Search Results (196)

Background: While sleep duration’s association with stroke is established, the combined influence of sleep onset time and duration on stroke subtypes remains inadequately explored. Since circadian biology links sleep onset timing to vascular risk via mechanisms operating independently of sleep duration, we quantified their joint contributions to the risk of stroke. Methods: In this population-based cross-sectional study, from 31 December 2021 to 31 March 2022, we recruited 8168 ischemic stroke cases, 3172 intracerebral hemorrhage cases, and 13,458 control participants across 152 survey centers in 28 counties in Hunan Province, China. Standardized computer-assisted interviews collected sleep parameters. Conjoint analysis identified protective sleep profiles. Results: Short sleep duration (<6 h) was consistently associated with elevated ischemic risk across all sleep onset times (p < 0.05 in all cases, i.e., sleep before 10 p.m. [odds ratio (95%CI): 1.886(1.606, 2.214)], 10–11 p.m. [1.740(1.336, 2.265)], 11 p.m.–12 a.m. [2.335(1.190, 4.581)], and after 12 a.m. [2.834(1.193, 6.728)]). A sleep duration of 6–8 h with a sleep onset time between 10 p.m. and 12 a.m. was associated with the lowest ischemic risk (p < 0.001 in all cases). Conversely, prolonged sleep (>8 h) with an early sleep onset time (<10 p.m.) increased ischemic risk (OR 1.194, 95% CI 1.090–1.308, p < 0.001), whereas a late sleep onset time (11 p.m.–12 a.m.) in long sleepers was protective (OR 0.580, 95% CI 0.352–0.956, p < 0.001). Similar trends were observed for ICH, though the effect sizes were attenuated. Conclusion: Sleep duration and onset time interact to influence stroke risk. Optimal cerebrovascular protection requires ≥6 h of sleep, ideally initiated between 10 p.m. and 11 p.m. These findings highlight sleep optimization as a potential modifiable target for high-risk populations. Full article

Background/Objectives: The accurate evaluation of stroke etiology in basilar artery occlusion (BAO) remains underexplored. This study aimed to explore a simple and practical method for predicting the in situ atherosclerotic thrombosis (ISAT) subtype of BAO. Methods: We retrospectively analyzed patients diagnosed with BAO at our institution between April 2015 and April 2025. ISAT was characterized by moderate-to-severe stenosis (>50%) at the occlusion site on angiography, while the cardioembolism (CE) subtype was defined as sudden-onset arterial occlusion with evidence of a cardiac source of embolism. The location of BAO was classified based on cerebral angiography findings as proximal, middle, or distal. Clinical and imaging characteristics were compared between CE and ISAT subtypes. Results: Among 33 patients, 8 (24%) were classified as having the ISAT subtype. Multivariable analyses revealed that the presence of atrial fibrillation (AF) (OR 0.03; 95% CI, 0.00–0.56) and a non-proximal occlusion site (i.e., middle or distal) (OR 0.02; 95% CI, 0.00–0.27) were independently associated with ISAT. Patients were stratified into four groups based on the presence or absence of proximal occlusion and AF. CE subtypes predominated in groups with either AF or no proximal occlusion (25/27, 93%), whereas ISAT was present in all patients with both proximal occlusion and absence of AF (6/6, 100%). The area under the curve for this classification was 0.955. The sensitivity, specificity, positive predictive value, and negative predictive value for diagnosing ISAT were 75%, 100%, 100%, and 93%, respectively. Conclusions: A simple classification based on the presence of proximal occlusion and AF status suggested the potential to facilitate preprocedural differentiation of ISAT subtype in BAO. Full article

