cardiology – European Stroke Organisation

ESSW – Session 7 – Far Horizons

Noémie — Wed, 06 Dec 2023 12:15:02 +0000

06/12/2023/in ESO /by Noémie

By: Anke Wouters, Rustam Al-Shahi Salman

ESO European Stroke Science Workshop 2023

Session 7: Far Horizons

Heavy snow disrupted the exit out of Garmisch, but despite this distraction, a lively debate followed.

Keynote debate: There are no limits to mechanical thrombectomy for acute ischaemic stroke due to medium and large vessel occlusion.

Prof. Mikael Mazighi: PRO

Prof. Mazighi started with a picture of his opponent swimming in the ice-cold Eibsee. Debating against superwoman Else Sandset is not an easy task, but everyone knows the indications for thrombectomy are increasing. Prof. Mazighi started with showing the data about patients with large core ischaemic stroke. In the TENSION trial, using mostly only CT for patient selection, 20% of the patients ended up being functionally independent. Also, the most recent trial, IN EXTREMIS LASTE, showed similar results with a reduction of mortality and an increased functional independence, however at the cost of an increased intracranial hemorrhage risk. The distal medial vessel occlusions (DMVOS) are another important new thrombectomy target with 4 RCTs currently including patients. DMVOS are very common (25-40%), but a higher bleeding risk is associated with a worse outcome. Therefore, we need other strategies to reduce the bleeding risk, with for example new antiplatelet strategies (ACTIMIS trial) or neuroprotective agents (TLR4 antagonists). Prof. Mazighi concluded by stating that there are no limits for mechanical thrombectomy, but that we do need a combined approach: good level of evidence (waiting for results of RCTs), optimisation of reperfusion, prevention of bleeding and adjunctive therapies.

Prof. Else Sandset: CONTRA

EVT is of course a highly effective treatment strategy with a NNT of 2.6 when used within 6 hours of ischaemic stroke onset, but still there are some limitations to this treatment. The most important limitation to EVT might be the fact that the treatment is still not available to many patients. Furthermore, the data for mild ischemic strokes and distal vessel occlusions, are still lacking and we need to wait for the results of the ongoing RCTs before treating those patients outside RCTs. Recent trials demonstrated a benefit of EVT in patients with large ischaemic cores, but the included patients might not be representative of the general population. Those patients were quite young and had a low number of comorbidities. Probably it is still important to consider the ‘frailty’ of a patient when considering EVT. Prof. Sandset ended here arguments with a patient-focussed perspective, by saying that it is important to take your time to talk to family and patients to achieve shared decision making in those situations.

After this intense debate, around 90% of the audience agreed that there are still some limits to mechanical thrombectomy.

Keynote lecture: Better translation for clinical recovery

Prof. Rick Dijkhuizen

Prof. Dijkhuizen spoke about the important translation of basic stroke recovery research to clinical trials. Research about stroke recovery has been limited by a lack of standardisation, variable clinical responses and incomplete recovery. Important initiatives have been initiated which provide recommendations to overcome these limitations: ISRRA, STAIR, Multi-PART. Treatment testing in animals should be standardised, multicentre and use translational outcome measures. Basic science studies remain important for detection of new pathways and targets for treatments. Translational imaging, like diffusion tract MRI or fMRI could potentially bridge the gap to clinical neurorecovery trials.

This was nicely demonstrated by prof. Dijkhuizen In the next part of his talk with the example of repetitive transcranial stimulation (rTMS). rTMS can be used post-stroke to modulate the cortical excitability. To bring rTMS from bench to bedside, a large platform was setup within UMC Utrecht. First, a meta-analysis showed that starting rTMS within 1-month post-stroke, was the most optimal timing. Preclinical research with rat models and skilled research as an outcome measure was started, for which the results are still blinded. In addition, a phase 2 clinical trial (B-stars), investigating the effect of contralateral cTMS (continuous theta burst stimulation) on upper limb recovery, has started. The results of this trial were recently published in Stroke (Vink et al. 2023) and showed a significant effect on upper limb recovery compared to the group with sham stimulation. A large national multicenter phase 3 RCT, called B-STARS² will soon start, and we are all looking forward to the results of a large, definitive trial in the field of neurorehabilitation.

Did GSSW get its priorities right? Evidence from international stroke research priority setting exercises

Prof. Terry Quinn (UK)

In the last talk of the 2023 GSSW edition, prof. Quin summarized ways of getting our research priorities on the right track. To define our priorities, we can use published data, the opinions of different experts or the research goals from guidelines. However, most importantly as academic researchers we need to synergize our research goal with people who suffered from a stroke. It is not always straightforward to get to know the real priorities of patients, because they might be reluctant to discuss certain topics with their physicians. Within the registry of Stroke Care Quality (RES-Q +) project, a chat bot was developed for patients to ask their questions more easily. Following social media is another strategy to get to know patient’s interests. In a more formal prioritisation exercise, all stroke stakeholders are included. The three most used methods are the: `James Lind Alliance`, `Global Health Forum Child Health and Nutrition Research Initiative` and the `Delphi Consensus method`. In stroke rehabilitation and long-term care, a top 10 of research questions included psychological and cognitive problems and fatigue among other things. However, it is important to note that priorities are likely to be contextual, vary with time and by included participants. A study about the effect of priority setting on published articles, didn’t show an impact on the articles that were published. To end this ESSW: Prof Quinn concluded that ESSW could focus on more of the priority areas and the priority for research is to focus on priority setting and implementation!

As ESSW 2023, closed, the snowy weather trapped most of us in Garmisch with no choice but to enjoy an extra snowy day in Garmisch to continue discussions with our colleagues!

The post ESSW – Session 7 – Far Horizons first appeared on European Stroke Organisation.

ESSW – Session 4 – OMICS, OH MY!

Noémie — Wed, 06 Dec 2023 12:10:29 +0000

06/12/2023/in ESO /by Noémie

By: Märit Jensen, Diana Aguiar De Sousa

ESO European Stroke Science Workshop 2023

Session 4: OMICS, OH MY!

The Friday afternoon session with the catchy title “OMICS, OH MY!” presented the first pro and con debate of this year’s ESSW and by this another new feature to the programme of the workshop.

The statement to be debated was: “Genomics will deliver specific stroke treatment in the next 5 years”.

