Cerebrovascular Diseases Extra最新文献

Purpose: To evaluate whether fluid-attenuated inversion recovery vascular hyperintensity (FVH) on post-treatment fluid-attenuated inversion recovery (FLAIR) can serve as a surrogate imaging marker of cortical hyperperfusion identified by arterial spin labeling (ASL) in patients with acute ischemic stroke (AIS) after endovascular therapy (EVT).

Materials and methods: We retrospectively enrolled 150 patients with AIS who achieved successful recanalization after EVT. Clinical data and post-treatment magnetic resonance imaging (MRI) sequences including diffusion-weighted imaging (DWI), FLAIR, and ASL were systematically collected. The 150 patients were categorized into four groups based on DWI and FVH status (A: DWI-, FVH-; B: DWI+, FVH-; C: DWI-, FVH+; D: DWI+, FVH+). Perfusion was evaluated within six predefined Alberta Stroke Program Early CT Score (ASPECTS) regions (M1-M6) per patient, yielding a total of 900 cortical regions analyzed. The perfusion status was evaluated based on visual assessment of absolute cerebral blood flow (CBF) maps derived from ASL, followed by statistical analysis.

Results: Among the 900 cortical territories, 250 (27.78%) were classified as Group A, 361 (40.11%) as Group B, 55 (6.11%) as Group C, and 234 (26.00%) as Group D. Inter-rater agreement for evaluating the status of post-treatment FVH was excellent (κ = 0.851). There were significant differences in perfusion characteristics across four groups (p < 0.001). In subgroup analysis, Group C exhibited a higher proportion of hyperperfusion compared to Group A (21.82% vs. 15.20%), although the difference did not reach significance (p = 0.442), while Group D demonstrated a significantly higher percentage of hyperperfusion relative to Group B (48.72% vs. 34.34%, p < 0.001).

Conclusion: Positive FVH may be associated with post-EVT cortical hyperperfusion in AIS patients following successful revascularization.

Objectives This study sought to investigate the severity of intracranial artery calcification (IAC) in relation to white matter hyperintensities (WMH), and whether the association was mediated by cerebral autoregulation (CA). Methods A total of 144 patients with cerebral small vessel disease were included in this study. The severity of WMH was assessed using Fazekas scores in FLAIR-MRI images. On non-contrast head computed tomography (CT) images, the severity of IAC was measured by IAC scores and further classified as intimal or medial calcification. As a proxy of CA, critical closing pressure (CrCP) was determined by analyzing blood pressure-flow velocity relationships in the middle cerebral artery. Mediation analyses were conducted to examine the proportion of mediation of CrCP on the association between IAC and WMH. Results IAC scores were found to be associated with WMH scores (β 0.364; 95% CI, 0.133-0.409; P <0.001). After multivariable adjustment, a statistically significant association was observed between IAC scores and higher CrCP values (β, 0.329; 95% confidence interval [CI], 0.129-0.528; P = 0.001). Mediation analyses revealed that CrCP partially mediated (10.3%) the association between higher IAC scores and increased WMH severity. The proportion of mediation was driven by a medial calcification pattern (13.9%). Conclusions This hospital-based study demonstrated the association between higher IAC scores and the severity of WMH in patients with cerebral small vessel disease, which can be partially mediated by cerebral autoregulation as indicated by CrCP, especially for the patients with predominantly medial calcification.

Introduction: Despite recent advances in stents and stenting techniques, ischemic complications associated with carotid artery stenting (CAS) remain unresolved. Although plaque characteristics have attracted attention as risk factors, only a few studies have focused on access routes. This study aimed to identify ischemic factors following CAS, including access routes and plaque instability, using computed tomography angiography (CTA).

Methods: We retrospectively collected the clinical data of consecutive patients who underwent CAS and preoperative CTA. The access route was evaluated as having aortic plaques and a stenosis at proximal segment lesions beyond carotid plaques (brachiocephalic/common carotid artery). Aortic plaques were further classified based on the presence or absence of calcifications. The outcome was the presence of hyperintense lesions (ipsilateral/non-ipsilateral/bilateral) on postoperative diffusion-weighted imaging (DWI). Multivariate analysis was conducted using two models: aortic plaques (Model 1) and calcified aortic plaques (Model 2).

