On Episode 13 of the Stroke Alert Podcast, host Dr. Negar Asdaghi highlights two articles from the February 2022 issue of Stroke: “Cannabis Use and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage” and “Infertility, Miscarriage, Stillbirth, and the Risk of Stroke Among Women: A Systematic Review and Meta-Analysis.” She also interviews Dr. Pierre Amarenco about his article “Intracranial Hemorrhage in the TST Trial.”
Dr. Negar Asdaghi:
1) Can marijuana use increase the risk of ischemic stroke in patients with aneurysmal subarachnoid hemorrhage?
2) Is there an association between infertility or miscarriage and development of stroke later in life?
3) Does lowering the bad cholesterol increase the risk of intracerebral hemorrhage?
We will cover these and much more in today's podcast. This is the latest in Stroke. Stay with us.
Dr. Negar Asdaghi: Welcome to another exciting Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami Miller School of Medicine and your host for the monthly Stroke Alert Podcast.
Dr. Negar Asdaghi: The February 2022 issue is the second installment of Stroke's annual Go Red for Women issue. This is to highlight the journal's continuous effort to bring to attention the research which focuses on reduction of sex disparities and enhancing inclusivity in stroke care. This issue of the journal features a number of articles from sex disparities in enrollment in randomized trials of stroke, to sex-related differences in ischemic stroke presentation, outcome of endovascular therapy, plaque composition of carotid stenosis, and the sex-dependent rupture rate of cerebral aneurysms and the risk of subarachnoid hemorrhage, which I encourage you to review in addition to listening to today's podcast.
Dr. Negar Asdaghi: Later in the podcast, I have the distinct honor of interviewing one the leaders in the field of secondary stroke prevention, Dr. Pierre Amarenco from Bichat University in Paris, to discuss the latest analysis of the association between LDL cholesterol levels and intracerebral hemorrhage risk in a sub-analysis of the Treat Stroke to Target trial, and what is next to come on cholesterol-lowering therapies post-ischemic stroke. But first with these two articles.
Dr. Negar Asdaghi: It should come at no surprise to our listeners that the use of marijuana in its variety of forms is increasing not only in the United States, but also across the globe, both for recreational purposes and also for treatment of a range of medical conditions. There's also a growing body of evidence to link marijuana use to cerebrovascular disorders, including ischemic and hemorrhagic strokes. In fact, national surveys in the United States show that over two million Americans with established cardiovascular disorders currently use or report having used marijuana in the past.
Dr. Negar Asdaghi: Aneurysmal subarachnoid hemorrhage is a hemorrhagic stroke subtype that is frequently complicated by cerebral vasospasm and delayed cerebral ischemia, or DCI. Now, we know that development of DCI can significantly increase the neurological morbidity and mortality related to the disease. So, the question is, can marijuana use increase the risk of DCI in subarachnoid hemorrhage? And what is the difference between cannabis and marijuana? And how are they even related to the brain and vascular disorders? Now, to answer these questions, we first have to do a quick review of three key points.
Dr. Negar Asdaghi: Key point number one: The word "cannabis" refers to all products derived from the plant cannabis sativa. This plant contains about 540 chemical substances. The word "marijuana" refers to parts of or products from the plant with substantial amounts of tetrahydrocannabinol, or THC. THC is the active ingredient of marijuana responsible for mediating its psychoactive effects through activation of G protein-coupled cannabinoid receptors, which are easier to remember as CB1 and CB2 receptors.
Dr. Negar Asdaghi: Key point number two: CB1 and CB2 receptors are diffusely expressed throughout the brain, but interestingly, CB1 receptors are also richly expressed across various vascular beds, including the cardiac and cerebral vessels. So, there we have it, a connection between marijuana and the blood vessels.
Dr. Negar Asdaghi: Key point number three: The differential activation of CB1 receptors in cerebral vessels may lead to vasoconstriction or vasodilation, potentially linking marijuana to vasospasm seen in aneurysmal subarachnoid hemorrhage, which then leads to DCI. But it should be noted that THC can also lead to ischemia through other mechanisms, such as altering the brain's oxidative capacity, impairing mitochondrial respiratory chain complexes, and increasing reactive oxygen species in free radicals. So, causing brain ischemia through mechanisms other than vasospasm.