Background: Dilated cardiomyopathy (DCM) is a major cause of heart failure and arrhythmic mortality; yet, its association with cerebrovascular events, particularly in the absence of atrial fibrillation (AF), remains insufficiently explored. Purpose: This study aimed to determine the prevalence, mechanisms, and anatomical distribution of stroke in patients with DCM and to assess the role of AF and structural remodeling in stroke risk. Methods: We retrospectively analyzed 471 patients who died with DCM at the Emergency County Clinical Hospital of Bihor between 1 January 2022 and 31 December 2024. Clinical records, neuroimaging, autopsy reports, and histopathological data were reviewed. Stroke subtypes were classified according to TOAST criteria (large artery atherosclerosis, cardioembolic, small vessel disease, other determined, undetermined) and hemorrhagic categories (intracerebral, subarachnoid). Demographic, echocardiographic, and comorbidity data were compared between patients with and without cerebrovascular events. Results: Of 471 patients with DCM, 45 (9.6%) had concomitant stroke: pure ischemic in 32 (71.1%), 7 (15.6%) showed ischemic with hemorrhagic transformation, and primary hemorrhagic in 6 (13.3%). The parietal lobe was most frequently affected. AF was present in 26 patients (57.8%) and was significantly associated with ischemic stroke (p = 0.004), though embolic strokes also occurred in sinus rhythm. Patients with stroke had significantly lower left ventricular ejection fraction (28.0 ± 13.7% vs. 34.0 ± 11.2%, p = 0.007) and larger atrial dimensions. Histopathological findings confirmed acute and chronic ischemic injury patterns, including “red neurons,” white matter vacuolization, and gliotic scarring. Conclusions: Stroke is a frequent and often underdiagnosed complication in DCM, predominantly ischemic and embolic in nature. Importantly, embolic events were observed even in patients without AF, suggesting that atrial remodeling in DCM may independently predispose to cerebrovascular risk. These results underscore the need for refined preventive strategies, including careful atrial assessment and exploration of whether anticoagulation may benefit selected high-risk DCM patients without AF, a question that requires confirmation in prospective trials. Potential embolic sources in DCM include atrial cardiopathy and left ventricular thrombus in the setting of severe systolic dysfunction; therefore, careful ventricular as well as atrial assessment is warranted in high-risk DCM. Full article

Background: Accurate localization of internal carotid artery (ICA) occlusion is critical for optimizing endovascular thrombectomy (EVT) strategies. Conventional multiphase CT angiography (mCTA) often omits the carotid bifurcation in delayed phases, limiting differentiation between true cervical ICA occlusion and pseudo-occlusion. Methods: We retrospectively analyzed 56 acute ischemic stroke patients with ICA occlusion who underwent EVT and extended-range mCTA between 2016 and 2020. The scan range of the second and third arterial phases was modified to include the carotid bifurcation. Imaging patterns were evaluated to distinguish bifurcation stenosis with superimposed occlusion from proximal ICA occlusion, and to infer thrombus location by comparing arterial opacification levels across phases. Results: Extended mCTA significantly improved visualization of ICA enhancement patterns in delayed phases (p < 0.001). Cases with bifurcation stenosis showed consistently lower and stable opacification levels across phases, whereas proximal ICA occlusion demonstrated progressive contrast advancement. Distal occlusion, particularly beyond the ophthalmic artery, showed higher opacification. Including the carotid bifurcation increased scan length by ~10%, with acceptable radiation exposure. Conclusions: Incorporating the carotid bifurcation into delayed mCTA phases enhances the ability to differentiate occlusion subtypes and estimate thrombus location. This refined imaging approach enables better EVT planning, including device selection and procedural timing, thereby improving patient outcomes in acute stroke care. Full article

Acute ischemic stroke (AIS) is one of the leading global causes of mortality and morbidity. Clearer understanding of stroke etiology is a major clinical objective to determine appropriate strategies for secondary stroke prevention. Histological and molecular analysis of clots retrieved during mechanical thrombectomy (MT) in AIS offers a unique opportunity to study clot composition and its relation to stroke etiology. The field of clot composition analysis has undergone substantial growth in recent years, driven in part by the establishment of MT as the standard of care, as well as its expanding indications. Although many features differ between large-artery atherosclerosis (LAA) and cardioembolic (CE) clots, application of these findings to predicting stroke etiology at a clinical level remains challenging. Moreover, a significant number of patients have multiple comorbidities or suffer a cryptogenic subtype. Next-generation techniques such as multiomic sequencing offer a powerful potential to elevate our understanding of clot pathology and provide the level of granularity required for clinical diagnosis and management. Herein, we provide an updated review of the current state of the field by exploring stroke etiologies and their relationship to clot pathology, including classic histologic features as well as more recent, emerging results from proteomic and transcriptomic analyses. Full article

