International Journal of Stroke最新文献

Background: To estimate the associations of stroke risk with plasma metabolites, metabolic risk score (MRS), the combinations of MRS with hypertension or lifestyle, and lifestyle-related metabolic signature. To assess the improvement of the stroke risk prediction model through the incorporation of MRS.

Methods: A total of 77,315 participants from the UK Biobank were included in this study. Xgboost and LASSO-Cox regression were used to select metabolites and construct MRS. Elastic net regression was utilized to construct the lifestyle-related metabolic signature. Multivariate Cox regression was used to estimate the associations between metabolites, MRS, the combinations of MRS with hypertension or lifestyle, lifestyle-related metabolic signature, and stroke risk.

Results: We identified 48, 63, 39, and 4 metabolites associated with the risk of stroke, ischemic stroke (IS), subarachnoid hemorrhage (SAH), and intracerebral hemorrhage (ICH), respectively. High MRS significantly increased the risk of stroke (HR = 2.65 (95% confidence interval (CI): 2.09-3.35)), IS (HR = 2.45 (95% CI: 1.89-3.17)), ICH (HR = 2.74 (95% CI: 1.55-4.85)), and SAH (HR = 4.64 (95% CI: 2.25-9.56)). In the combination analyses, compared with normal systolic blood pressure (SBP) and low MRS, normal/high SBP, and high MRS significantly increased stroke risk (HR = 5.80 (95% CI: 2.75-12.27)/6.37 (95% CI: 3.22-12.62)). A favorable/unfavorable lifestyle and high MRS also significantly increased stroke risk (HR = 2.38 (95% CI: 1.73-3.28)/3.86 (95% CI: 2.63-5.67)) compared with a favorable lifestyle and low MRS. Incorporating MRS into the 15-year stroke and IS risk prediction model increased the areas under the curves (AUCs) from 0.746 to 0.766 and from 0.771 to 0.811, respectively. The metabolic signature was correlated with adherence to a healthy lifestyle (r = 0.414; P = 2.22e-16) and inversely associated with stroke risk (HR = 0.80 (95% CI: 0.73-0.86)).

Conclusions: Various metabolites and MRS were significantly associated with the risk of stroke, IS, ICH, and SAH. Individuals with a high MRS may face an elevated stroke risk among populations with high SBP or unhealthy lifestyle, even those with normal SBP or healthy lifestyle. MRS provided modest improvement to the stroke risk prediction model. The lifestyle-related metabolic signature could reduce 20% stroke risk.

Background: Emerging evidence indicates a frequent occurrence of atrial fibrillation (AF) detection among patients with established causes of ischemic stroke unrelated to AF. This systematic review and meta-analysis aimed to evaluate AF detection rates in stroke patients with large or small vessel disease, considering the AF detection modality and duration of cardiac rhythm monitoring.

Aims: We conducted a comprehensive search of PubMed and Scopus databases up to 2 March 2024, to identify randomized controlled trials, non-randomized prospective studies, and retrospective studies assessing the frequency of AF detection in stroke patients with large or small vessel disease. The primary outcome of interest was the rate of AF detection. We utilized inverse-variance weights to produce the pooled prevalence (effect size (ES)) and 95% confidence interval (CI) of patients diagnosed with post-stroke AF.

Summary of review: In the analysis of 14 eligible studies encompassing 4334 patients, AF was identified in 154 out of 2082 patients with strokes attributed to small or large vessel disease, yielding a pooled prevalence of 6.27% (ES; 95% confidence interval (CI): 3.18-10.17, I² = 87.83%). Among patients with large vessel disease strokes, AF was diagnosed in 79 out of 1042 patients, accounting for a pooled prevalence of 5.07% (ES; 95% CI: 1.30-10.33, I² = 77.05%). Similarly, among those with small vessel disease strokes, AF was detected in 75 out of 1040 patients, with a pooled prevalence of 5.03% (ES; 95% CI: 1.96-9.06, I² = 78.05%).

Conclusions: AF is often found in ischemic stroke patients with large or small vessel disease. Detection rates increase with longer cardiac rhythm monitoring. The safety and benefits of oral anticoagulation for these AF episodes are uncertain.

Background: Cerebral venous disruption is one of the characteristic findings in cerebral small vessel disease (CSVD), and its disruption may impede perivascular glymphatic drainage. And lower diffusivity along perivascular space (DTI-ALPS) index has been suggested to be with the presence and severity of CSVD. However, the relationships between venous disruption, DTI-ALPS index, and CSVD neuroimaging features remain unclear.