Dr. Negar Asdaghi: So, with these three points in mind, in the current issue of the journal, in the study titled "Cannabis Use and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage," Dr. Joshua Catapano from the Department of Neurosurgery at the Barrow Neurological Institute and colleagues report on the outcomes of 1,014 aneurysmal subarachnoid hemorrhage patients treated over a 12-year period at their institution from August 2007 to July 2019.
Dr. Negar Asdaghi: The primary exposure was cannabis use, which was detected by routine urine toxicology at the time of hospital presentation with subarachnoid hemorrhage. Patients were also screened for the use of other vasoactive substances, including cocaine, amphetamines, and also tobacco use. The primary outcome was DCI defined as cerebral infarction detected either by CT or MRI or proven on autopsy after exclusion of procedure-related infarctions.
Dr. Negar Asdaghi: And here's what they found. Number one: Overall, 36.2% of their patient population with aneurysmal subarachnoid hemorrhage developed DCI. 50.2% of their total population had poor functional outcome defined as modified Rankin Scale of over two by the time of discharge, and 13.5% died. These are important reminders that aneurysmal subarachnoid hemorrhage remains a deadly form of stroke, despite modern neurosurgical and neurocritical care advances in treatments.
Dr. Negar Asdaghi: Number two: 4.5% of their patient population tested positive for cannabis. And here's the alarming finding of their study. The rate of DCI was significantly higher in those who were positive for cannabis, that was 52%, versus only 35% in those negative for cannabis. This association was not seen with other vasoactive agents such as cocaine and methamphetamine. Now, radiographic vasospasm was also significantly more common in cannabis users, the rate of which was 88% in cannabis users than in non-users, which was 70%.
Dr. Negar Asdaghi: Now, number three: When they adjusted for baseline patient characteristics, presenting Hunt and Hess classification, and other vasoactive substances and active smoking, cannabis use was independently associated with an increased likelihood of development of DCI. So, what did we learn from this study? Active cannabis users were 2.7 times more likely to develop ischemic stroke post-aneurysmal subarachnoid hemorrhage as compared to their non-user counterparts. This is one of the largest studies to potentially link marijuana to development of cerebral ischemia in this population.
Dr. Negar Asdaghi: There is now ample scientific evidence to connect some pregnancy-related complications, such as gestational hypertension, gestational diabetes, preeclampsia, and some pregnancy outcomes, such as preterm birth or having small-for-gestational-age infants, to an increased long-term risk of cerebrovascular events in the mother. Infertility, miscarriage and stillbirth are also common abnormalities in the process of conceiving and being pregnant, but whether there is an association between these abnormalities and development of future vascular disorders in women is not clear.
Dr. Negar Asdaghi: In the current issue of the journal, in the study titled "Infertility, Miscarriage, Stillbirth, and the Risk of Stroke Among Women," Dr. Chen Liang from the School of Public Health at the University of Queensland in Brisbane and colleagues report on the results of a systematic review and meta-analysis on this topic. So, let's dive into it.
Dr. Negar Asdaghi: First, a brief look at their methodology. After a comprehensive literature search, a total of 18 studies were included in this meta-analysis, including over 7,800,000 women between the ages of 23 to 63 with a mean follow-up of 3.8 to 19 years. So, a big study. Five studies evaluated the association between infertility and stroke. Infertility was defined in broad terms as either a formal diagnosis or receiving fertility treatment or testing through databanks or medical records. And the other 13 studies explored the association between a history of either miscarriage and/or stillbirth and the main outcome of the study, which was stroke.
Dr. Negar Asdaghi: In 11 studies, the outcomes of ischemic and hemorrhagic strokes were specified, four studies only reported on the ischemic stroke, and the rest did not identify the stroke subtype. So, what did they find? Well, their first finding was on the association between infertility and stroke. Overall, the five studies included over 4,600,000 women, and this association was inconsistent due to heterogeneity of the results between the different studies. But, when excluding the one study from Asia, which created most of the heterogeneity in results, infertility was indeed found to be associated with a 17% increase in the risk of stroke in the mother. In terms of possible causes, well, they looked at common infertility etiologies and vascular risk factors, and not surprisingly, they found many connecting points.