Background/Objective: Plant-based diets are gaining global attention for their positive impact on health and sustainability; however, the nutritional value and health effects differ across plant food categories. We investigated the association of three plant-based diet indices and incident cardiovascular disease (CVD) and its subtypes. Methods: This study consisted of 10,030 Korean adults aged 40–69 years from the Korean Genome and Epidemiology Study (KoGES) in Ansan and Ansung. Using a validated food frequency questionnaire from the community-based cohorts of the KoGES, we derived three dietary indices based on food intake: (1) Overall Plant-Based Diet Index (PDI), (2) Healthful Plant-Based Diet Index (hPDI), and (3) Unhealthful Plant-Based Diet Index (uPDI). We analyzed the association between three plant-based diet indices and the incidence of CVD using a multivariate Cox proportional hazards regression model, adjusted for demographic and other CVD risk factors. Results: During 99,751 person-years, 597 CVD cases occurred. None of the three plant-based diet indices (PDI, hPDI, uPDI) were significantly associated with overall risk of CVD. When stratifying results by types of CVD, individuals with the highest adherence to uPDI had a higher risk of coronary heart disease (CHD), compared to the lowest group [HR (95% CI) = 1.62 (1.12–2.33), p-trend = 0.008], but not stroke [HR (95% CI) = 0.97 (0.66–1.42), p-trend = 0.964]. There were no associations between adherence to PDI and hPDI and the incidence of CHD and stroke. Conclusions: In this prospective cohort of Korean adults, none of the three plant-based diet indices were associated with CVD risk, whereas higher adherence to an unhealthful plant-based diet was associated with increased risk of CHD, but not stroke. These findings highlight the importance of plant food quality in CHD prevention and warrant confirmation in other populations. Full article

Background/Objectives: Stroke is a cerebrovascular disorder characterized by vessel occlusion or rupture, resulting in brain damage and subsequent physical impairment. Recent studies have implicated hevin–calcyon protein binding in the repair of brain injury. Secreted protein acidic and rich in cysteine–like 1 (SPARCL1) encodes hevin. This study investigated SPARCL1 gene polymorphisms in ischemic stroke to identify potential biomarkers for brain injury treatment. Methods: we examined the associations of SPARCL1 polymorphisms (rs1049544, rs1130643, rs7695558, rs1049539) with ischemic stroke. This case–control study involved 387 controls and 509 patients with ischemic stroke. Genotyping was performed via real-time polymerase chain reaction with the TaqMan™ SNP Genotyping Kit. Results: The rs1049544 polymorphism was significantly associated with ischemic stroke prevalence (GG vs. CC: adjusted odds ratio [AOR] = 0.642, p = 0.043; GG + GC vs. CC: AOR = 0.671, p = 0.045). Additionally, rs1049544 was significantly associated with large-artery disease prevalence (GG vs. CC: AOR = 0.489, p = 0.028; GG + GC vs. CC: AOR = 0.527, p = 0.033), and rs1130643 (TT vs. TC: AOR = 0.362, p = 0.039) was associated with cardioembolism prevalence in ischemic stroke subtype analysis. In haplotype analysis, G-G (rs1049544/rs7695558; odds ratio = 4.942, p = 0.001) and C-T (rs1049544/rs1049539; odds ratio = 0.776, p = 0.043) haplotypes were associated with ischemic stroke prevalence. Although some genotypes were not individually associated with ischemic stroke, the presence of the rs1049544 C allele appeared to enhance risk. Conclusions: These findings suggest that SPARCL1 polymorphisms are associated with ischemic stroke and may be considered potential biomarkers for risk assessment. Full article