Results: Among the 115 patients who underwent CAS, the mean age was 74.7 years, and 16 (13.9%) were female. Aortic arch plaques were detected in 33 (28.7%) cases, and calcified plaques in 10 (8.7%). Plaques at proximal segment lesions were detected in 27 (23.5%) cases. DWI lesions were detected in 49 (42.6%) cases; 41 (35.7%) on the ipsilateral side, 19 (16.5%) on the non-ipsilateral side, and 11 (9.6%) bilaterally. The following variables were significantly associated in the univariate analysis: age (ipsilateral, p = 0.005; non-ipsilateral, p = 0.007; bilateral, p = 0.005), proximal segment lesions (ipsilateral, p = 0.04; non-ipsilateral, p = 0.002; bilateral, p = 0.02), aortic plaques (non-ipsilateral, p < 0.001; bilateral, p < 0.001), and calcification (non-ipsilateral, p < 0.001; bilateral, p < 0.001). For ipsilateral lesions, proximal segment lesions were associated in both models (Model 1: odds ratio [OR], 4.30; 95% confidence interval [95% CI], 1.5-13.5; p = 0.006, and Model 2: OR: 4.40; 95% CI: 1.6-13.5; p = 0.004). For non-ipsilateral and bilateral lesions, aortic plaques (non-ipsilateral: OR: 5.33; 95% CI: 1.8-16.5; p = 0.002; bilateral: OR, 13.16; 95% CI: 3.0-93.4; p = 0.001) and calcification (non-ipsilateral: OR: 11.55; 95% CI: 2.6-63.0; p = 0.001; bilateral: OR: 18.51; 95% CI: 3.7-106.5; p = 0.0003) were associated in both models.

Conclusion: Ischemic lesions are likely to occur after CAS, depending on the access route. CTA, which allows the evaluation of access routes, is a useful modality for predicting ischemic lesions after CAS.

Introduction: Spontaneous cervical artery dissection (CeAD) is an important cause of ischemic strokes in young adults. The pathophysiology as well as risk factors are largely unknown. Recurrences are considered rare and primarily to occur within the first 3 months. The frequency of asymptomatic recurrences varies in recent studies. This study seeks to determine the risk of all recurrent dissections in an unselected consecutive patient population after initial diagnosis.

Methods: Of 218 patients referred between October 2014 and December 2024, 102 were included in the final analysis. Patients' medical records were reviewed to determine demographics, including associated risk factors and antithrombotic treatments used. Reports from relevant imaging at routine follow-up and at repeat admissions were acquired to determine recurrence rates of CeAD and new cases of stroke.

Results: 7 (6.9%) patients had CeAD recurrencies after the index event, of which 6 occurred after 6 months and 2 (28.6% of recurrencies) were asymptomatic. A family history of dissections (RR: 6.9, CI: 1.7; 27.3, p = 0.006) or radiologically verified tortuous cervical arteries (RR: 9.8, CI: 2.8; 34.3, p = 0.0003) were significantly associated with recurrence. By 1-year follow-up, 56 patients had persisting vessel sequelae from the index CeAD. Stroke occurrences after the index CeAD was 2.9% (n = 3) and did not occur in patients with CeAD recurrence. All patients received antithrombotic treatment for at least a year.

Conclusion: Recurrence of CeAD and stroke occurrence were low after the index event. CeAD were often asymptomatic and occurred later than previously reported. Long-term, regular follow-up and stroke-preventive treatments are essential to reduce morbidity from repeat CeAD and strokes, especially in patients with relevant family history or known artery tortuosity.

Post-stroke atrial fibrillation (AFib) is a frequent yet undetected complication, particularly in resource-limited settings, where systematic screening remains challenging. Timely identification is essential for guiding anticoagulation strategies and reducing recurrent stroke risk. This scoping review synthesizes evidence on predictive strategies integrating artificial intelligence, circulating biomarkers, and advanced rhythm-monitoring modalities in adults with ischemic stroke or transient ischemic attack without known AFib. Predictive variables from conventional clinical scores and modern AI-based models were harmonized into a unified framework, highlighting incremental contributions from natriuretic peptides, imaging radiomics, and electronic health record-derived laboratory parameters. A novel analytical construct-area under the curve (AUC)-cost-feasibility mapping-was introduced to compare diagnostic strategies, including risk scores, handheld and patch electrocardiography, smartwatch-based photoplethysmography (with ECG confirmation required for diagnosis), and implantable loop recorders, with explicit consideration of scalability in low- and middle-income countries. Based on this synthesis, a tiered diagnostic pathway is proposed, combining clinical risk stratification with biomarker-guided triage (particularly NT-proBNP and MR-proANP) to inform allocation of extended monitoring resources, thereby optimizing diagnostic yield and cost-effectiveness. Persistent knowledge gaps include the absence of standardized biomarker thresholds, limited head-to-head evaluations of AI-enabled workflow in post-stroke populations, insufficient external validation in diverse populations, and a lack of prospective cost-effectiveness analyses. By integrating predictive domains, quantifying performance-cost trade-offs, and outlining an implementation-oriented, risk-stratified strategy, this review aims to inform AFib screening after stroke from theoretical innovation toward context-adapted clinical application, offering a structured framework to guide both research and practice in diverse healthcare environments.

Background: We aimed to describe imaging characteristics in stroke hospitalizations with nonspecific/unspecified vascular region subcodes and to assess for systematic bias in the use of these subcodes.

Methods: We captured first ischemic stroke hospitalizations from 2018-2022 at a single stroke center. We reviewed imaging studies to classify a gold standard of vascular region blinded to ICD-10 subcodes in 200 randomly selected hospitalizations: 100 with nonspecific/unspecified subcodes and 100 with specific subcodes oversampled for posterior circulation strokes. We assessed for systematic bias in the use of nonspecific/unspecified subcodes using multilevel logistic regression, with primary provider included as a random intercept. Separate models were applied to the full population of strokes and to those that underwent imaging review.