Dr. Negar Asdaghi: For example, polycystic ovarian syndrome is a common cause of infertility and is frequently associated with insulin resistance and type 2 diabetes. Endometriosis, another cause of infertility, is commonly associated with hyperlipidemia and hypertension as a result of chronic systemic inflammation. Another example is premature ovarian insufficiency that could increase the risk of stroke through elevated follicle-stimulating hormone, a lower level of estrogen, and a relatively elevated level of androgen.
Dr. Negar Asdaghi: So, their next finding was on the association between miscarriage and stillbirth in stroke. As you know, both of these conditions, so miscarriage and stillbirth, describe pregnancy loss at various stages. A stillbirth is the loss of fetus after the 20th week of development while a miscarriage refers to a loss of pregnancy before the 20th week of gestation. Women with a history of miscarriage had a 7% increased risk, and those with a history of stillbirth had a 38% increase in the risk of stroke later in life. Now, since having a miscarriage is a very common occurrence, it's important to pay attention to their dose response sub-analysis. When data was available on the number of miscarriages or number of stillbirths, increased risk of stroke was apparent among women with three or more miscarriages, but not two or less. For stillbirths, similarly, a history of repeated stillbirths was associated with increased risk of stroke, but evidence on association for a single stillbirth with stroke was insufficient.
Dr. Negar Asdaghi: These are important findings to keep in mind when reviewing these results, and importantly, when counseling patients in routine practice. Now, in terms of causes, the authors discuss a variety of associated mechanisms, such as persistent endothelial dysfunction, a common cause for both pregnancy loss and vascular disease, elevated level of homocystine, autoimmune disorders, including presence of antiphospholipid antibodies and a cause for both pregnancy loss and development of arterial stenosis, noting that especially for the autoimmune conditions, specifically in the case of the APS syndrome, pregnancy loss is likely to be repeated, which is consistent with the findings of their subgroup analysis and dose response analysis in the paper, showing that repeated miscarriages and stillbirths are more likely associated with a higher risk of stroke rather than a single event.
Dr. Negar Asdaghi: So, bottom line, what my takeaway from this study is, that many factors that can cause infertility, miscarriage and stillbirth can also cause vascular disorders, and these associations should be kept in mind when treating women at a younger age for fertility and pregnancy-related complications.
Dr. Negar Asdaghi: Intensive therapy to lower serum lipid levels with the use of statins is recommended after transient ischemic attack or ischemic stroke of atherosclerotic origin. Treatment with statins has been shown to reduce the risk of major vascular events in the stroke population, but there remains a concern regarding an increased risk of development of intracranial hemorrhage with this therapy. Whether this increased risk of ICH is a class effect related to treatment with statins, or is associated with a certain low target levels of LDL cholesterol, is uncertain.
Dr. Negar Asdaghi: The Treat Stroke to Target randomized trial tested the hypothesis that a target level of LDL cholesterol of less than 70 milligram per deciliter would be superior to a target range of 90 milligrams to a hundred milligram per deciliter in reducing the overall cardiovascular events after an ischemic stroke or TIA in patients with evidence of atherosclerosis. The primary results of the trial was published in New England Journal of Medicine in early 2020.
Dr. Negar Asdaghi: In the current issue of the journal, in the study titled "Intracranial Hemorrhage in the Treat Stroke to Target Trial," the trial investigators report the results of a pre-specified analysis of the TST trial to evaluate the baseline and on-treatment predictors of incident ICH. I'm joined now by Dr. Pierre Amarenco, who's the first author of the study and one of the primary investigators of the TST trial, to discuss this paper. Dr. Amarenco is an internationally renowned neurologist who absolutely needs no introduction to the Stroke readership, but as always, an introduction is nice.
Dr. Negar Asdaghi: He's a Professor of Neurology and the founder of the Department of Neurology and Stroke Center, as well as the SOS-TIA Clinic, at Bichat University Hospital in Paris. He's a leader in the field of secondary prevention of stroke with special interests in treatment of patients with TIA and mild stroke. He has served as the primary investigator of multiple randomized trials of antithrombotic therapies, lipid modifying agents, and acute revascularization treatments. Dr. Amarenco leads the international TIA registry involving centers from 21 countries around the globe. Welcome to our podcast, Pierre. Thank you so much for joining us all the way from Paris.
Dr. Pierre Amarenco: Good afternoon, Negar. Thank you for asking me.
Dr. Negar Asdaghi: Well, thank you for being here. Let's start with the Treat Stroke to Target trial. It addresses an important gap in the secondary prevention of ischemic stroke literature. Can you please start us off with an overview of the trial?
