cardiac risk stratification scores to better get a sense if there may be a utility for aspirin in that setting. But as I said, for secondary stroke prevention for patients who have had a stroke, um, you know, we almost routinely will start them on an antiplatelet agent. Um, we have clear clinical evidence that starting a baby aspirin can reduce your risk of a stroke, uh, MI or death by about 13%. A common clinical question that will arise is, what do you do if your patient has had a stroke and is already start, is already taking a baby aspirin? Um, you know, this is kind of a, uh, survey of, uh, of neurologists in the field back in 2021 about what they do in that clinical scenario, and you can just see that, uh, there's a variety of approaches that you, you will see, um, a good number of patients just maintain on aspirin. Uh, there will be some people that will switch over. To Plavix and then others that will choose to place on dual antiplatelet or switch to anticoagulation. So a variety of different approaches. What I always advise people is to think about aspirin or just antiplatelet therapy in general as a seatbelt to prevent, um, for, uh, to prevent a worsening of a car accident. Um, so, you know, when a patient has a stroke, the first question I'm asking myself are kind of what are the driving risk factors that led to the stroke in the first place? Is it the blood pressure? Is it the cholesterol? Is it the diabetes? Is there something else going on at play? And really focusing on that type of risk mitigation and Really just thinking of aspirin or any antiplatelet agent as really just a seatbelt to prevent things from getting worse. Um, you know, the one thing I do caution people against is we do have clinical research that suggests higher doses of aspirin. Aspirin are associated with a higher risk of bleeding. Um, Uh, and we do not have clear clinical evidence that higher doses of aspirin are associated with a lower risk of stroke. So given the risk of bleeding associated with higher risks of higher doses of aspirin without any clear clinical benefit, I do not routinely increase aspirin, um, aspirin dosing. Um, rather, I will usually maintain someone on aspirin or entertain switching over to Plavix based on, um, the patient's preferences. Um, one of the fundamental changes that have occurred as it pertains to secondary stroke prevention is the role and the utility of dual antiplatelet therapy, so aspirin in conjunction with a medication like Plavix, um, after a minor stroke or a TIA. To review Fundamentals of where the utility of dual antiplatelet therapy comes from, you can imagine that for a stroke survivor over time, the risk of a recurrent event is highest early on after the initial stroke and then starts to level off over time. In the field in research, um, we know that aspirin or mono platelet monotherapy is helpful for a risk reduction, um, and we are aware that being on dual antiplatelets or two blood thinners are associated with a higher risk of bleeding than just being on. One blood thinner. And so the question became, is there an optimal protection window early on after an initial stroke to offer additional plate, uh, sorry, offer additional protection with the use of a secondary, um, antiplatelet agent. And this is the question that a lot of landmark trials, um, were focused on back in 20 2013 and then 2018, both in China as well as, um, in the US and multiple countries that were fundamentally looking at the role of dual antiplatelets. Therapy. And this is a complex mechan graph, but really just showing that these trials used a variety of combinations of both aspirin and Plavix for a variety of days after a minor stroke or a TIA. And really the fundamental of these trials and where our guideline approach to using dual antiplatelet therapy landed on is that 21 days was thought to be the most optimal time window for using two antiplatelet agents, most commonly aspirin 81 mg. And Plavix 75 mg. And then after that 21 day period, transitioning to monotherapy, so transitioning to just a baby aspirin after that time point, with the understanding that that was the balancing between the optimal stroke prevention and bleeding risk. Um, these studies back in 2018, um, really looked at minor strokes, so, uh, minor symptoms after a stroke, formerly classified as an NIHSS less than 4 or a TIA. But since then there have been studies looking at the same paradigm with other forms of antiplatelet therapy, including ticagrelor, showing equivalence in the results. There have also been multiple studies in the past couple of years that have expanded the use of dual antiplatelet therapy in a variety of ways. This is the Inspire study from 2024 that is now instead of Looking at acute presentation, so initiation of dual antiplatelet therapy within 24 hours after an event like this, kind of bringing it out to 72 hours. As I mentioned, the highest risk is earliest on for a recurrent event. And the, the real takeaway of these studies is that, you know, even up to 72 hours initiation of these medications is still useful, though the, the overall effect or impact of that is less when it's initiated. Within the 48 to 72 hour window as compared to within 24 hours. So starting these medications early is important, though there is a benefit if you start them up to about 72 hours from the initial event. There have also been newer studies, um, from 2024, um, broader, broadening, sorry, um, expanding, um, the, the overall deficits from the stroke, as I mentioned. Um, dual antiplatelet therapy was traditionally only used for a minor stroke, um, an NIHSS of less than 4. But we have evidence even from a