Stroke最新文献

Background: Subarachnoid hemorrhage (SAH) following aneurysmal rupture remains a devastating cerebrovascular event with limited predictive biomarkers. Accurate prediction of aneurysm rupture risk remains a clinical priority, as it could improve risk prediction and reveal potential therapeutic targets. Leveraging UK Biobank proteomic data, we aimed to identify protein markers associated with SAH risk using observational and genetic analyses.

Methods: We analyzed data from 52 916 participants enrolled in the UK Biobank. The analysis involved 3 steps: (1) Longitudinal cox proportional hazards analyses between normalized circulating levels of 2923 proteins and incident nontraumatic SAH (aneurysmal or nonaneurysmal) adjusting for age, sex, ancestry, smoking status, hypertension, hyperlipidemia, and diabetes; (2) Proteins identified in step 1 (false discovery rate-adjusted P<0.05) underwent Mendelian randomization using cis-protein quantitative trait loci; (3) cellular expression profile of significant proteins were examined using single-cell transcriptomic from immunophenotypic atlas of human hematopoietic progenitors.

Results: We identified 123 incident SAH cases; the mean follow-up was 7.06 years (SD, 3.53), the mean age was 59.28 (SD, 7.13), and 62% were females. SLAMF1 (signaling lymphocytic activation molecule family member 1) and NINJ1 (Ninjurin 1) were significantly associated (SLAMF1: HR per SD increase, 2.18 [95% CI, 1.49-3.18]; adjusted P<0.001; for NINJ1: HR, 1.85 [95% CI, 1.43-2.40]; adjusted P=0.004). Mendelian randomization confirmed the association for SLAMF1 (Inverse Variance Weighted approach OR, 1.73 [95% CI, 1.26-2.38]), with directionality supported through reverse Mendelian randomization (P>0.05). Single-cell transcriptomic analysis demonstrated high SLAMF1 expression in CD4-CTM, CD4-activated, and CD4-naive cells, indicating a possible immunologic role in SAH pathophysiology.

Conclusions: Our combined analytical approach identified SLAMF1 as a protein associated with increased SAH risk. SLAMF1, a receptor involved in modulating innate and adaptive immune responses, has been implicated in inflammatory and autoimmune diseases. SLAMF1 and related proteins represent promising biomarkers for SAH risk, potentially enhancing risk stratification, guiding preventive strategies, and informing future therapeutic development. Further research is necessary to explore its mechanistic role in SAH development.

Background: Early neurological deterioration (END) is a frequent complication of acute ischemic stroke. Although END worsens clinical outcomes, standardized treatment strategies remain undefined, resulting in variability in clinical practice. This study examines real-world treatment patterns for END and compares the effects of different strategies on neurological and functional outcomes.

Methods: This study analyzed data from a nationwide, prospective, multicenter stroke registry in South Korea, including patients with noncardioembolic stroke who developed END due to stroke progression between January 2019 and August 2024. END was defined as new or worsening neurological symptoms meeting National Institutes of Health Stroke Scale criteria (≥2-point total or ≥1 point in consciousness or motor subscores) with radiological confirmation. Patients were classified into conservative management, antithrombotics change, and induced hypertension (iHTN). The primary outcomes were neurological improvement, defined as a ≥2-point reduction in the National Institutes of Health Stroke Scale score, and 3-month functional outcome measured by modified Rankin Scale ordinal shift. Secondary outcomes included good functional recovery (modified Rankin Scale score, 0-2) and composite vascular events (death, stroke, and myocardial infarction). Multivariable analyses adjusted for age, sex, prestroke modified Rankin Scale, initial National Institutes of Health Stroke Scale score, vascular risk factors, the TOAST (Trial of ORG 10172 in Acute Stroke Treatment) classification, acute thrombolysis, and laboratory covariates.

