It was fun and exciting to meet up again with colleagues from all around the world for this year’s ESOC 2025 in Helsinki, Finland. The city embraced us with fine Southern Finnish Sun as Mira Katan and Daniel Strbian welcomed over 4,000 participants from >100 countries. We enjoyed amazing talks and high-quality posters in all different fields of stroke research so far. I got the opportunity to share some of the posters that caught my eye during the session on Wednesday (Conference Day 1) at the networking event.
Among the posters on ACUTE ISCHEMIC STROKE MANAGEMENT, I would like to highlight RESIDUAL RECURRENCE RISK AFTER ATRIAL FIBRILLATION-RELATED STROKE: A SYSTEMATIC REVIEW AND META-ANALYSIS by Jane Buckley et al. from Dublin, Ireland. They argue that there is limited data on the residual risk of recurrent stroke in patients with atrial fibrillation (AF). They did a systematic review and meta-analysis of studies which enrolled patients with prior ischemic stroke and AF and follow-up for ≥1 year. The primary outcome was recurrent ischemic stroke. The secondary outcomes were any recurrent stroke and intracerebral hemorrhage (ICH). The analysis was repeated in patients whose qualifying event occurred despite oral anticoagulation (OAC). Among 21 studies with 76,191 patients (136,186 years follow-up), the median proportion of OAC use across was 91%. The pooled cumulative incidence of recurrent ischemic stroke was 3.67% per year. The risk was higher in observational cohorts (4.14%/year) compared with RCTs (2.26%/year, P heterogeneity <0.001). The risk of any recurrent stroke was 5.11%/year and ICH was 0.62%/year. In patients with stroke despite OAC, the risk was 7.21%/year for ischemic stroke, 8.96%/year for any stroke and 1.4%/year for ICH. They conclude that despite modern prevention therapy, the residual recurrence risk after AF-related stroke is high and exceeds the rate around 2-fold in RCTs and they estimate that 1 in 6 patients will have a recurrent ischemic stroke within 5 years. These data demonstrate an urgent need to develop new secondary prevention strategies after AF-related stroke. Also, these data can serve as a quantitative basis for future intervention trials. The study was published simultaneously in JAMA Neurology doi:10.1001/jamaneurol.2025.1337.
Aino Korhonen et al. from Helsinki, Finland contributed the poster MATERNAL AND NEONATAL TREATMENT OUTCOMES OF PREGNANCY-RELATED ANEURYSMAL SUBARACHNOID HEMORRHAGE – NATIONWIDE REGISTER-BASED OBSERVATIONAL STUDY. They analysed clinical progression, treatment and outcomes of aneurysmal subarachnoid hemorrhage in pregnancy (paSAH) in a nationwide observational study in Finland from 1987-2016. In total, 28 patients were hospitalised with paSAH. In addition, paSAH caused two deaths at home and one death at the emergency department before any treatment. Ten hospitalised patients had lost their conscience at stroke onset. 21 patients were treated by aneurysmal clipping, 4 patients by endovascular coiling and 3 patients by both procedures. Most procedures (n=23, 82.1%) were performed before childbirth. The most frequent method of delivery was elective caesarean section (CS) (n=12, 42.9%) followed by emergency CS (n=9, 32.1%). All children of the hospitalised patients survived. Vasospasm occurred in 5 (17.9%) cases and delayed cerebral ischemia (DCI) in 3 (10.7%) cases. Overall maternal mortality was 9.7% (n=3). There were no deaths during the hospitalisation. The median mRS at 90 days was 1 for the hospitalised patients. They conclude that the outcome of paSAH was encouraging as all hospitalised patients and their unborn children survived and the outcome seems to be reassuring, albeit complications such as vasospasm and DCI occurred in some patients. These data are very important as in pregnant women of all stroke subtypes, studies and outcomes are rather arbitrary and unknown and regarding treatment, clinicians have a rather challenging task to get through.
From the topic INTRACEREBRAL HEMORRHAGE, I would also like to highlight the following poster on ASSOCIATION OF DIRECT ORAL ANTICOAGULANTS AND VITAMIN K ANTAGONISTS WITH INTRACEREBRAL HEMORRHAGE LOCATION by Otto Lankinen et al. from Helsinki, Finland. They tackled the question if intracerebral hemorrhages (ICH) related to oral anticoagulation (OAC) are also predominantly located in cerebellar locations in patients treated with direct oral anticoagulants (DOAC). Previous data indicate that vitamin K antagonist (VKA) associated ICHs are enriched in cerebellar location. They included all non-traumatic ICH patients in a single center cohort from 2015-2019. ICH location and the extent of brain white matter lesions (WML) from the admission brain imaging as well information on OAC use were analysed from medical records. Among 1,020 ICH patients, 49 (4.8%) were DOAC-ICH and 133 (13.0%) VKA-ICH. Interestingly, cerebellar location was overrepresented among DOAC-ICH (N=8, 16.3%) and VKA-ICH (N=14, 10.5%) compared to non-OAC-ICH (N=37, 4.4%, P<0.001). In an adjusted model, cardiovascular comorbidities, WML, DOAC-ICH (OR 5.01) and VKA-ICH (OR 3.36) were independently associated with cerebellar ICH location. DOAC-ICH and VKA-ICH were not associated with supratentorial lobar, supratentorial deep, or brainstem locations. They conclude that both DOAC-ICH and VKA-ICH are overrepresented in cerebellar locations, and the association is even stronger for DOAC-ICH. This warrants further studies to understand pathological mechanisms behind the increased risk for cerebellar ICH in OAC patients e.g. different pathophysiological properties like sympathetic nerve distribution.