couple of years ago, bringing this up to an NIHSS of 10, so getting into the mode, minor and moderate stroke range. A lot of the decisions about starting dual antiplatelet therapy started in the Acute setting during an ED visit or a hospitalization. So as a PCP in the community setting, you are usually not involved in the actual initiation of dual antiplatelet therapy. However, I think the big takeaway from this research is that a lot of our stroke survivors, a lot more of our stroke survivors are being started on dual antiplatelet therapy after they're hospitalized. and so to have awareness of that. Um, and as I mentioned, really remembering that that time window, that 21 days is the traditional time window in which we're using those, um, dual antiplatelet therapy agents. If I can see one of the most common, if I could say one of the most common things I see in the community is patients are indefinitely placed on. On these agents after a stroke, and no one has gone back to identify that the dual antiplatelet therapy was intended only for that 21 day period. So that transition to monotherapy is an important step, um, and that's where I think we can all work together to making sure we review that when patients follow up for their stroke, post-stroke care. Now transitioning to cholesterol management, you know, high-intensity statins are still the first-line therapy for secondary stroke prevention, and our studies from the early 2000s, um, including SPARCle from 2026, 2006, still target an LDL goal less than 70. This is still the fundamental evidence that we have for this. Um, you know, the one thing when I, when it comes to statin management is really ensuring that we re-review and reevaluate cholesterol levels after, um, a stroke, um, after the initiation of a high-intensity of statin, to ensure that we're actually approaching goal or at goal. And if they're not at goal, really thinking about second-line therapies to get patients. To goal. There are multiple new medications, including PCSK9 inhibitors that are available for patients who struggle to get their cholesterol to goal. And I do think that this is an area that we need to start being more aggressive for, especially when we suspect atherosclerotic disease or cholesterol management is the primary reason the stroke occurred in the first place. There aren't, um, very clear primary prevention guidelines, um, for an LDL goal, though I do say it's always reasonable to consider an LDL goal less than 100 for patients you suspect are higher risk for a stroke, um, through diet, exercise, or considering a statin medication. Uh, one other thing I'd like to highlight is the emerging research regarding GLP-1 medications. This has been an area of focus, um, with our clinic and um an area that we've been looking into. You know, as we are all aware, GLP-1 medications, there's a lot of new research, um, using these medications to help with both obese. Obesity for patients with diabetes, but also obesity with cardiovascular risk factors, with studies being published, including select showing in patients who are obese and have cardiovascular risk factors, initiation of a GLP-1 medication can actually reduce their risk of a cardiovascular event. Um, we do not have clear evidence for improvements in secondary stroke prevention yet. Um, we do have emerging evidence for this area, um, but we do not have a large scale landmark study in the. US yet. Um, though I am starting to talk about patients, talk about these types of therapies in patients who have diabetes and or are obese, um, as I do suspect this is going to be an area that we're going to be paying more attention to in the future. And just to point out that the select study that looked at cardiovascular outcomes, though they did see a smaller percentage of patients, a slightly smaller percentage who had a stroke on this therapy, this wasn't significant. That's not to say that I don't expect to see studies showing potential significance once we target a more high-risk cerebrovascular disease population. Blood pressure management. Um, you know, the AHA recommends, um, for long-term blood pressure management, um, when we think about, um, optimizing, um, patients and reducing risk for both heart disease and stroke, targeting a blood pressure goal of less than 130/70. 80 as tolerated. There aren't any specific medications that have been useful for the management of blood pressure, patient blood pressure for stroke survivors. So really just taking into account a patient's medical comorbidities. A common question I get is, you know, my patient, I've been told, has intracranial atherosclerotic disease, narrowing of blood vessels. Shouldn't we be targeting a higher blood pressure in that setting to help overall perfusion of the brain? Um, this is really talking about this concept of blood pressure dependence, or this idea that there is a difference in terms of Blood pressure and perfusion in the brain and the onset of neurological symptoms. Um, you know, this is something that we do see, um, from time to time, um, in patients. However, you know, one important thing to mention is that even though patients do exhibit signs of intracranial narrowing or intracranial atherosclerotic stenosis, is that Over time, they do end up building collateral blood vessels in the brain. Those collateral blood vessels end up helping overall perfusion in the brain. So even in patients who have, um, intracranial atherosclerotic disease, we still want to target this blood pressure if, if, if it is, um, uh, if it is tolerated. Um, so even if patients may have been previously Symptomatic. If there's been a significant amount of