Aims: To investigate the association between venous integrity and perivascular diffusion activity, and explore the mediating role of DTI-ALPS index between venous disruption and CSVD imaging features.

Methods: In this cross-sectional study, 31 patients (mean age, 59.0 ± 9.9 years) were prospectively enrolled and underwent 7-T magnetic resonance (MR) imaging. DTI-ALPS index was measured to quantify the perivascular diffusivity. The visibility and continuity of deep medullary veins (DMVs) were evaluated based on a brain region-based visual score on high-resolution susceptibility-weighted imaging. White matter hyperintensity (WMH) and perivascular space (PVS) were assessed using qualitative and quantitative methods. Linear regression and mediation analysis were performed to analyze the relationships among DMV scores, DTI-ALPS index, and CSVD features.

Results: The DTI-ALPS index was significantly associated with the parietal DMV score (β = -0.573, p corrected = 0.004). Parietal DMV score was associated with WMH volume (β = 0.463, p corrected = 0.013) and PVS volume in basal ganglia (β = 0.415, p corrected = 0.028). Mediation analyses showed that DTI-ALPS index manifested a full mediating effect on the association between parietal DMV score and WMH (indirect effect = 0.115, Pm = 43.1%), as well as between parietal DMV score and PVS volume in basal ganglia (indirect effect = 0.161, Pm = 42.8%).

Conclusion: Cerebral venous disruption is associated with glymphatic activity, and with WMH and PVS volumes. Our results suggest cerebral venous integrity may play a critical role in preserving perivascular glymphatic activity; while disruption of small veins may impair the perivascular diffusivity, thereby contributing to the development of WMH and PVS enlargement.

Background: Estimating the incidence of end-stage kidney disease (ESKD) in stroke survivors is important to assess and predict clinical course, improve post-stroke quality of life, and ultimately reduce health burden.

Aim: Our objective was to assess the risk of ESKD in patients compared to a matched stroke-free control cohort.

Methods: A nationwide retrospective cohort study was conducted in 315,326 stroke subjects and 390,781 matched stroke-free control subjects. Health examination results and claims data were collected from the Korean National Health Insurance Service during 2010-2018. Cox proportional hazard models were used to assess the risk of ESKD in the stroke cohort.

Results: During a mean follow-up period of 4.3 years, the incidence of ESKD was 1.83 per 100,000 person-years in the stroke cohort versus 0.57 per 100,000 person-years in the control cohort. The stroke cohort exhibited a significantly higher risk of developing ESKD compared to the matched control, with an adjusted hazard ratio (aHR) of 1.79 (95% confidence interval (CI) = 1.67-1.93). Stroke survivors were associated with a higher risk of developing ESKD, regardless of the severity of disability (aHRs of 1.93, 95% CI = 1.69-2.21 for severe disability; 1.71, 95% CI = 1.41-2.07 for mild disability; and 1.78, 95% CI = 1.65-1.92 for no disability), compared to the matching control cohort. The elevated risk was observed in both hemorrhagic stroke (aHR = 1.96, 95% CI = 1.73-2.23) and ischemic stroke (aHR = 1.75, 95% CI = 1.62-1.89).

Conclusions: This study demonstrates that stroke patients have a significantly higher risk of incident ESKD. This highlights the need for heightened clinical awareness and improved monitoring of kidney function in this population.

Background- Increased times from symptom onset to puncture (TSOP) and from puncture to reperfusion (TPTR) are associated with worse outcome in ischemic stroke patients treated with endovascular therapy (EVT) in the early time window (<6 hours). However, these associations are less described in the late window (>6 hours), where patients may benefit from EVT because of a more favorable imaging profile (late window paradox). We sought to compare the effect of these timeframes between these two periods on efficacy and safety outcomes.Methods- The ETIS Registry (Endovascular Treatment in Ischemic Stroke) is an ongoing, prospective, observational study in 21 centers that perform EVT in France. We included adult patients with an anterior occlusion, successfully treated by EVT (mTICI 2b-3) between January 2015 and June 2023, with a known time of stroke onset. The cohort was divided into 2 groups according to the TSOP (≤6h vs >6h). Primary outcome was favorable outcome (modified Rankin Scale 0-2 at 90 days).Results- 7,516 patients were included, with 5,936 patients being treated ≤6h and 1,580 >6h. In the early window, TSOP and TPTR were associated with worse outcomes at 90 days (adjusted OR=0.68 per hour; 95%CI, 0.64-0.73; p<0.001 and aOR=0.92 per 10 minutes increment; 95%CI, 0.90-0.94, p<0.001, respectively). TSOP was not associated with worse outcomes at 90 days in the late window (p=0.955), but TPTR was associated with worse outcomes (aOR=0.91 per 10 minutes increment; 95%CI, 0.86-0.96, p=0.001), every 10 additional minutes in TPTR being associated with a 1.7% (95%CI, 0.6%-2.7%) decreased probability of favorable outcome.Conclusions- Only EVT procedural time is associated to unfavorable outcomes at 90 days in late window patients. These results highlight how the late window paradox may end at the start of EVT and underscore the need for timely management, particularly for the EVT, even for late window patients with a presumed more favorable imaging profile.