Hugh Markus made the start taking the optimistic view voting for “yes”. He had a difficult task as the pre-debate survey already revealed that the majority of scientists in the audience appeared to be on the sceptic side with regards to the near future promises of genomics for stroke treatment. To support his case, Hugh Markus reminded everybody of the fact that genomics already has led to the identification of new treatment in cardiovascular disease providing the example of PCSK9 inhibitors for treatment of hypercholesterolaemia. In the second part of his talk, he described the prospects of mendelian randomization for the identification of potential therapeutic approaches. Finally, he pointed out that the era of genetic modification to treat stroke has just begun. As an example, he referred to the success in healing sickle cell disease with CRISPR-based gene editing which has been approved in the UK some weeks ago. Other approaches relying on genetic modification are currently being tested for example for cholesterol reduction using base editing of the PCSK9 gene. Against this background, Hugh Markus concluded that the advent of specific novel stroke treatment informed by genomics in the next 5 years is within reach.

Ynte Ruigrok took the role of the opponent. In an enthusiastic talk, she aimed at convincing the audience using five persuasive arguments, ingeniously structured to form the memorable acronym ‘FIASCO’. To start with, given the complexity of the genome and factors involved in stroke, she raised doubts that targeting a single genetic target would work. She also questioned why the next 5 years would bring more progress than the 5 years following the launching of GWAS which also came along with many hopes and promises but failed to deliver. Ynte Ruigrok pointed out that most of the drugs linked to targets identified by genomics had been identified based on other (non-genomic) approaches. Just 1 of 13 identified targets in this milestone analysis had not been known or tested before. This saying she made an excusing remark to the session chairs, Stephanie Debette and Martin Dichgans, who happen to be leading authors of the mentioned paper. Both took it with a smile – no offence taken.

After pros and cons were exchanged the audience was asked again. Obviously Ynte Ruigrok made some good points as the result of the voting was even stronger towards scepticism with 84% voting that genomics will NOT deliver specific stroke treatment in the next 5 years. The talks were followed by a lively discussion acknowledging the huge advances in genomics and also the prospects for future treatments based on genomics while the 5 years perspective might be overoptimistic.

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ESSW – Session 6 – New Horizons

Noémie — Tue, 05 Dec 2023 09:56:15 +0000

05/12/2023/in ESO /by Noémie

By: Corinne Benakis, Arthur Liesz

ESO European Stroke Science Workshop 2023

Session 6: New Horizons

Keynote lecture: Uric acid in stroke: the next frontier

Angel Chamorro (Spain)

Prof. Chamorro started his lecture on uric acid in stroke by first introducing he metabolism of uric acid, which is the end product of purine metabolism in humans. Uric acid is found as an end product in urine, usually known to form crystals and accumulate in joints when in high concentration. In lower concentration, uric acid is an antioxidant, and neutralizes free radicals with potential beneficial effect in ageing and cancer. Prof. Chamorro made the analogy of uric acid as a “vacuum cleaner”. In 2002, he and his team published results that showed that an increase of uric acid in patients with acute ischemic stroke is an independent predictor of good clinical outcome, highlighting the importance of oxidative damage induced early in the ischemic cascade. He re-emphasized the huge disappointment of “neuroprotection failure” in translating positive pre-clinical research to clinical trials. He addressed that perhaps this failure was due to mostly targeting the early excitotoxic events mediated by excessive glutamate toxicity but that might not be relevant since the time course of glutamate peaks very acutely after stroke but quickly recovers thereafter. In contrast, the formation of radical species continues to rise after stroke, especially in the penumbra participating in the no-reflow phenomenon. Hence, he emphasized neuroprotective strategies should be a “redox-centered neuroprotection” strategy, especially targeting the salvageable penumbra tissue in combination with mechanical thrombectomy.

URICO-ICTUS 2b/3 was a randomised, double-blind, placebo-controlled trial, that recruited patients with acute ischaemic stroke (The Lancet Neurology 2014), with a primary outcome of patients with excellent outcome at 90 days. The study showed an absolute treatment effect of 8% but no significance. The speaker mentioned the relatively small number of patients recruited that would make finding any significant results difficult.

He then took the audience on to describe the efforts taken by the Stroke Preclinical Assessment Network (SPAN) to test uric acid in preclinical stroke models. SPAN consisted of six research laboratories that conduced preclinical stroke modelling, with a coordinating center which was solely involved in drug preparation, randomization, collection and management of data, assessing blinded outcomes and performing statistical analysis. Outcome was addressed at 30 days based on behavioural improvement post-stroke as primary end-point. Of all drugs tested, among the four stages (including rodent models with comorbidities: hypertensive, obesity) only uric acid showed efficacy on the primary outcome which was validated iuntil the final stage 4 (validation in a rat model). These very impressive and promising results were published this year in Science Translational Medicine. The next frontier is to perform an interventional clinical trial in patients receiving endovascular thrombectomy (AURORA) in combination with uric acid. The stroke field is following the outcome of such intervention closely, as it could bring important benefits for stroke patients, their relatives and clinical stroke practice.

Prof. Chamorro received a nice round of applause and the first question asked him to explain the rationale behind limiting this kind of clinical trial to patients with thrombectomy. Prof. Chamorro mentioned that ideally uric acid would be administrated to any stroke patients, however it is important now that beneficial effect of uric acid is proven in highly responsive patients. This was followed by a question regarding the best timing of drug administration, and whether blood biomarkers can be used to test efficacy or perhaps to stratify receiver patients. Because previous work showed that the level of uric acid peaks immediately after reperfusion, uric acid will be administered immediately when the thrombectomy is decided. Biomarkers are now not the focus of the study, but rather primary outcome. A participant raised that giving uric acid may be counter intuitive since it can induce gout, however this was a highly epi-phenomenon among the patients enrolled and not specific to the treatment and might underlined pre-existing condition. There was then some debate from participants regarding the interpretation of sub-group analysis, that could be either futile or meaningful. What matters at the end is overall benefit for the patient and perseverance will tell us more.

Stephanie Debette

Multiomics into vascular brain health

Stephanie Debette’s scientific presentation delved into the pressing issue of vascular brain disease, which still lacks adequate treatment. She emphasized that genomics could potentially offer a targeted approach to address this condition, revealing over 150 genetic risk loci associated with vascular brain disease, mostly small vessel disease (SVD) with increased risk of stroke and dementia. However, the mechanisms underlying these genetic risk variants remain poorly understood.

Debette highlighted Montaner et al.’s work in Nat Rev Neurol 2020 (co-authored by Alba Simats, next speaker in this session), showcasing the transition from stroke treatment to multiomics strategies, stressing the importance of circulating biomarkers in understanding the underlying biology and hastening omics-driven discoveries in vascular diseases.