time that has passed since that period of time, then I do think about reintroducing blood pressure medications to help overall target this goal, because uncontrolled high blood pressure over time ends up just being a vicious cycle that ends up contributing to intracranial atherosclerotic disease. So it is important to be cognizant about that risk factor. I also like to highlight that good blood pressure control is not just important for both cardiovascular health, um, as well as stroke prevention, but really thinking about things like dementia or cognitive impairment later in life. And so this is very much a targetable, treatable area that we can advocate for our patients so that they have good functioning, um, uh, uh, cognitive health, uh, in their later years as well. And then, um, we also want to highlight all sorts of lifestyle modifications that are important for good cerebrovascular health. This includes things like diet. Um, I like talking to my patients about the Mediterranean diet, which promotes a variety of fruits and vegetables, a smaller emphasis on red meats, avoiding fried fatty foods, um, and really trying to focus on protein from things like fish or poultry. Um, in terms of exercise, highlighting good moderate intensity cardiovascular exercise, targeting about 30 minutes a day, 5 days a week, you know, with moderate intensity exercise, what I tell patients are activities that keep you moving and keep you sweaty. So, um, activities like hiking, swimming, biking, jogging, using an elliptical, um, these are the activities we want to emphasize and He promote in our patients. And then patients um who've had a stroke, it's really through a team-based approach, both with primary care, cardiology, endocrinology, um, to really help manage their overall risk factors, um, for the betterment of their care. Um, so with that, um, I want to transition to some common clinical scenarios that we may see in the outpatient setting and just ways in which we think about in managing these scenarios. The first patient is a 65-year-old who has your traditional cardiovascular risk factors, and he's seeing you after a transient episode of right-hand weakness. And during your physical exam, you noticed a left carotid bruit, ho ho ho. And so astutely, you want to get vessel imaging, and we, we discussed emphasis on obtaining neck vessel imaging. So we'll get a carotid ultrasound to look at the flow velocities, including the peak systolic velocity and the end diastolic velocity. And then we'll get a CTA to look at the lumen of the blood vessel and look for any signs of plaque or carotid artery disease. And what you can see is that we have these elevated peak systolic velocities, as well as a CTA showing greater than 70 degree stenosis. You see this nice raging plaque right here. And so this is an example of a patient who likely had a TIA secondary to an artery to artery stroke due to symptomatic carotid stenosis. And, you know, um, uh, management, uh, for carotid stenosis is its own evolving field. Um, I have a whole separate hour-long talk on carotid stenosis, and there's actually been even newer evidence in this past year regarding carotid stenosis. Um, however, just to highlight some of the key Impacts as it pertains to our patients who've had a TIA and a stroke, you know, the strongest clinical evidence for intervention beyond medical management is for, um, carotid stenosis greater than 70%. So, um, this is the patient population we want to urgently consider a therapeutic. Interventions for. There are multiple different ways we can surgically intervene, um, both an open carotid endarterectomy, cleaning out the blood vessel, um, as well as a stent. There are newer procedures like a TCAR procedure that involves the placement of a stent with cerebral, uh, control of cerebral perfusion flow. But some of the key hallmarks as we think about the urgency for intervention when you identify this is that, um, uh, recommended times for intervention for symptomatic stenosis greater than 70% are. Within 2 weeks because this is going to be your highest risk period. And so these are patients, um, if they haven't been evaluated in an ED or have been hospitalized for this, want to be urgently evaluated for potential intervention. Um, as it pertains to which type of surgical management is better, stenting or open, you know, there are multiple factors we consider, including the patient's age, medical core morbidities, including cardiac morbidities, as well as the site of the lesion, whether radiation may have been at play for this lesion. And so, Usually these are patients that are discussed in an interdisciplinary setting. At UCSF, we have a joint conference with our neurosurgeons as well as our neurointerventionalists in which we discuss these patients to best determine what type of intervention might be both in the patient's goals of care, but also ultimately the best to help prevent stroke. An interdisciplinary approach in general is, is probably the best for for these patients. And, um, I'll move on to another case. Um, this is a 45-year-old who also has a history of hypercholesterremia, and she has had a recent stroke in her left hemisphere in the setting of proximal intracranial atherosclerotic disease. Um, to give you a sense of what this looks like, when we look at her intracranial vessels, you can see what looks Like part of her vessel just missing, um, but what is a severe narrowing of that vessel, a severe stenosis of that vessel, and as you can see downstream of this vessel on her MRI scan, she's had a stroke in her left hemisphere. And so what we would refer to this as is artery to artery disease