Dr. Pierre Amarenco: Yes. The objective of Treat Stroke to Target trial was to evaluate in 2,860 patients with ischemic stroke of atherosclerotic origin randomized into a target LDL cholesterol less than 70 milligram or a target LDL cholesterol 90 to 110 milligram per deciliter to see the benefit in the lower target group as compared to the higher target group. That was the purpose of the TST trial.
Dr. Negar Asdaghi: And the trial, Pierre, was terminated early. Do you mind commenting for our listeners as to why this happened?
Dr. Pierre Amarenco: Yes. The TST trial had a very long duration. It was an academic trial with low funding, funded by the French government, which is not quite the same as the NIH-funding trials. To give you an example, patient cost was $1,500 for the whole duration of the trial per patient. Around $1,500 per patient. So, it was a very low funding, and because of that, after nine years, we had to stop. But we had recruited all patients, and we had a three-year follow-up, so we could have a meaningful result.
Dr. Negar Asdaghi: So, perfect. So, just to recap for our listeners: Over eight-year period of time, despite the early termination, you had 2,860 patients enrolled, and so the termination of the trial was administrative reasons alone, as you mentioned. And so what were the primary outcomes of the trial?
Dr. Pierre Amarenco: The primary outcome of the trial was a reduction of 22% in this primary outcome, which was the composite of ischemic stroke and non-stroke, microinfarction, vascular death, and urgent revascularization for coronary or carotid ischemic event.
Dr. Negar Asdaghi: Okay, so the primary outcome was reduction of vascular events, truly, whether cardiac or in the brain. But now coming to the issue that is going to be addressed in your current paper, there remains a concern in the secondary prevention literature regarding an increased risk of intracerebral hemorrhage with statin therapy. Before we talk about the paper again, I want to give us a little bit of a background regarding the roots of this concern. Where does this all stem from?
Dr. Pierre Amarenco: In fact, when you do a meta-analysis of all statin trials, there is no increase of hemorrhagic stroke, particularly trials in primary prevention of stroke. However, in trials in secondary prevention, which include mostly HPS trial with simvastatin and SPARCL trial with atorvastatin, there was a 60% increase in hemorrhagic stroke. That did not outweigh the benefit observed in this trial, but there was a concern about statin in secondary prevention, particularly high dose statin.
Dr. Pierre Amarenco: So, in SPARCL, we did a post-stroke analysis looking at predictors of hemorrhagic stroke, and we found that, as usual, age and male sex increase risk of hemorrhagic stroke, but the most important was uncontrolled hypertension and atorvastatin. Atorvastatin stayed into the model. We know that atorvastatin reduce LDL cholesterol, that low LDL cholesterol in SPARCL was not associated with hemorrhagic stroke. So, there was a paradox because atorvastatin stayed into the model and we know that atorvastatin lower LDL cholesterol importantly. It is possible that something goes wrong between statin and vascular disease in the brain. In SPARCL, we looked at stroke subtypes at the baseline, and we found that atherosclerotic stroke, TIA and cryptogenic stroke were not associated with hemorrhagic stroke. But we found also that patients randomized with brain hemorrhage, 2% of the sample, and patient randomized with lacunar stroke were at increased risk of hemorrhagic stroke.
Dr. Pierre Amarenco: So, altogether, we can say that small vessel disease of ischemic type or hemorrhagic type were associated with hemorrhagic stroke, and we know that small vessel disease is associated with high blood pressure. So, the fact that we found uncontrolled hypertension as a predictor of hemorrhagic stroke in SPARCL was logical since also we found that small vessel disease was a predictor.
Dr. Negar Asdaghi: So, very important points that you mentioned, and I, again, want to repeat them for our listeners. And I think it's one of my questions later on to ask about independent predictors of hemorrhage, but based on the cumulative literature for what we knew before the current study, you had mentioned uncontrolled hypertension, small vessel disease, which is sort of a marker of both ischemic and hemorrhagic events in the brain, were all independent predictors of development of ICH. Whether statin therapy or low target level of LDL adds to that fueling, that fire, or not was something that you wanted to really decipher in the TST trial. I think we're ready to hear about the methodology of your current paper, if you could tell us, please.