The integration of omics biomarkers such as metabolites, methylation, microRNAs, and proteins, along with genetic information, was emphasized to establish causal relationships, though research in multiomics for stroke has been hindered by limited sample sizes, predominantly focusing on blood-based biomarkers as shown in Chen Nat Comm 2020 and Mishra Nature 2022, utilizing Mendelian Randomization to obtain clues for causality.

Another referenced study by Sliz et al (Circulation 2022) described using mendelian randomization that circulating metabolites are associated with white matter hyperintensities (WMH). Metabolites are either endogenous or from exogenous sources like diet and chemical exposures, associating specific metabolites with risk factors for vascular brain disease, although the precise correlations are not fully investigated.

Debette discussed epigenomics, citing Yang, Brain 2023, and the importance of proteomics due to its proximity to function. Her focus leaned towards plasma proteins, as exemplified in Kuipers JCBFM 2022, which highlighted a cluster of proteins, including coagulation factors, associated with white matter hyperintensities (WMH). Employing a pQTL approach (protein quantitative trait loci), Debette outlined her study associating 21 proteins with a higher risk of SVD, specifically mentioning cathepsin b and immune response enrichment. This research would significantly enhance the prediction of SVD. She posed critical questions in her conclusion, pondering whether the proteins linked to SVD could predict stroke and dementia while exploring the feasibility of developing drugs targeting these proteins. She emphasizes that taking a more global approach towards vascular brain health by integrating multiomics to not only address risk prediction, but also early prevention and to accelerate the development of new drugs. And the development of interdisciplinary experts would significantly accelerate discovery.

Alba Simats

Innate immune memory after stroke drives inflammatory cardiac dysfunction

Alba Simats’ presentation exemplified the profound impact of post-stroke inflammatory responses, and it’s influence on other diseases like atherosclerosis, diabetes, and heart dysfunction. The chronic inflammatory state persisting in stroke patients over time raises questions about its consequences on peripheral organs, such as the heart.

Within a month of stroke, increase of myeloid cells were identified in various peripheral organs, particularly highlighting the dominance of monocytes/macrophages exhibiting a pro-inflammatory signature. Remarkably, the heart emerged as the most affected organ in this cellular population, exhibiting altered left ventricle diastolic dysfunction, a finding mirrored in the SICFAIL previously describing cardiac dysfunction in stroke patients.

Investigations into cardiac fibrosis, collagenase and MMP9 accumulation in the heart showed as association with with an increase in heart and circulating inflammatory CCR2+ monocytes expressing MMP9. A cohort of cardiac autopsy samples from stroke and control patients further substantiated these findings, demonstrating fibrosis, MMP9, CCR2+ expression, and inflammatory genes in the hearts of stroke patients.

Insights into bone marrow as a potential source of these monocytes wasrevealed, showcasing increased monocytes/neutrophils and their precursors after one month post-stroke. Notably, both pluripotent stem cells and monocytes from the bone marrow exhibited distinct gene profiles similar to those in the periphery, speculating that the inflammatory cardiac monocytes originate and are polarized in the bone marrow.

A groundbreaking experiment, showing causality, involved bone marrow transplantation from stroke-affected mice to mice lacking bone marrow, demonstrated that progenitor cells and monocytes carrying the Ly6C high marker exhibited identical signatures, leading to similar cardiac dysfunction characterized by increased fibrosis and MMP9 expression in the heart. The potential therapeutic avenue of inhibiting monocyte infiltration from the bone marrow to the heart using a dual chemokine inhibitor showed promising results. Blocking monocyte access to the heart not only restored left ventricle volume but also decreased cardiac fibrosis, hinting at a potential intervention strategy for post-stroke cardiac complications. These are the first evidence that stroke impacts cardiac function chronically mediated by recruitment of inflammatory monocytes to the heart.

Floris HBM Schreuder

Inflammation after Intracerebral Hemorrhage

Floris HBM Schreuder’s presentation on “Inflammation in Intracerebral Hemorrhage (ICH): The Ugly, The Bad, and The Good” highlighted the nuanced nature of inflammatory responses in this condition. He outlined the phases of inflammation, emphasizing both detrimental and beneficial aspects. Hence, the classical view of good and bad inflammation in ICH is more complicated.

The road map of his talk navigated through three main areas: the role of inflammation in ICH, mechanisms of secondary brain injury, and therapeutic approaches.

In discussing the role of inflammation in ICH, Schreuder focused on the transition to a hemorrhagic phenotype, attributing it to reduced clearance in Amyloid beta deposition, leading to vessel fragmentation (loss of smooth muscle cells) and subsequent perivascular inflammation.

ICH develops into hematoma growth but also to an accumulation of parenchymal blood components inducing secondary brain injury with BBB breakdown, inflammation and perhematomal edema. This was portrayed as a time-dependent process, where the inflammatory response played a complex role.

Preclinical studies faced limitations due to induced ICH via collagenase or blood injection, which do not necessarily recapitulate the complex inflammatory cascade in human ICH. Importantly there is still only limited data derived from investigating human brains and systemic inflammation. He highlighted the recent meta-analysis showing association with circulating inflammatory biomarkers and clinical outcome following ICH (Kirby et al. Wellcome Open Res 2023).

Therapeutic strategies to mitigate post-ICH inflammation include surgical blood removal and reducing perihematomal edema: The Dutch ICH surgery trial, and a new sub-study DIST-INFLAME to investigate immunoprofile between surgically versus conservatively treated patients are investigating these approaches. Schreuder stressed the need for early intervention due to the vulnerability of ICH patients to infections, posing the question of whether modulating inflammation, possibly with steroids like Dexamethasone, could be effective or if this type of intervention is alreafdy a “closed case” considerating previous (futile) studies using this intervention..

Ongoing trials targeting inflammation and potential therapeutic avenues like neutralization of IL-1b as a target were discussed; including potential complications and the their limitations. Schreuder concluded by emphasizing the importance in targeting multiple phases and mechanisms of ICH, such as stopping ICH growth, treat hypertension, reduce secondary brain inflammation (IL1b), promote repair (stem cell strategy?) and rehabilitation, combining experts from different fields from the emergency to the rehab teams. He finished his talk mentioning there is certainly possibility of leveraging inflammation for therapeutic intervention in ICH while acknowledging the complexity and challenges involved.