Aneurysmal subarachnoid hemorrhage (aSAH) is a severe stroke subtype often complicated by symptomatic cerebral vasospasm (sVP), contributing to delayed cerebral ischemia and poor outcomes. Immune dysregulation, particularly T-cell imbalances and pro-inflammatory cytokines, is implicated in vasospasm development. Soluble immune checkpoint proteins—CTLA-4 (sCTLA-4) and PD-L1 (sPD-L1)—regulate immune homeostasis and may serve as biomarkers or modulators of inflammation in aSAH. This prospective cohort study included 179 aSAH patients, divided into sVP+ (n = 48) and sVP− (n = 131), plus 50 healthy controls. Serum sCTLA-4 and sPD-L1 levels were measured on days 1, 5, and 9 post-ictus using Luminex xMAP. Associations with clinical outcomes were analyzed using non-parametric statistics and hierarchical clustering. Both sCTLA-4 and sPD-L1 were significantly elevated in sVP+ patients versus sVP− and controls, increasing over time. sCTLA-4 was significantly higher in sVP+ on days 5 (p = 0.001) and 9 (p < 0.001), and sPD-L1 on days 5 and 9 (both p < 0.001). Clustering revealed distinct expression patterns between sVP+ and sVP− groups. Elevated sCTLA-4 and sPD-L1 levels are associated with sVP after aSAH and may serve as biomarkers for early immune dysfunction, offering insights into potential therapeutic targets. Full article

Introduction: Previous studies have reported sex differences in stroke. There are few Asian studies. This study was performed to investigate sex differences in stroke risk factors and mechanisms in a multi-ethnic Asian population. Methods: Data on patients admitted to Raffles Hospital for stroke were analysed. Data were extracted on sex, age, hypertension, diabetes mellitus (DM), hyperlipidaemia, smoking, heart disease, and prior cerebrovascular events (pCeVD). Stroke was subtyped into haemorrhagic stroke (HS) or ischaemic stroke (IS) based on brain scan. IS mechanism was categorised using Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, while the clinical syndrome by Oxfordshire Community Stroke Project (OCSP) classification. Results: Data were collected on 1165 patients, mean age 65.6 ± 12.9 yr; 47.4% female, 83.0% Chinese, with hypertension (63.5%) and hyperlipidaemia (60.3%) being the most common risk factors. HS comprised 23.5%. On regression analysis, compared to males, females had older age (OR 1.03, 95%CI 1.02–10.4) and DM (OR 1.60, 95%CI 1.11–2.30), but less smoking (OR 0.09, 95%CI 0.07–0.13), pCeVD (OR 0.67, 95%CI 0.49–0.93), and HS (OR 0.71, 95%CI 0.51–0.98). There were no differences in HS mechanisms, or IS mechanisms or syndromes. Sex–ethnic differences were found (p < 0.001), with more Chinese and fewer Indians among females compared to males. Conclusions: This study corroborates previous studies of significantly older age and more diabetes mellitus, but less smoking and haemorrhagic stroke among female stroke patients compared to males; differences in HS and IS mechanisms were not found. Novel in this study is that sex–ethnicity differences were found. Future studies should prospectively validate these sex/ethnic differences. Full article

Background: Stress hyperglycemia (SH), a transient elevation in blood glucose levels during acute stress such as stroke, has been increasingly recognized as a critical determinant of clinical outcomes. This review aims to evaluate the association between SH and clinical outcomes across different stroke subtypes and its role as a prognostic indicator. Methods: The current literature review was conducted through a comprehensive literature search of PubMed, Scopus, and Web of Science electronic databases. Initial title and abstract screening was conducted by two independent reviewers depending on the relevance to the topic of interest. Final study inclusion was based on the clinical relevance and agreement between reviewers. Results: Current evidence links SH with higher stroke severity (Higher national institutes of health stroke scale (NIHSS)), larger infarct volumes, increased risk of hemorrhagic transformation, and worse functional recovery (Lower modified rankin scale (mRS)), especially in ischemic stroke. In hemorrhagic stroke, SH is associated with hematoma expansion, perihematomal edema, and worsening neurological function. Although SH has been shown to be a reliable stroke outcome predictor, there is no scientific consensus regarding the most reliable measurement method. The use of absolute blood glucose values may not accurately reflect SH, particularly in diabetic patients, where chronic baseline hyperglycemia complicates interpretation. This underscores the necessity for individualized assessment rather than a uniform interpretation. Clinically, the early detection of SH may provide enhanced monitoring and supportive care; however, rigorous glucose management remains contentious due to the risk of hypoglycemia. Conclusions: This review synthesizes evidence from recent studies and supports SH as a prognostic marker of both short- and long-term adverse outcomes in stroke patients. Further research is warranted to evaluate the efficacy of targeted glycemic treatments on such outcomes. Full article