Dr. Pierre Amarenco: So, in TST, of course, because of this background, we pre-specified an analysis of incident hemorrhagic stroke. So, we looked at patients with incident hemorrhagic stroke versus those without, and we did a multivariable analysis to look at predictors, and that was the methodology of the paper we use for this specific paper.
Dr. Negar Asdaghi: And what were the primary results?
Dr. Pierre Amarenco: So, the primary result was that after a median of three years follow-up, we found 31 hemorrhagic stroke in the lower target group and 28 hemorrhagic stroke in the higher target group, and the difference was not significant. In the paper, we show a graph with a distribution of hemorrhagic stroke according to the level of LDL cholesterol three months before the hemorrhagic stroke, and it is striking to see that half of the events occurred for an LDL cholesterol above 100 milligram per deciliter and half of the events occurred for an LDL cholesterol below 100 milligram per deciliter. So, clearly, in TST trial, like in SPARCL trial, we did not find a relationship between low LDL cholesterol and incident hemorrhagic stroke.
Dr. Negar Asdaghi: So, very important information for all practicing neurologists and stroke neurologists out there. I want to recap, again, very important numbers that you mentioned. Achieving low LDL cholesterol target, even very low numbers, as you mentioned, was not a predictor of development of intracerebral hemorrhage in the trial. And, as you mentioned, half of them, actually it occurred even before achieving the target LDL for the trial. But you did find some other significant predictors of ICH in the study. Can you please elaborate on those?
Dr. Pierre Amarenco: Yes, we found predictors, and the only predictors we found, in fact, were uncontrolled hypertension, exactly what we found in SPARCL. So, uncontrolled hypertension is really something important, and anticoagulant treatment, which was not found in SPARCL. So they were the only predictors, uncontrolled hypertension and anticoagulant treatment with of use therapeutic implications. When you put patients on a low level of LDL cholesterol, when you target the low level, you have to tightly control blood pressure, which is always a case in secondary prevention of stroke, but particularly when you target the low LDL cholesterol, and then anticoagulant treatment, of course, you have to monitor closely blood pressure and also the level of anticoagulation.
Dr. Negar Asdaghi: So, it's, again, I want to repeat what you mentioned, because it seems like we've been blaming the wrong person all along, concentrating on this issue of statins or low LDL levels being associated or the causative reason for development of intracerebral hemorrhage, and forgetting about the obvious, which is uncontrolled hypertension and now the new finding of being on oral anticoagulants, which is not unexpected. Pierre, my next question was on SPARCL trial, but you've already alluded to the SPARCL study. I'm going to repeat and ask the question regarding SPARCL, because for years and years as practicing neurologists, we've referred to the results of SPARCL, and you already alluded to some of the similarities between the two trials, but is there something else as you compared TST with SPARCL that you want to mention in terms of patient population included in both studies or the differences in the results?
Dr. Pierre Amarenco: The most important difference was that in SPARCL, there was a placebo group, which was not the case in TST since we compared two levels of LDL cholesterol. So, literally all patients were on statins in TST trial, which was not the case in SPARCL since half of the patients were on statins. So, that was the main difference, but the concept of TST clearly came from SPARCL sub-analysis. In SPARCL sub-analysis, we found that achieving an LDL cholesterol less than 70 milligram was associated with a benefit compared to patients with an achieved LDL cholesterol of 100 milligram per deciliter. But that was a post-stroke analysis in SPARCL, and so we had to confirm this, which is why we did the TST trial, which was clearly a follow-up of the SPARCL trial. And then we confirmed what we found in SPARCL, that is low LDL cholesterol was not associated with incident hemorrhagic stroke while there was a benefit of achieving a low LDL cholesterol target compared to a higher target.
Dr. Negar Asdaghi: All right, so just the follow-up question on the LDL levels. Statins are, of course, not the only agent to use to achieve a lower level of LDL cholesterol. There's a growing literature with the PCSK9 inhibitors, especially in patients with acute coronary syndrome, to lower the LDL levels. How are the findings from those studies of PCSK9 inhibitors on the risk of ICH compared to your study?