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ESSW – Session 5 – Too much, too young

Noémie — Mon, 04 Dec 2023 11:24:22 +0000

04/12/2023/in ESO /by Noémie

By: Anke Wouters, Rustam Al-Shahi Salman

ESO European Stroke Science Workshop 2023

Session 5: Too much, too young

Keynote Lecture: Stroke in the young: what are we missing?

Speaker: Frank-Erik De Leeuw, RadboudUMC

Professor De Leeuw, gave an excellent keynote lecture summarizing the missing aspects of stroke in the young. Stroke patients of 18-50y old were considered as young strokes. The increase in the incidence of more than 50% during the last years is very worrisome. In his talk, prof. De Leeuw summarized three key factors about young stroke that we are currently missing: Cryptogenic causes, prognosis and adverse events.

How can we find the unknown causes of these strokes in the young?

Data from the Odyssey study were shown in which 1322 young ischemic stroke patients were included between 2013 and 2017 in 17 centers in the Netherlands. Around 25-30% of these patients had a cryptogenic stroke according to the TOAST-classification. However, risk factors like high temperature, physical exercise, flu-like episodes… all increased the risk of having a cryptogenic stroke in those young patients. Furthermore, according to geographical data, patients living in rural areas were at a greater risk compared to those living in urban areas in the Netherlands. Cancer was another important risk factor that was addressed. In stroke patients, the excess risk of having cancer was higher in young patients compared to older stroke patients. Probably it is not useful to screen all young stroke patients for cancer but only selected patients who are at the highest risk. Known risk factors are anemia, cryptogenic stroke and stroke in three brain regions.

What are we missing about prognosis?

It is important to keep in mind that all individual patients are different, and that the recurrence stroke risk depend on the underlying cause of the stroke. For example, after cervical artery dissection the recurrence risk is very high in the first two weeks, but the risk of recurrence is very low in the long-term, in contrast for patients with underlying atherosclerosis the risk is always high and will increase further over the years. This information can help to inform patients more accurately in clinical practice.

What about the secondary prevention?

Probably the use of antithrombotic therapy should be managed individually depending on both the bleeding and ischemic stroke risk. From the data collected in the Netherlands, the bleeding and ischemic risk are very similar after 5-10 years. Hence, the European guidelines suggest that you can discuss stopping secondary prevention with your patients after 3-5 years if a complete etiological work-up didn’t reveal a cause. Evidence from future clinical trials might be needed to more accurately define if and when we can stop antithrombotic treatment.

This excellent keynote lecture was followed by a lively discussion.

Why is the incidence of stroke in the young rising?

Speaker: Linxin Li (UK)

Dr. Li nicely described the rising incidence of ischemic stroke in the young patients in the last 20 years based on data from the Oxford vascular study. Although the absolute incidence of young stroke showed considerable levels of inconsistencies in other high-income countries, this was consistently less favorable compared to older ages. She nicely demonstrated that the time-trend in the young stroke could not be explained by changes in diagnostic work-up, stroke definition and adjudication, patient behaviour, hospital admission policy or changes in traditional vascular risk factors. Although there is still a high prevalence in modifiable risk factors in young stroke patients which are under-recognized and under-treated. Next, still a lot of research should be done regarding the role of emerging risk factors (migraine, previous auto-immune disease, exercise,…).

Novel types of hereditary small vessel disease: evidence for a unifying mechanism?

Speaker: Elisabeth Tournier-Lasserve

Professor Tournier-Lasserve focused on hereditary causes of small vessel disease. Causative mutations are only identified in 20-25% of the referred patients. Perturbation of the cerebrovascular matrisome is a convergent pathway but through different mechanisms. She nicely demonstrated with the COL4A1 example (HANAC and PADMAL phenotypes), how mutational consequences can be distinct from one class of mutations to another and lead to different small vessel disease (SVD) phenotypes. Many other anomalies can cause an up or down regulation of COL4A1/2 genes and might explain some unresolved SVD cases in the future. Probably a combination of DNA sequencing and functional protein/mRNA fibroblast analysis will be needed to identify them.

Closing comments: PFO as a window on heterogeneity of treatment effect.

Speaker: Guillaume Turc

Professor Turc talked about the selection of people with ischaemic stroke who should undergo PFO closure. The PFO-Associated Stroke Causal Likelihood (PASCAL) classification system is mostly used in clinical practice to select patients for PFO-closure. 15% of young people with ischaemic stroke would be included in the `unlikely` PASCAL category, meaning the stroke was probably not caused by the PFO. Hence these patients are unlikely to derive any benefit from PFO closure (but 95% CI are wide). To determine patients at a high risk for recurrent stroke, a detailed PFO anatomy is important. Data show that patients with both a large shunt and an atrial septal aneurysm are at the highest risk of having a recurrent stroke (SCOPE collaboration) and have the highest treatment effect of PFO closure. Therefore, in the current 2021 AHA/ASA guidelines PFO anatomy has a central role in stratifying patients for PFO closure.

After a lengthy and insightful discussion, the second day of the ESSW was wrapped up.

The post ESSW – Session 5 – Too much, too young first appeared on European Stroke Organisation.

ESSW – Session 3 – Methods Matter

Noémie — Mon, 04 Dec 2023 11:09:05 +0000

04/12/2023/in ESO /by Noémie

By: Thomas Meinel, Diana Aguiar De Sousa

ESO European Stroke Science Workshop 2023

Session 3: Methods Matter

Dr. Sarah McCann

In her excellent keynote lecture on meta-research, Dr. McCann challenged the preclinical stroke research community with an alarming in-depth analysis of published laboratory stroke studies analyzing key quality metrics. A large proportion of preclinical research is not reproducible in humans, mostly due to significant weaknesses of design and reporting.

Weaknesses include selective outcome reporting and publication bias. Frequently, animal models are also not reflective of the human disease population, e.g. an antihypertensive drug tested in young healthy male mice as opposed to an older, more often female human population that this drug would then be used in.

The same tools that we take for granted in clinical research, namely large-sized registries, multicenter studies, randomization and blinding of performing the treatment and outcome assessment are useful tools to overcome those methodological flaws in preclinical studies. Successful examples of such large collaborations are the Stroke Preclinical Assessment Network (SPAN) and INFORM-Stroke.