Ischemic stroke is a complex, multifactorial disorder with a significant heritable component. Recent developments in genome-wide association studies (GWASs) have identified several common variants associated with clinical outcomes, stroke subtypes, and overall risk. Key loci implicated in biological pathways related to vascular integrity, lipid metabolism, inflammation, and atherogenesis include 9p21 (ANRIL), HDAC9, SORT1, and PITX2. Although polygenic risk scores (PRSs) hold promise for early risk prediction and stratification, their clinical utility remains limited by Eurocentric bias and missing heritability. Integrating multiomics approaches, such as functional genomics, transcriptomics, and epigenomics, enhances our understanding of stroke pathophysiology and paves the way for precision medicine. This review summarizes the current genetic landscape of ischemic stroke, emphasizing how evolving methodologies are shaping its prevention, diagnosis, and treatment. Full article

Intracerebral hemorrhage (ICH), a severe stroke subtype common in the elderly, often results in high morbidity and mortality, with limited treatment options for long-term recovery. While glial scar formation is increasingly recognized as key to central nervous system (CNS) repair, its role and characteristics in the aging brain post-ICH remain unclear. This study investigated glial scar formation after ICH (100 μL autologous blood injected into the right basal ganglia model) in aged Fischer 344 rats and assessed the effects of deferoxamine (DFX) treatment. Histological and immunohistochemical analyses were conducted on days 7, 28, and 60 post-ICH using cell-specific and iron-related markers, with DFX administered at 100 mg/kg daily for 14 days in separate groups. Over time, the lesion core showed increased hemosiderin accumulation and astrogliosis. By day 60, the area of astrogliosis corresponded to an area with persistent neuronal loss (DARPP-32-negative). Glial composition shifted from microglia dominance on day 28 to astrocyte predominance by day 60. DFX treatment reduced iron deposition, astrogliosis, and DARPP-32-negative regions while enhancing oligodendrocyte presence. Iron-related markers (HO-1, ferritin, Perls’ staining) and PDGFRβ-positive fibrotic cells were concentrated in the scar core. These findings provide novel insights into scar formation after ICH in aged rats and suggest DFX as a potential therapy to improve outcomes in elderly stroke patients. Full article

Amyloidosis, often referred to as “the great imitator”, is a condition characterized by the abnormal deposition of amyloid proteins in various tissues, potentially leading to organ dysfunction. When these deposits localize in the brain, they can disrupt neurological function and present with diverse clinical manifestations, making diagnosis particularly challenging. Cerebral amyloidosis is a rare entity that frequently mimics other neurological disorders, often resulting in significant delays in recognition and management. This case highlights the diagnostic challenge posed by cerebral amyloidosis and underscores its unique presentation. We present the case of a 76-year-old male with a history of rheumatoid arthritis (RA) who developed progressive right-sided weakness over several months. Three years prior, he experienced numbness on the right side of his face and upper limb. Initial imaging identified a small lesion in the left thalamic region, which was originally diagnosed as a glioma. However, due to the worsening of his clinical symptoms, further evaluation was warranted. Subsequent imaging revealed lesion growth, prompting a biopsy that ultimately confirmed the diagnosis of intracerebral amyloidoma. This case underscores the necessity of considering amyloidosis in the differential diagnosis of atypical neurological deficits, particularly in patients with systemic inflammatory conditions such as RA. The initial presentation of hemiparesis resembling a stroke, coupled with non-specific imaging findings and a prior misdiagnosis of glioma, highlights the complexity of cerebral amyloidosis. Only through brain biopsy was the definitive diagnosis established, emphasizing the need for improved diagnostic modalities to facilitate early detection. Further subtyping of amyloidosis, however, requires mass spectrometry-based proteomics or immunohistochemistry to accurately identify the specific amyloid protein involved. Clinicians should maintain a high index of suspicion for cerebral amyloidosis in patients with RA who present with progressive neurological deficits and atypical brain lesions. Early recognition and accurate diagnosis are essential to guiding appropriate management and improving patient outcomes. Full article