Despite the progress made in understanding the management and outcomes of Moyamoya angiopathy (MMA), several aspects of the disease remain largely unknown. In particular, evidence on the disease history and management of MMA is lacking, mainly due to methodological and selection biases in the available studies and the lack of large, randomized prospective studies. Therefore, the care of MMA patients remains limited to a few expert centers worldwide, and management is often based on local expertise and available resources. Over the years, recommendations or expert opinions have been written to provide guidance to physicians in the treatment of this condition with the goal of reducing the risk of stroke recurrence and long-term disability. However, there is no complete agreement between the available guidelines and recommendations due to differences in the articles addressed, methodologies, expertise, and validated approaches to literature review. This lack of consensus on the management of MMA may confuse clinicians and highlight some important issues and points. The aim of this comprehensive review article is to critically examine three recent guidelines and recommendations on MMA, discussing their differences and similarities and highlighting gaps in MMA care that need to be covered.

Background: Acute ischemic stroke (AIS) or transient ischemic attack (TIA) is the most common neurological manifestations of patients with antiphospholipid syndrome (APS). Incidental diffusion-weighted imaging (DWI) positive subcortical and cortical lesions, or acute incidental cerebral microinfarcts (CMI), are microscopic ischemic lesions, detectable on MRI for 10-14 days only. We aimed to look at the prevalence of acute incidental CMI in a cohort of patients with APS and their association with subsequent AIS or TIA.

Methods: This is a population-based cohort study of adults with APS diagnosis using International Statistical Classification-9 (ICD-9) and supporting laboratory results between January 2014 and April 2020. We included any patient undergoing brain MRI (index event) during the year prior APS diagnosis or at any time point following diagnosis. Age-matched subjects with negative APS laboratory workup were used as a control group. In the first analysis, we compared acute incidental CMI prevalence in both groups. We then performed a second analysis among APS patients only, comparing patients with and without acute incidental CMI for AIS or TIA as the primary outcome. Cox proportional hazards models used to calculate hazards ratio (HR) and 4 years cumulative risk.

Results: 292 patients were included, of which, 207 patients with APS. Thirteen patients with APS had acute incidental CMI on MRI (6.3%), compared with none in the control group (p = 0.013). Following multivariable analysis, APS was the sole factor associated with acute incidental CMI (p = 0.026). During a median follow-up of 4 years (IQR 3.5, 4) in patients with APS, following multivariable analysis, acute incidental CMI was associated with subsequent AIS or TIA (HR 6.73 [(95% CI, 1.96-23.11], p < 0.01).

Conclusion: Acute incidental CMI are more common among patients with APS than in patients with negative APS tests, and are associated with subsequent AIS or TIA. Detecting acute incidental CMI in patients with APS may guide etiological workup and reevaluation of antithrombotic regimen.

Background: In patients with an acute ischemic stroke, the penumbra is defined as ischemic tissue that remains salvageable when reperfusion occurs. However, the expected clinical recovery congruent with penumbral salvage is not always observed.

Aims: We aimed to determine whether the magnetic resonance imaging (MRI)-defined penumbra includes irreversible neuronal loss that impedes expected clinical recovery after reperfusion.

Methods: In the prospective French Acute Multimodal Imaging Study to Select Patients for Mechanical Thrombectomy (FRAME) and an observational cohort of patients with large vessel occlusions undergoing endovascular treatment, we quantified penumbral integrity by fluid-attenuated inversion recovery (FLAIR) changes. We studied the influence of recanalization status on the evolution of penumbral FLAIR changes and studied penumbral FLAIR changes as predictor of tissue fate and functional outcome on the 90-day modified Rankin Scale (mRS).