The recently launched CoReS hub aims to bring together primary researchers and evidence synthesists to provide infrastructure and support systems to empower the community in the performance of systematic reviews on preclinical evidence. Journal policies have also modestly helped to improve design and reporting of animal experiments such as adopted by Nature publishing group and Stroke. Open data policies are another piece of the puzzle to enhance the transparency and external validity. The suggestions have been incorporated into design guidelines (EDA), and publication guidelines (ARRIVE).

The discussion acknowledged the urgent need for improvement and great potential of the proposed improvements.

Overall, the analysis and proposed solutions are a highly relevant contribution to improve validity, transparency, and reproducibility of laboratory stroke research. Following those recommendations ultimately means less waste in preclinical research, less potential harm for patients and more robust and fruitful translational research.

Professor Maren Ranhoff Hov

In her outstanding lecture on innovative trial designs with the example of cluster randomized trials in the prehospital setting, Professor Ranhoff Hov pointed out the particularities and challenges of prehospital research. Learning from the trauma community, that put into place a very standardized approach to ensure fast and high-quality care, she mentioned the potential of such an approach to address the heterogeneity of stroke presentations, especially for those presenting with less severe or less specific symptoms and other hurdles for a rapid activation of the stroke chain of survival. One such approach was the ParaNASPP trial, that used prehospital NIHSS assessment by an app. Since randomization and blinding is not possible on a patient-level, the design was a stepped-wedged cluster randomized trial. This also allowed to provide training of the cluster sequentially. The downside of this approach include a potential secular effect during the trial, especially given the fact that the COVID pandemic happened during recruitment. As an example, the delay of on-scene time of about 5 minutes is not necessarily only due to the use of the prehospital app, but might (partially) be a pandemic effect. She encouraged the stroke research community to engage in prehospital research making use of novel technical solutions such as videocalls and mobile apps with live communication to the stroke center.

Professor Joanna Wardlaw

Professor Joanna Wardlaw presented the tremendous effort to update and expand the STRIVE recommendations for imaging features of small vessel disease in the STRIVE-2 update. This included an analysis of adoption of the recommendations, which was mostly good, but there is ongoing debate mostly about the best term for “recent small subcortical infarcts”. The update includes novel and emerging features such as cortical superficial siderosis as well as small cortical infarcts as well as recommendations on image acquisition and analysis. For sure, those recommendations will continue to influence guidelines and improve research and patient care.

Professor Will Whiteley

How to do research under the time pressure of a pandemic was the topic of the last talk of the session. There was a massive inflation of research, but weaknesses included lack of collaboration with duplicative, small studies instead of larger, well conducted studies. The peer review system failed to filter dogmatic and flawed research. Positive developments to provide timely and truthful information include the use of master protocols, rapid governance, and easy data flow. Since the information should be available freely, researchers should use preprints, as well as open data and open code. In the next pandemic, policy makers should quickly set up few, but well designed and large projects providing sufficient funding combining several perspectives. One such positive example is the RECOVERY trial.

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ESOC 2022 Session Report – ESC-ESO Joint Symposium: Evaluation of cardiac source of stroke

Lara Le Noan — Fri, 06 May 2022 08:53:40 +0000

06/05/2022/in ESO, ESOC /by Lara Le Noan

By Dr. Inna Lutsenko, ESO Social Media and PR Committee

@inna_lutsenko

Chairs: Marta Rubiera (Spain) and Wolfram Döhner (Germany)

How can I see inside the heart? The basics of POCUS assessment in neurologist’s hands

Theodoros Karapanayiotides from Greece opened the session of collaborative Symposium the ESO and the European Society of Cardiology. He started his talk with an introduction of “POCUS” – point of care ultrasound, a portable device, which does not make neurologists depend on the radiology department in the cases when an immediate ultrasound diagnosis is necessary. With a POCUS a patient may be scanned while in an ambulance on the way to an emergency room or even in remote areas. The advantage of the POCUS is its availability in neurological departments. POCUS is not a full cardiac examination, a semi qualitative, but permits to estimate the left/right ventricle size in the parasternal long axis. Common pathologies, which might be diagnosed with a POCUS are

heart failure with an enlargement of the left atrium in a four chamber view, confirming with the global hypokinesia of the left atrium,
“ballooning deformation of the heart” – Takotsubo cardiomyopathy when heart changes its shape in the so called “octopus trap”
Constrictive cardiomyopathy with a total collapse of left ventricle,
apical left ventricular thrombus
aortic arch in suprasternal view, where large atheromas could be detected in the ascending and descending aorta,
and even the distensibility and diameter of vena cava with central venous pressure could be measured.

POCUS is not used though for the PFO diagnostics, in these cases we should refer the patient to a cardiologist with the use of the transesophageal ultrasound. Theodoros Karapanayiotides concluded that POCUS is not intended for full investigation of cardiogenic/cryptogenic stroke, but this is an extension/complement to physical examination, which could provide rapid answers to specific questions.

Troponin elevation in acute stroke: when to worry when to wait

Jan Scheitz from Germany started his talk with a clinical case with a 77 years old female, having a right MCA syndrome with NIHSS 7 and onset-to-admission time 12 hours. She had diabetes, her vital signs were normal and ECG was unspecific and troponin was elevated in admission (hs-c TnT 70 ng/L (5-times ↑ URL). The question was raised whether it is an acute myocardial infarction and how to proceed. Jan Scheitz reminded us that troponin is a special biomarker for the condition of the heart contraction and it could reflect any heart pathology, such as myocardial damage and necrosis. High sensitivity troponin helps us to reveal the heart changes in the general population.

What do we have if we look closely at the patients with elevated troponin level before sending the patient to the CT lab? In the The TRoponin ELevation in Acute Ischemic Stroke (TRELAS) Study which was done in Charite, Berlin, among 2,123 consecutive acute ischemic stroke patients prospectively screened at two tertiary hospitals, 13.7% had cTn elevation (>50ng/l). Further studies are needed to clinically identify the minority of patients with AIS and angiographic evidence of a culprit lesion. In a case of the elevated troponin level in acute ischemic steroke Jan recommends as a first step to differentiate acute or chronic myocardial injury. In case of an acute stroke (hs-cTn ↑ (> 99th Percentile) we should suspect stroke-associated myocardial injury.

Characteristics associated with post-stroke troponin elevation:

Older age, burden of cardiovascular risk factors,
Chronic kidney disease,
Presence of structural and coronary heart disease:

History of CAD, AFIB, Heart Failure
Correlates with LF-EF, WMA, ECG (QT c time, repolarization changes)
Stroke severity, embolic infarct pattern, stroke lesion site.