Results: Among 3067 patients with END due to stroke progression, 1840 (60.0%) received conservative management, 747 (24.4%) underwent antithrombotic changes, and 480 (15.7%) were treated with iHTN. Neurological improvement occurred in 34.2% of patients, with the highest in the iHTN group (41.5%) compared with the conservative (32.2%) and antithrombotics change groups (34.4%; P<0.001). In adjusted analyses, iHTN increased the odds of neurological improvement (adjusted odds ratio, 1.55 [95% CI, 1.25-1.92]) and a favorable 3-month modified Rankin Scale shift (adjusted odds ratio, 1.24 95% CI, 1.03-1.48]) compared with conservative management, particularly in patients with large artery atherosclerosis. Antithrombotics change showed no significant association with neurological or functional recovery.

Conclusions: In patients with noncardioembolic ischemic stroke who developed END due to stroke progression, iHTN was associated with favorable clinical outcomes.

Background: Cardiovascular and cerebrovascular diseases are significant global health challenges and leading causes of death worldwide. Although there is substantial evidence supporting the positive effects of statins for both primary and secondary prevention of these diseases, evidence is lacking regarding the benefits in people with dementia. This study investigated the associations between statin use and cardiovascular and cerebrovascular hospitalizations in nursing home residents with and without dementia.

Methods: This retrospective cohort study of nursing home residents with and without dementia using insurance claims data was conducted in Germany between January 2015 and December 2019. Propensity score-based models were used to evaluate the association of statin use with hospitalizations due to cerebrovascular and cardiovascular events among nursing home residents with and without dementia. Subgroup analyses were performed based on the presence or absence of atherosclerotic cardiovascular disease, dementia type, presence of hyperlipidemia, and newly prescribed statin use, as well as age groups, care dependency level, and sex.

Results: The final sample included data from 96 162 individuals, 37 262 without dementia, and 58 900 with dementia. Statin use was associated with an increased risk of hospitalization due to cardiovascular or cerebrovascular events among people with dementia (hazard ratio [HR], 1.06 [95% CI, 1.01-1.12]; P=0.023). Moderate and high statin intensity was associated with an increased risk of hospitalization (moderate: HR, 1.15 [95% CI, 1.07-1.23]; P<0.001; high: HR, 1.55 [95% CI, 1.15-2.10]; P=0.005) In subgroup analyses, we found an association between statin use and increased risk of hospitalization among individuals without atherosclerotic cardiovascular disease (HR, 1.30 [95% CI, 1.12-1.52]; P<0.001), with vascular dementia and Alzheimer disease (HR, 1.18 [95% CI, 1.06-1.32]; P=0.003; HR, 1.14 [95% CI, 1.00-1.31]; P=0.047, respectively) as well as among newly prescribed statin users (HR, 2.71 [95% CI, 2.33-3.15]; P<0.001). Among individuals without dementia, we found no differences (HR, 1.03 [95% CI, 0.96-1.11]; P=0.397) in the primary analysis and subanalyses except for the high statin intensity group (HR, 1.51 [95% CI, 1.04-2.19]; P=0.029) and among participants with newly prescribed statins (HR, 1.99 [95% CI, 1.56-2.52]).

Conclusions: In our study, statin use was associated with an increased risk of hospitalization due to cardiovascular or cerebrovascular events among people with dementia. These findings highlight the need for further research and cautious consideration of statin use in people with dementia.

Delays in stroke diagnosis contribute to long-term disability. Many patients still face barriers to effective risk factor management, timely detection, and access to poststroke rehabilitation. The emergence of artificial intelligence-enabled, consumer-facing health technologies offers a transformative opportunity to address these gaps across the stroke care continuum. This review examines the evolving role of artificial intelligence-powered devices, including smartwatches, smartphones, wearable sensors, and ambient home-based technologies, in enabling precision stroke care. For stroke prevention, these tools facilitate scalable monitoring of cardiometabolic and stroke-specific risk factors. For early detection, artificial intelligence algorithms applied to multimodal sensor data can identify subtle neurological impairments and support real-time triage. In recovery, artificial intelligence-enhanced remote monitoring and virtual supervision offer scalable models for delivering personalized rehabilitation outside of specialized centers. Although most of these innovations remain in early development, they signal a paradigm shift toward accessible, individualized, and data-driven stroke prevention and management.