Results: Recanalization status did not modify the evolution of rFLAIR signal intensity (SI) over time in the total cohort, but was associated with lower SI in the FRAME subset (b = -0.06, p for interaction = 0.04). Median rFLAIR SI was higher at baseline in the subsequently infarcted penumbra compared to the salvaged (ratio = 1.07, standard deviation (SD) = 0.07 vs 1.03, SD = 0.06 p < 0.0001, n = 150). The severity and extent of rFLAIR SI changes did not predict 90-day functional outcome in univariate (p = 0.09) and multivariate logistic regression (p = 0.4).

Conclusions: Recanalization status did not influence the evolution of penumbral FLAIR changes. FLAIR SI changes in the baseline penumbra were associated with tissue fate, but not functional outcome.

Background and aim: Some patients with intracerebral hemorrhage are on antithrombotic agents at the time of the event and these may worsen outcome, but the relative risk of different oral anticoagulants and antiplatelet agents is uncertain. We determined associations between pre-onset intake of antithrombotic agents and initial stroke severity, and outcomes, in patients with intracerebral hemorrhage.

Methods: Patients with intracerebral hemorrhage admitted within 24 h after onset between January 2017 and December 2020 and recruited to the Japan Stroke Data Bank, a hospital-based multicenter prospective registry, were included. Enrolled patients were classified into four groups based on the type of antithrombotic agents being used on admission. The outcomes were the National Institutes of Health Stroke Scale (NIHSS) score on admission and modified Rankin Scale (mRS) of 5-6 at discharge.

Results: Of a total 9810 patients with intracerebral hemorrhage (4267 females; mean age = 70 ± 15 years), 77.1% were classified into the no-antithrombotic group, 13.2% into the antiplatelet group, 4.0% into the warfarin group, and 5.8% into the direct oral anticoagulant (DOAC) group. Median (interquartile range) NIHSS score on admission was 12 (5-22), 13 (5-26), 15 (5-30), and 13 (6-24), respectively, in the four groups. In multivariable analysis, the prestroke warfarin use was associated with higher NIHSS score (adjusted incidence rate ratio = 1.09 (95% confidence interval (CI) = 1.06-1.13), with the no-antithrombotic group as the reference), but the antiplatelet group (1.00 (95% CI = 0.98-1.02)) and DOAC group (0.98 (95% CI = 0.95-1.01)) were not. The rate of mRS 5-6 at discharge was 30.8%, 41.9%, 48.6%, and 41.5%, respectively, in the four groups. In multivariable analysis, prestroke warfarin use was associated with mRS 5-6 (adjusted odds ratio = 1.90 (95% CI = 1.28-2.81), with the no-antithrombotic group as the reference), but the antiplatelet group (1.12 (95% CI = 0.91-1.37)) and DOAC group (1.25 (95% CI = 0.88-1.77)) were not.

Conclusion: Patients who were taking warfarin prior to intracerebral hemorrhage onset suffered more severe intracerebral hemorrhage as evidenced by higher admission NIHSS and higher discharge mRS. In contrast, no increase in severity was seen with antiplatelet agents.

Background: The global prevalence of ischemic stroke in young adults is increasing, leading to a significant social impact. Fabry disease is a recognized cause of ischemic stroke in young patients, and although disease-modifying treatments are available, further evidence is needed to confirm their effectiveness in reducing the incidence of ischemic strokes.

Aims: This study aimed to identify undiagnosed Fabry disease in young adult patients with ischemic stroke in a Taiwanese cohort.

Methods: This multicenter, prospective cohort study enrolled patients aged 20-55 years who had experienced an ischemic stroke or transient ischemic attack (TIA) within 10 days, from 1 January 2016 to 31 December 2020. Screening for Fabry disease was performed using a dry blood test to measure α-galactosidase activity in male patients and blood globotriaosylsphingosine (lyso-Gb3) levels in female patients. For patients with positive screen results, genetic diagnosis of Fabry disease was pursued through Sanger sequencing of the GLA gene, covering all exons and a segment of intron 4.

Results: A total of 977 patients (659 male, 68%) were enrolled from seven hospitals across Taiwan. Four patients (0.4%, all male) had positive screening results, and two patients (0.2%) were genetically diagnosed with Fabry disease. Case 1 had the GLA c.658C>T mutation and experienced ischemic stroke in the bilateral occipital regions. Case 2 had the GLA c.640-801G>A mutation and experienced an ischemic stroke in the left superficial watershed area.

Conclusion: The prevalence of undiagnosed Fabry disease in this cohort of Taiwanese young adults with ischemic stroke or TIA was 0.3% among the young male population. Understanding the prevalence of undiagnosed Fabry disease in young adults with ischemic stroke could help shape future Fabry disease screening policies.

Data access statement: The collected data will be available upon reasonable request from the corresponding author.