To summarize: neurologists should differentiate acute and chronic injury and for this to lead serial troponin measurements. In case of chronic myocardial injury, re-stratify vascular risk profile and perform (outpatient) cardiac assessment. In acute myocardial injury – establish cause in a timely manner. Use conventional risk schemes and cardiac imaging to stratify risk of type 1 myocardial infarction.

What the heart hides: How to perform basic and advanced cardiac monitoring in your stroke unit

In his presentation, Martin Köhrmann from Germany underlined that cardiac monitoring includes: evaluation of biomarkers (CHD, CAD, MI), evaluation of structural changes and function (heart ultrasound), evaluation of vasculature if needed and evaluation of electric changes (ECG). Stroke Arrhythmia Monitoring Database (SAMBA) was a prospective, monocentric study with 641 patients from the Stroke Unit. Daily standardized rhythm analysis of acquired ECG data was done. SAMBA consisted of several substudies: SAMBA-SR: detection of Arrhythmias (Kurka et al. Stroke; Kallmunzer et al. Stroke; Seifert et al. J Neuol), SAMBA-AF: detection of atrial fibrillation (Kallmunzer et el.; Stroke), SAMBA HR: clinical impact of heart rate dynamics (Kallmunzer et al.; J Stroke Cerebrovasc Dis.) and Impact on Early Repolarization Pattern (Bobinger et al.; Clin Res Cardiol).

Standardized Algorithm for ECG analysis should include:

24-h spectrum of HR dynamics
Identification of drops and raises > 20/min
Changes in width of spectrum
Tachycardia > 120/min and Bradycardia < 40/min
Automatically detected arrhythmias and alarms

Arrhythmia after Stroke:

25% of all patients have relevant arrhythmia
24% of these are clinically evident
77% direct therapeutic consequences (1 CPR, 13 pacemaker/ICD, medication)
Tachycardic > bradycardic
Clearly time dependent after stroke
Predictors: Age, NIHSS on admission.

Biomarkers of Cardiac and Vascular Thrombogenicity and Stroke Risk

Presented by Magnus Bäck, Sweden

Several mechanisms take part in a cardiac thrombogenicity: endothelial dysfunction, vasoconstriction, thrombosis, inflammation, smooth muscle proliferation, biomarkers of inflammation: IL-6, CCRP, n-3, PUFA, coagulation and platelet aggregation with elevated D-dimers, fibrinogen, etc. Biomarkers can also distinguish the source of thrombus.

Left atrium thrombogenicity can be evaluated by ultrasound monitoring. Cardiac thrombogenicity can be systemic. In the center is inflammation that can help to distinguish cardiac and vascular thrombogenicity.

CRP is higher in non-cardioembolic cases. Omega-3-fatty acids in atherosclerosis can be biomarkers for inflammation. DHA fatty acids decreased the risk of ischemic stroke. DPA decreases the risk of cardioembolic stroke.

Stroke prevention in cardiac interventions: TAVI, ablations.

Presented by Jan Kovac, United Kingdom

Heart interventions which coil lead to the acute brain injury are mechanical thrombectomy (pivotal, but not limited to), LAA Closure, embolic protection for Cardiac Interventions and ablations. Postulated Mechanism is the reduction of the left atrial appendage blood flow from dysrhythmia. AF slows LAA blood flow and disrupts laminar flow. More complex LAA internal characteristics such as “cauliflower” morphology puts even low CHA2DS2 – VASc score AF patients at significantly higher embolic risk than the simpler chicken wing or windsock morphologies. There are 90% nonvalvular atrial fibrillation related emboli detected in left atrial appendage closure. Most of the atrial fibrillation comes from the left atrial appendage.

Can pulmonary vein isolation (PVI, AF Ablation) prevent Stroke?

Historical studies such as AFFIRM/RACE showed no difference in risk of stroke between rate and rhythm control strategies for AF. There are multiple observational studies demonstrating a reduced incidence of stroke post-ablation (Bunch et al./Korean National Health Insurance Service (NHIS) database). Meta-analyses also supported the reduced stroke risk post ablation (although in the majority of studies included, anticoagulation was continued post-ablation). Randomized Prospective studies demonstrated that there is no randomized prospective data to suggest ablation is associated with a reduction in risk of stroke (CABANA trial). There are several ongoing studies LAA vs NOACs: CHAMPION – AF clinical trial, PFO trial.

Heart Brain Interventionist 2022 (And Beyond):

Cardiology is moving beyond boundaries of heart disease
Stroke is often related to heart conditions
Stroke prevention and treatment is multidisciplinary
Several New Skills required for all specialties
Cooperation and pathway access requires collaboration of all stakeholders
Important issue of training quality and outcome control
Stroke Specialist – Referrer, Gate Keeper and Quality Controller!

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Is inflammation the next therapeutic target in intracerebral hemorrhage?

Lara Le Noan — Mon, 11 Apr 2022 08:08:11 +0000

Aristeidis H. Katsanos, MD, PhD

McMaster University and Population Health Research Institute

@ArKatsanos

Intracerebral hemorrhage (ICH) is a devastating disease with an estimated incidence of 24.6 cases per 100,000 person-years. While just under a third of strokes are ICH, they account for 49% of the global burden of death from stroke. Despite the advances in primary and secondary ischemic stroke prevention, neither the incidence nor the case fatality rates of ICH have substantially decreased since 1980, in contrast to the case of ischemic stroke. As both ICH incidence and case fatality increase with age, the burden of ICH-related morbidity and mortality and ensuing healthcare expenditures are expected to increase substantially with our aging demographics over the coming decades.

Experimental, epidemiological and clinical trial data have highlighted that inflammation is a key mediator in the development of vascular events, including stroke. Evidence from large-scale randomized controlled clinical trials, summarized in a previous post , suggest that inhibition of inflammatory pathways in patients with coronary artery disease can ameliorate the risk of future cardiovascular events, including stroke prevention. In addition to the association with ischemic events, inflammatory processes also seem to be implicated in the resulting brain injury following an ICH. ICH seems to trigger an immunological reaction and systemic inflammatory response that contributes to secondary brain injury, following the initial mechanical forces of an expanding hematoma (primary injury). Hematoma-related blood components, such as iron, induce oxidative stress and the aggregation of immunocytes, both resident in the central nervous system and recruited from the peripheral circulation, with evidence from experimental and observational clinical studies suggesting an increased expression of inflammatory cytokines in brain microglia and the peripheral blood of patients with acute ICH. Inflammatory markers in the early acute phase of ICH have been associated with both hematoma enlargement and worsened patient outcomes. ICH-induced inflammatory response results in cytokines release, which promote neutrophil infiltration, and augment further the ongoing neuroinflammation, brain injury and cerebral edema.