or symptomatic intracranial artery disease, um, and the management of this is a somewhat more nuanced. Unlike our carotid artery that we just spoke about in which we're talking about surgical procedures. As it pertains to intracranial arteries, um, medical management is, um, still considered superior to surgical management for these, um, these narrowing, these stenotic blood vessels. Maximum medical management in this case is, um, usually a course of dual antiplatelets, so two antiplatelet agents, and this is a case in which we will extend the window in which we use these antiplatelets from the 21 day, as I was speaking with earlier, to about 90 days in order to maximize their highest risk time period. Um, as I mentioned, we usually do not, um, discuss stenting for these cases. We focus on ensuring that they've been maximally medically managed. Um, so our blood thinners are, are part of that maximum medical management. And then the incorporation of things like statin therapy, working on their other risk factors, um, thinking about their overall, um, lifestyle changes, um, to avoid unnecessary interventions or surgery, and importantly, avoid a stroke. Um, I'm going to start, stop, finish this last case, and then we can transition to some questions. Um, this is a 30-year-old female who had a recent stroke. She has no traditional cardiovascular risk factors. However, she's found to have a PFO. So I mentioned this earlier for our young patients without. Cardiovascular risk factors. We are commonly, um, doing a cardiac ultra, uh, sorry, a cardiac ultrasound with a bubble study to evaluate for a PFO. Um, a PFO is going to be your connection between your venous and arterial circulation, in which a clot can form and then travel from one system into another and cause a stroke. The evaluation of patients with a PFO and consideration of closure of a PFO should be done in an interdisciplinary setting with both experienced cardiologists to understand the, um, PFO closure procedure, um, as well as with neurologists who are experienced and understand, um, uh, uh, how to perform and review a stroke in the young workup and strokes. Affiliated with that. When we consider patients with PFO-related strokes, we use various risk stratification scores. This is the rope score, which really boils down to understanding the patient's age, really targeting younger patients and ensuring they don't have traditional cardiovascular risk factors. This is the patient population in which we suspect most benefits from PFO closure. And then we structural card information from structural cardiology regarding aspects of the PFO itself. Do they have high risk features or low risk features in order to have the best, most thorough evaluation with the patient to ensure they understand the impact of a PFO-related procedure. Um, we have multiple experienced cardiologists who routinely perform these PFO closures using various devices. Um, and we usually discuss these cases in a multidisciplinary approach. And so these are, these are patients that involve both consultation with cardiology and neurology. I'm going to pause there. I'm going to end with one slide briefly regarding referrals to our clinic. We obviously, all we do is see patients at, at our stroke clinic with a history of cerebrovascular disease, and we are more than happy to see your patients. Um, you know, in terms of tips for referral. When referrals come in, we want to ensure that they're associated with an appropriate diagnosis because our referrals go through initial stages of an automated, automated processing to try to get your referral into the most appropriate clinic and the fastest. Ensuring it comes in with an appropriate diagnosis like an ischemic stroke is going to be helpful rather than saying something like numbness or weakness. Um, I also, um, tell providers in the community to consider which clinics may be best suited for consultation. Um, our stroke clinic primarily focuses on stroke prevention, so really understanding why strokes occur and how to prevent them. Um, and, but there are other other specialty clinics here, um, clinics, uh, focused on memory impairment, as well as clinics focused on headache. And so if a patient's had a history of a stroke, but the primary reason for the referral is for headache management or concerns about memory, your referral may be best suited to, um, referring to our other tertiary clinics here at UCSF. Um, and all referrals that come to our stroke clinic, we treat as urgent. We try to schedule as soon as possible, because we understand that this diagnosis is an important one that requires an appointment. This is why we have been working so hard in order to make our clinical clinic available for appointments. Um, so, um, if you want to escalate your request, if you feel like there's a patient that should be seen in a more urgent manner, this would be one where, um, I'd recommend you reaching out to me directly, and I'll include my email at the end. Um, to try to escalate the matter. Um, and remember that if you think you have a patient that has had a TIA or a stroke, um, uh, uh, or you're getting a call about that, it's always best to refer them to an emergency department for an acute evaluation, um, prior to a referral in our, to our clinic. Our clinic is primarily focused on secondary stroke prevention. We are not doing an acute evaluation in our clinic, uh, appointments. Um, I've included our clinic phone number and fax number as well as a website, um, and I'm happy to take questions. Published August 21, 2026 Created by Related Presenters Anirudh Sreekrishnan, MD Neurology • Vascular Neurology View full profile