The causal nature of sex hormone-binding globulin (SHBG) in the pathogenesis of stroke remains uncertain. We explored whether SHBG levels are causally associated with stroke via cardiometabolic traits. A network two-sample Mendelian randomization (MR) study was conducted to determine the mediating roles of cardiometabolic traits in the causal effects of SHBG levels on stroke subtypes. Further two-sample MR analyses were performed to explore the inverse associations between significant cardiometabolic mediators and SHBG levels. The MR results indicated a protective effect of genetically increased SHBG levels on any stroke (odd ratio [OR] = 0.941; 95% confidence interval [CI]: 0.898, 0.984), any ischemic stroke (OR = 0.951; 95% CI: 0.922, 0.981), and small-vessel stroke (OR = 0.871; 95% CI: 0.765, 0.977). Moreover, genetically elevated SHBG levels were associated with lower waist circumference (WC, β = −0.091; 95% CI: −0.136, −0.046), waist-to-hip ratio (WHR, β = −0.057; 95% CI: −0.084, −0.030), triglycerides (TG, β = −0.188; 95% CI: −0.249, −0.127), systolic blood pressure (β = −0.799; 95% CI: −1.068, −0.530), and diastolic blood pressure (β = −0.436; 95% CI: −0.605, −0.267), and a reduced risk of type 2 diabetes mellitus (OR = 0.684; 95% CI: 0.400, 0.968) in both the discovery and replication datasets. The proportions of such cardiometabolic traits that mediated the causal effects of SHBG levels on any stroke, any ischemic stroke, or small-vessel stroke ranged from 17.8% to 52.7%; while the mediating effects of SHBG levels on the causal associations between WC, WHR, and TG and stroke ranged from 18.4% to 68.3%. Our findings suggest a protective effect of genetically elevated SHBG levels on stroke risk via key cardiometabolic mediators, primarily WC, WHR, and TG. The mediating roles of SHBG levels in the causal links from WC, WHR and TG to stroke risk were also established. These pathways support SHBG as a potential biomarker and therapeutic target in stroke prevention. Full article

Background/Objectives: The hemoglobin-to-red blood cell distribution width (RDW) ratio (HRR) reflects the status of inflammation and oxidative stress size. Previously, it has been suggested that HRR is associated with cardiovascular diseases (CVD). However, evidence has been limited for examining the association between HRR and the incidence of specific cardiovascular events (e.g., cardiovascular disease, stroke, congestive heart failure) and all-cause cardiovascular death and non-cardiovascular death, adjusting for known confounders. Methods: Data from the National Health and Nutrition Examination Survey (NHANES) in the year cycle of 1999–2018 were collected. HRR was calculated as the ratio of hemoglobin divided by the RDW. The outcomes were CVD, including stroke, congestive heart failure, atherosclerotic cardiovascular diseases (ASCVD), coronary artery disease as well as all-cause death including cardiovascular death and non-cardiovascular death. Univariate and multivariate analyses were performed to explore the association between HRR and outcomes. Restricted cubic spline curves were delineated. Results: In total, 47,719 participants were eligible for further analysis. In multivariate analysis adjusting for all confounding factors, higher HRR levels were significantly associated with a decreased risk of CVD. Compared to Q1 (<9.86), the odds ratio (OR) and 95% confidence intervals (95% CI) in Q2 (9.86–10.96), Q3 (10.96–11.97), and Q4 (≥11.97) were 0.79 (0.66, 0.94), 0.59 (0.48, 0.73), and 0.53, (0.42, 0.67), respectively, for predicting CVD. Similar results were observed for different subtypes of CVD, including stroke, congestive heart failure, and ASCVD. Notably, for predicting coronary heart disease, only Q3 was significant compared to Q1 (0.70, [0.54, 0.92], p = 0.010). HRR was significant for predicting all-cause death, cardiovascular death, and non-cardiovascular death. Additionally, HRR had the highest discriminative ability for predicting all-cause death compared with that of hemoglobin and RDW. Conclusions: A higher HRR was associated with a lower risk of CVD and death. Moderate levels of HRR were associated with the lowest risk for coronary heart disease. HRR had better discriminative ability than hemoglobin and RDW. Full article