Anakinra in Cerebral Haemorrhage to Target Secondary Injury Resulting From Neuroinflammation (ACTION) is a phase 2, multicentre, prospective, randomized, three-armed (1:1:1) trial assessing the effect of high-dose and low-dose anakinra compared to standard medical management on cerebral edema, serum inflammatory markers and functional outcomes of patients suffering from a spontaneous ICH. Colchicine for the prevention of vascular events after an acute intracerebral hemorrhage (CoVasc-ICH) is another vanguard-phase, randomized, placebo-controlled, multicenter clinical trial with the overarching goal to investigate the safety and efficacy of low-dose colchicine for the prevention of major cardiovascular events and brain injury after an acute spontaneous ICH.

Although current evidence is still insufficient to support the implementation of anti-inflammatory treatment strategies after an acute intracerebral hemorrhage, there are two ongoing randomized control clinical trials which are targeting the inflammatory cascade to ameliorate the cardiovascular risk and improve the functional outcomes of this fragile patient population.

REFERENCES

van Asch CJ, et al. Incidence, case fatality, and functional outcome of intracerebral haemorrhage over time, according to age, sex, and ethnic origin: a systematic review and meta-analysis. Lancet Neurol. 2010;9:167-76.
Feigin VL, et al. Update on the Global Burden of Ischemic and Hemorrhagic Stroke in 1990-2013: The GBD 2013 Study. Neuroepidemiology. 2015;45:161-76.
Shi SX, et al. IL (Interleukin)-15 Bridges Astrocyte-Microglia Crosstalk and Exacerbates Brain Injury Following Intracerebral Hemorrhage. Stroke. 2020;51:967-974.
Silva Y, et al. Molecular signatures of vascular injury are associated with early growth of intracerebral hemorrhage. Stroke. 2005;36:86-91.
Ma Q, et al. NLRP3 inflammasome contributes to inflammation after intracerebral hemorrhage. Ann Neurol. 2014;75:209-19.

Conflict of interest statement

Dr. Katsanos serves as the co-Principal investigator for the Colchicine for the prevention of vascular events after an acute intracerebral hemorrhage (CoVasc-ICH), supported by the Canadian Institutes of Health Research and the Population Health Research Institute

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Capsular Warning Syndrome: not all TIAs remain the same

Lara Le Noan — Fri, 01 Apr 2022 05:53:46 +0000

Giuseppe Reale, MD^1,2; Marco Moci, MD².

¹Fondazione Policlinico Universitario A. Gemelli IRCCS, UOC Neuroriabilitazione ad Alta Intensità

²Università Cattolica del Sacro Cuore – Roma, Dipartimento di Neuroscienze

Transient Ischemic Attack (TIA) is usually characterized by transient focal neurological signs such as speech disturbances, hemiparesis or partial visual loss, without any neuroimaging evidence of cerebral ischemia^1,2. Short-term risk of stroke after TIA is high: according to the most used score for assessing such risk, ABCD2 score, the risk of stroke within the first 48 hours ranges from 1% to 8.1%, depending on symptoms, their duration, patients’ age, hypertension and diabetes³. However, not all focal neurological signs are the same. This is the case of Capsular Warning Syndrome (CWS) that constitutes a subgroup of all TIAs. First described by Donnan et al in 1993, CWS consists of acute, transient, stereotypical sensory and/or motor symptoms affecting the face, arm and/or leg. There has to be an absence of cortical signs and it has to occur within a seven-day period after an index TIA^4–6.

The most comomn manifestation of CWS is with a pure hemiparesis, the number of episodes mostly ranging between 3 to 10 (even in a single day), their mean duration being about 6 minutes, and appearing in “clusters”^4–6. Although CWS is only responsible of 1.5-4.5% of all TIAs, the risk of ischemic stroke is likely high, with an incidence ranging between 17% and 70%. A recent review even showed that 74% of these patients had infarction on neuroimaging, which is far above the 8% risk detectable with ABCD2 score^4–6. The ABCD3-I score proposed in 2010 added occurrence of at least two TIAs – a so called ‘dual TIA’ – to the stroke risk score^7–9 and this was later validated in a Chinese population. However, when the recurrences of symptoms in a patients with a CWS is regarded as a ‘dual TIAs’, the risk of subsequent stroke is likely underestimated¹⁰. Pathophysiological mechanisms that might explain such increased risk of ischemic stroke are still unclear. Several mechanisms might contribute to the ischemic damage, including penetrating small vessel disease, hemodynamic impairment, branch-artery disease, artery-to-artery embolism and peri-infarct depolarization⁶.

Regarding treatment, dual antiplatelet therapy is the mainstay for all TIAs, CWS included⁶^,¹¹^,¹². Other potential therapies are matter of investigation, such as intravenous tirofiban (overlap loading Clopidogrel 300 mg and Aspirin 100 mg), which has been suggested as a potential intervention toreduce fluctuations in CWS patients¹³. When a DWI-FLAIR mismatch on MRI in the acute symptomatic phase is present, choosing thrombolytic therapy is reasonable.

In conclusion, CWS represent a non-neglectable sub-group of TIAs, it is characterized by several episodes of transient subcortical neurological symptoms and has a high risk of stroke progression. Therefore, when evaluating a TIA, suspecting CWS could have a significant impact on patients’ management strategies, especially in terms of monitoring during the early stage.