Among the PRE-HOSPITAL SERVICE ORGANISATION abstracts I want to emphasise on EPILEPSY AND STROKE: BIOMARKER DISCOVERY AND THERAPEUTIC ADVANCES by Saykha Ilkhomova et al. from Tashkent, Uzbekistan. They highlight the bidirectional relationship of epilepsy and stroke, however, the mechanisms linking these conditions remain poorly understood, and targeted interventions are lacking. They conducted a prospective cohort study involving 750 participants including 250 with post-stroke epilepsy (PSE), 250 with epilepsy without stroke, and 250 controls. Laboratory analyses included inflammatory markers (IL-6, TNF-α) and neurotrophic factors (BDNF). Imaging techniques (MRI, PET) evaluated structural and functional changes. They found that elevated IL-6 and TNF-α levels were significantly associated with PSE (RR = 4.3; p =0.003). Imaging revealed cortical thinning and microvascular dysfunction, prominent in PSE cases (OR = 3.7; p = 0.01). A predictive model combining IL-6, TNF-α, and imaging findings achieved 81% accuracy in identifying high-risk patients (p < 0.001). This study highlights inflammation as a critical link between epilepsy and stroke. This biomarker-driven risk stratification can serve as a basis for targeted anti-inflammatory intervention trials tackling a transformation in the management of PSE.
From the topic CLINICAL PRACTICE, MANAGEMENT AND CARE, the poster FUNCTIONAL STROKE MIMIC A COMPARATIVE COHORT STUDY OF CT-BASED MULTIMODAL NEUROIMAGING AND LONG-TERM OUTCOME by Filipa Bastos et al. from Lausanne, Switzerland caught my eye. They argue that functional stroke-like episodes represent an increasingly recognised stroke mimic (FSM) though little is known about brain perfusion imaging and long-term outcome in these patients. They conducted a retrospective single center analysis from 2003-2017 and gathered data on consecutive patients with FSM who underwent acute perfusion-CT (PCT) and compared them to all contemporaneous acute ischemic strokes (AIS) undergoing PCT from the Acute-Stroke-Registry-and-Analysis-of-Lausanne (ASTRAL). Long-term outcome data were obtained from clinical visits and telephone interviews. In total, 25 FSM and 3201 AIS were included. They found that patients with FSM were significantly younger than AIS (median 43 vs. 73 years), had higher incidence of psychosis/depression-related disorders, and over half had prior history of functional disorders. FSM patients presented with less visual field defects, more decreased vigilance and more sensory deficits. Acute CT-based neuroimaging was essentially normal in FSM, including PCT. IVT rates were similar in both groups (48% vs 43%). Follow-up data for 22/25 FSM patients revealed a lower mRS at 3 and 12 months (median 1 vs. 2, padj <0.01) and lower mortality at 12 months (0% vs 20%, padj 0.04). After a median of 9 years of follow-up, FSM failed to functionally improve more (mRS) and 55% experienced further unexplained neurological events. They conclude that FSM revealed normal acute CT-based neuroimaging, but still high thrombolysis rates. Long-term observation revealed high rates of recurrent functional events and persistent disability, suggesting the need for more effective treatment and regular follow-up in these patients.
The last poster is for all coffee, tea and energy drink consumers out there. In the category DIAGNOSIS / ETIOLOGY I want to highlight the poster ACUTE NON-ALCOHOLIC STIMULANT BEVERAGE CONSUMPTION AS A TRIGGER FOR CRYPTOGENIC ISCHEMIC STROKE IN THE YOUNG: FINDINGS FROM THE SECRETO STUDY by Phillip Ferdinand et al. from Stoke-on-Trent, UK on behalf of the SECRETO study team. The SECRETO study is a multi-center study investigating cryptogenic stroke (CIS) in individuals aged 18-49 years. This analysis investigated the role of non-alcoholic stimulant beverages as potential triggers for CIS in a young population. Beverage consumption during the hazard periods (1 and 2 hours preceding stroke onset) was compared to usual consumption in control periods. A total of 598 patients were included in the analysis. Relative risks (RR) for acute coffee consumption were 1.729 (95% CI 1.056-2.831) during the 1-hour hazard period and 2.147 (95% CI 1.401-3.291) during the 2-hour hazard period. Tea consumption was also linked to elevated risk, with RRs of 3.935 (95% CI 1.036-14.951) at 1 hour and 4.894 (95% CI 1.915-12.503) at 2 hours. Cola or energy drink consumption showed no significant association in the 1-hour hazard period (RR 3.415, 95% CI 0.767-15.206), but a significant risk increase was observed during the 2-hour hazard period (RR 3.696, 95% CI 1.176-11.619). They conclude that acute consumption of coffee, tea, and cola or energy drinks may act as trigger factors for CIS in young adults. These findings highlight the need for awareness of dietary triggers in this population and warrant further investigation into underlying mechanisms. So we better think twice before grabbing a second or third cup of coffee 🙂
I hope my brief summaries inspire you and that you keep your fingers crossed for the final publications of the studies.