Background: Despite a rising public health burden, there have been few population-based studies of chronic subdural hematomas (cSDH) in the United States. We provide the first estimates of cSDH incidence and mortality in a large, representative U.S. population.

Methods: In a representative 5-county region of Southern Ohio and Northern Kentucky, all adults with cSDH in 2019 and 2020 were identified and adjudicated by study physicians. Incidence rates were estimated and standardized to the US population based on age, sex, and race; 30-day and 1-year mortality rates were also estimated. The cause of death was determined using the National Death Index.

Results: A total of 353 patients with cSDH were identified. The median age was 76 (IQR, 65-85), 231 were men (65.4%), and 78 were Black (22.1%). Clinical frailty was prevalent among patients (the median retrospective score on the clinical frailty scale was 4), and only 128 (36.3%) were functionally unimpaired at baseline. The regional incidence rate was 16.3 cases/100 000 persons/y (95% CI, 13.9-19.0). Incidence was age- and sex-dependent, with men 85 and older having an incidence rate of 354.8 cases/100 000 persons/y (95% CI, 242.7-500.9). When adjusted to national demographics, the estimated overall US incidence rate was 17.3 cases/100 000 persons/y (95% CI, 14.7-19.9). The 30-day mortality rate after cSDH was 9.4% (95% CI, 6.5-12.9), and the 1-year mortality rate was 32.9% (28.0-38.0). Early mortality (≤30 days) was often partly or fully attributed to the cSDH (48.4% versus 16.1%; P=0.0004), whereas the most common causes of later mortality were neurodegenerative and cardiovascular diseases (27.2% and 28.4%, respectively).

Conclusions: Our contemporary population-level data show that cSDH is common in the US and primarily afflicts patients with a high degree of functional impairment and frailty. While short-term mortality is low, longer-term mortality is high and often related to comorbid illnesses.

HIV-associated comorbidities, including cardiovascular and cerebrovascular events, are frequent diseases in people living with HIV. Notably, the prevalence of ischemic stroke is 3× higher in people living with HIV than in noninfected individuals, making it one of the most significant cerebrovascular events in people living with HIV. Despite this close association, the mechanisms involved in the enhanced incidence of ischemic stroke in HIV infection remain poorly understood. A chemokine CCL2 (C-C motif chemokine ligand 2), acting via its receptor CCR2 (C-C chemokine receptor type 2), is a prominent chemoattractant involved in the recruitment of CD4+T cells and monocytes/macrophages, which are primary targets for HIV infection. Due to its role in directing leukocyte migration into the brain and enhancing blood-brain barrier permeability, CCL2 is also a critical mediator of neuroinflammation after brain damage, such as ischemic stroke. In this review, we examine the role of the CCL2/CCR2 signaling pathway in HIV infection, its influence on the progression of ischemic stroke outcome and recovery, and propose the CCL2/CCR2 axis as a possible therapeutic target in people living with HIV.

Background: The health outcomes currently reported in aneurysmal subarachnoid hemorrhage (aSAH) research lack consistency and do not sufficiently reflect what is important to people most affected. The objective of this article was to establish consensus on the aspects of health (domains) clinicians and researchers should measure in aSAH research.

Methods: Informed by 2 international prioritizing surveys (involving 239 participants from over 25 countries and 6 continents), we used established consensus methodology in a hybrid in-person/online consensus meeting to establish which domains of health researchers should measure in aSAH research. Sixty-nine participants with lived experience with aSAH (35%), clinical and research leaders (62%), or from aSAH-related charity (3%) took part. International multidisciplinary working groups established consensus definitions for each domain.

Results: Consensus (>70% endorsement) was sought on a proposed group of 6 domains of health, and failing that, each domain individually. The 6 domains which reached consensus and were formally defined are (1) health-related quality of life, (2) survival, (3) cognition and executive function, (4) functional outcome, (5) delayed cerebral ischemia and cerebral infarction, and (6) rebleeding and aneurysm obliteration.

Conclusions: This International Position Statement reports the consensus process undertaken and the core domain set established to guide the choice of outcomes for evaluating new treatments for aSAH. It will ultimately help shape the future aSAH research agenda.