REFERENCES

Sorensen AG, Ay H. Transient ischemic attack: definition, diagnosis, and risk stratification. Neuroimaging Clin N Am. 2011;21:303–313, x.
Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann E, Hatsukami TS, Higashida RT, Johnston SC, Kidwell CS, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40:2276–2293.
Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, Sidney S. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007;369:283–292.
Paul NLM, Simoni M, Chandratheva A, Rothwell PM. Population-based study of capsular warning syndrome and prognosis after early recurrent TIA. Neurology. 2012;79:1356–1362.
Donnan GA, O’Malley HM, Quang L, Hurley S, Bladin PF. The capsular warning syndrome: pathogenesis and clinical features. Neurology. 1993;43:957–962.
Sales C, Calma AD. Stroke warning syndrome. Clinical Neurology and Neurosurgery. 2022;213:107120.
Merwick A, Albers GW, Amarenco P, Arsava EM, Ay H, Calvet D, Coutts SB, Cucchiara BL, Demchuk AM, Furie KL, et al. Addition of brain and carotid imaging to the ABCD2 score to identify patients at early risk of stroke after transient ischaemic attack: a multicentre observational study. Lancet Neurol. 2010;9:1060–1069.
Knoflach M, Lang W, Seyfang L, Fertl E, Oberndorfer S, Daniel G, Seifert-Held T, Brainin M, Krebs S, Matosevic B, et al. Predictive value of ABCD2 and ABCD3-I scores in TIA and minor stroke in the stroke unit setting. Neurology. 2016;87:861–869.
Kiyohara T, Kamouchi M, Kumai Y, Ninomiya T, Hata J, Yoshimura S, Ago T, Okada Y, Kitazono T, Fukuoka Stroke Registry Investigators. ABCD3 and ABCD3-I scores are superior to ABCD2 score in the prediction of short- and long-term risks of stroke after transient ischemic attack. Stroke. 2014;45:418–425.
Song B, Fang H, Zhao L, Gao Y, Tan S, Lu J, Sun S, Chandra A, Wang R, Xu Y. Validation of the ABCD3-I Score to Predict Stroke Risk After Transient Ischemic Attack. Stroke. 2013;44:1244–1248.
Johnston SC, Easton JD, Farrant M, Barsan W, Conwit RA, Elm JJ, Kim AS, Lindblad AS, Palesch YY, Clinical Research Collaboration, Neurological Emergencies Treatment Trials Network, and the POINT Investigators. Clopidogrel and Aspirin in Acute Ischemic Stroke and High-Risk TIA. N. Engl. J. Med. 2018;379:215–225.
Wang Y, Wang Y, Zhao X, Liu L, Wang D, Wang C, Wang C, Li H, Meng X, Cui L, et al. Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack. N Engl J Med. 2013;369:11–19.
Li W, Wu Y, Li X-S, Liu C-C, Huang S-H, Liang C-R, Wang H, Zhang L-L, Xu Z-Q, Wang Y-J, et al. Intravenous tirofiban therapy for patients with capsular warning syndrome. Stroke Vasc Neurol. 2019;4:22–27.

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Stroke care during the COVID-19 pandemic: Running a marathon with hurdles

Lara Le Noan — Fri, 25 Mar 2022 05:33:26 +0000

By Aristeidis H. Katsanos, MD, PhD

Twitter: @ArKatsanos

Coronavirus disease 2019 (COVID-19) outbreak was declared by the World Health Organization (WHO) on March 11, 2020. Healthcare delivery, including stroke care, has faced unprecedented challenges due to the impact of the COVID-19 pandemic.

International organizations, including the European Stroke Organisation, focused from the very start of the COVID‐19 pandemic on protecting hospital staff and at the same time preserving the quality of patient care. Despite concerns for increased in-hospital delays, the “protected code stroke” measures implemented during the active waves of the COVID-19 pandemic resulted in similar rates and time to reperfusion therapies during the first wave of the pandemic.

The association between the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and cardiovascular diseases, including stroke, has been an even more puzzling challenge for researchers and healthcare providers. Several studies reported an increased risk of cerebrovascular events in patients infected with SARS-CoV-2, suggesting that a hypercoagulable state induced by the viral infection could be the etiology for cryptogenic strokes in younger individuals. On May 2021, public attention was shifted to a surge of cases of cerebral venous sinus thrombosis (CVST) associated with a thrombosis and thrombocytopenia syndrome induced by viral vector-based vaccines against the SARS-CoV-2. As international regulatory authorities continued to emphasize the overwhelming benefit for vaccination against SARS-CoV-2, swift diagnosis and appropriate treatment initiation for patients with CVST associated with Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT) became of paramount importance to improve the dire prognosis associated with this condition.

According to several cohort studies from different parts of the world, patients admitted with stroke during the first wave of the COVID‐19 pandemic had more severe syndromes and a five-time higher risk for in‐hospital mortality compared to the pre-pandemic era. Based on these alarming findings, cohort studies performed during the second wave of the COVID-19 pandemic reported a decrease in stroke severity, in‐hospital strokes, and in‐hospital stroke mortality compared to the first wave of the pandemic.

After two continuous years of struggling to preserve best care practices during these challenging times, stroke teams are left with decreased stamina. Understaffing and extended shifts were the results of prophylactic staff quarantine or COVID-19 illness. Many of the stroke physicians and hospital staff around the globe have been infected with SARS-CoV-2. Unfortunately some have passed away, while others are suffering from the consequences of long-COVID syndrome.

Despite the successes in some of the challenges imposed by the COVID‐19 pandemic, the race is not over. In order to reach the finish line with the least possible casualties, healthcare providers and scientific communities should strive not only to maintain the quality of stroke care, but also address the long-standing unmet needs of stroke team members and patients. The invaluable experience gained from this marathon should be used as the ground to set new standards in stroke care when the pandemic is finally over.

REFERENCES

Markus HS, Brainin M. COVID-19 and stroke-a global world stroke organization perspective. Int J Stroke. 2020;15:361–364.
Katsanos AH, Palaiodimou L, Zand R, et al. Changes in Stroke Hospital Care During the COVID-19 Pandemic: A Systematic Review and Meta-Analysis. Stroke. 2021;52:3651-3660.
Khosravani H, Rajendram P, Notario L, et al. Protected Code Stroke: Hyperacute Stroke Management During the Coronavirus Disease 2019 (COVID-19) Pandemic. Stroke. 2020;51:1891-1985
Katsanos AH, Palaiodimou L, Zand R, et al. The Impact of SARS-CoV-2 on Stroke Epidemiology and Care: A Meta-Analysis. Ann Neurol. 2021;89:380-388.
Ferro JM, de Sousa DA, Coutinho JM, Martinelli I. European stroke organization interim expert opinion on cerebral venous thrombosis occurring after SARS-CoV-2 vaccination. Eur Stroke J. 2021;6:CXVI-CXXI.
Aguiar de Sousa D, van der Worp HB, Caso V, Cordonnier C, Strbian D, Ntaios G, Schellinger PD, Sandset EC; European Stroke Organisation. Maintaining stroke care in Europe during the COVID-19 pandemic: Results from an international survey of stroke professionals and practice recommendations from the European Stroke Organisation. Eur Stroke J. 2020 Sep;5(3):230-236.

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