Dr. Pierre Amarenco: The findings of four-year trial with evolocumab and ODYSSEY OUTCOMES trial with alirocumab was that going to less than 40 milligram per deciliter or even 30 milligram in mean per deciliter in four-year trial was not associated with an increased risk of hemorrhagic stroke. For example, in four year, the risk of hemorrhagic stroke was 0.21% in the evolocumab group versus 0.18% in the placebo group. And in ODYSSEY OUTCOMES trial, it was 0.2% in both groups. So, clearly, going to a very, very low level of LDL cholesterol was not associated with an increased risk of hemorrhagic stroke. To give a comparison, in TST, in the lower target group, we had a 1.25% risk of incident hemorrhagic stroke versus 0.9% in the higher target group. There was a slight increase, but that was not reaching statistical significance, and it was not associated with low LDL cholesterol.
Dr. Negar Asdaghi: Perfect. So, quite reassuring, these results from various trials, again, showing and reassuring that the risk of intracerebral hemorrhage seems to not be significantly associated with lower target levels of LDL cholesterol. Now, we do have time, Pierre, I want to digress a little bit from your current study and ask a question that comes up rather frequently in routine practice. And that is the association between statin therapy, lower levels of LDL and incident ICH in the setting of microbleeds that are found typically incidentally on an MRI study. Do you think there is any possible interaction between the two, or are there plans to look at this as part of TST?
Dr. Pierre Amarenco: Yes. I would like first to say that I don't like the term "microbleeds" or "microbleeding" because it is scary for the patients. I have plenty of patients coming to my outpatient clinic because they are afraid of what they have read on the radiologist report, "microbleeds." "Doctor, my brain is full of microbleeds." I prefer to use the term "microdeposit of hemosiderin," which is descriptive, which is associated with small vessel disease.
Dr. Pierre Amarenco: So, regarding the relationship between microdeposit of hemosiderin and incidence of intracranial hemorrhage on statin, in fact, we don't know the relationship, but we can't say that in SPARCL, there was an association between small vessel disease of hemorrhagic or ischemic type with incident hemorrhage on atorvastatin 80 milligram per day. So, these patients with microdeposits of hemosiderin have small vessel disease, and then they may be at risk of more hemorrhagic stroke. So, in these patients, I would be cautious, and on high dosage of statin. I prefer to use low dosage associated with ezetimibe or with PCSK9 inhibitor to go low for LDL cholesterol, but not with statins. So, this is the way I'm used to do when there is a lot of microdeposit of hemosiderin in my patient, but it has not been tested in clinical trials.
Dr. Negar Asdaghi: So, very important, again, to repeat and recap what you mentioned. First of all, love the term "microdeposit of hemosiderin," and I'm going to use that with my patients. I totally agree with you that telling someone, "Oh, there's tons of blood in your brain," is not quite a good start. But definitely, again, as you mentioned, these are markers of small vessel disease, both for ischemic stroke and hemorrhagic. So, it's important to, again, address the causes of small vessel developments and etiologies very aggressively. And, as you mentioned, the jury's still out whether the statin class affect an association with incident ICH or an association between low target levels of LDL cholesterol, and more to come on that in the future. Pierre, just to end our podcast, what would be your top two takeaway messages for our listeners on the topic of target LDL and incident ICH?
Dr. Pierre Amarenco: Well, the message is simple. Targeting an LDL cholesterol of less than 70 milligram per deciliter in atherosclerotic ischemic stroke non-significantly increases the risk of subsequent intracranial hemorrhage. Incident intracranial hemorrhage were not associated with low LDL cholesterol level. And we found two predictors of incident intracranial hemorrhage, which were uncontrolled hypertension and anticoagulant therapy, which has important clinical implication for our patients.
Dr. Negar Asdaghi: Dr. Pierre Amarenco, it's been a pleasure interviewing you on the podcast today, and we look forward to having you back with more on this topic.
Dr. Negar Asdaghi: And this concludes our podcast for the February 2022 issue of Stroke. Please don't forget to check out this month's table of contents for the full list of publications, including a series of Focused Updates on vascular brain health organized by Dr. Steve Greenberg.
Dr. Negar Asdaghi: February is also a special month for our stroke community, with our annual International Stroke Conference, which this year is held as a hybrid event, both face-to-face in New Orleans and simultaneously as a virtual event for those who cannot attend it in person, as the fight against the COVID-19 pandemic continues. Reminding us all that with every challenge, there comes new ways to live, to cope, and to rise above it all. And we're here to do just that with staying alert with Stroke Alert.
Dr. Negar Asdaghi: This program is copyright of the American Heart Association, 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more, visit AHAjournals.org.