Results: We identified 5,234 first ischemic stroke hospitalizations, of which 2,224 (43%) received a nonspecific/unspecified vascular region subcode. Out of the 100 ICD-10 nonspecific/unspecified stroke location cases that underwent imaging review, 85 had acute infarcts in specific locations: 45 anterior circulation, 40 posterior circulation, and 15 with no infarct. Factors associated with the use of nonspecific/unspecified subcodes were low NIHSS scores and non-neurological specialist but not anterior versus posterior vascular distribution. The proportion of variance explained by the models was modest (pseudo-R² 0.16).

Conclusions: Most ischemic stroke hospitalizations coded with nonspecific/unspecified ICD-10 vascular region subcodes had imaging-confirmed infarcts in specific vascular regions. These strokes tended to have a lower NIHSS and were overrepresented by posterior circulation lesions. The modest variance explained in the use of nonspecific/unspecified codes indicates that much of the coding is influenced by random variation or unmeasured factors. Future studies in other healthcare systems are needed to verify these findings and evaluate for other predictors. Researchers using these subcodes should recognize the limitations and incorporate sensitivity analyses to evaluate potential bias in results.

Background: While obesity is a known risk factor for ischemic stroke, its prognostic value remains uncertain. We examined the independent and combined effects of body mass index (BMI) and waist-to-hip ratio (WHR) on early stroke outcomes across subtypes.

Methods: In this prospective cohort study, 714 patients with acute ischemic stroke or TIA were enrolled over six months. BMI and WHR were assessed on admission. Stroke severity (NIHSS) and functional outcome at discharge (modified Rankin Scale, mRS) were recorded. Stroke aetiology was classified using TOAST and ESUS criteria. Multivariable regression and restricted cubic spline models were applied.

Results: A U-shaped association emerged between BMI and both stroke severity and recovery, with overweight patients (BMI 25.0-29.9 kg/m²) showing the lowest NIHSS and highest independence rate (mRS 0-1: 65%). Underweight and obese patients had significantly worse outcomes (p < 0.001). WHR was an independent predictor of higher stroke severity (β = +2.8; 95% CI: 2.1-3.5) and poor outcome (OR = 0.70; 95% CI: 0.52-0.94), and showed additive prognostic value when combined with BMI. A sex-specific interaction suggested a greater benefit from overweight in women (OR = 1.72; p = 0.02). Subtype analysis revealed a U-shaped BMI association in cardioembolic stroke (p = 0.014), but not in ESUS.

Conclusions: BMI and WHR show distinct, nonlinear, and sex- and subtype-specific associations with stroke severity and outcome. WHR outperforms BMI and enhances prognostication when combined. These findings challenge the obesity paradox and support integrating adiposity phenotypes into individualized stroke risk models.

Stroke in Young Adults in Asia Background Stroke in young adults is a worldwide problem with long term physical and socioeconomic implications. The largest burden of disease is expected to impact Asia. Stroke in young adults is defined broadly as strokes occurring between the ages of 18-49 and include ischaemic stroke and intracerebral haemorrhage. The objective of this review is to focus on the important aspects of epidemiology, risk factors, genetic contributions as well as evaluation, management and outcome of stroke in young adults within the Asian context. Summary This publication is an overview of recent literature from many countries in Asia. Population and hospital level data offer insight into common and unique aetiologies of pre-mature ischaemic stroke and intracerebral haemorrhage in young adults. In young adults, prognosis and outcomes were worse in intracerebral haemorrhage compared to ischaemic stroke. Stroke prevention should be emphasized while rapid access to acute stroke reperfusion and interventional therapies can benefit younger patients. More research should be performed in young adults with stroke in order to reduce the short and long term mortality in both stroke subtypes, improve primary as well as secondary prevention and define further the role of next generation sequencing for cryptogenic stroke. Key Messages Stroke in young adults in Asia reveal the interplay between complex genetic factors, traditional risk factors and unique aetiologies. Socioeconomic status and healthcare access are other important factors affecting the care of these patients.

Introduction: Parenteral heparin is widely used as bridging therapy while optimizing oral anticoagulation (OAC). Newer direct-acting OACs (DOACs) attain therapeutic effect very quickly. We report the use of dabigatran as bridging therapy during warfarin optimization for cardioembolic stroke in two patients who opted to receive warfarin for long-term anticoagulation for secondary stroke prevention.

Case presentations: Patient A was a 60-year-old man with hypertension, hyperlipidaemia, and gout who was admitted with a sudden onset of left-sided weakness. Clinically, he was alert but had right gaze preference and left-sided hemiplegia. The clinical diagnosis was of a right cortical stroke. He underwent intravenous tPA augmented with sonothrombolysis - the National Institute of Health Stroke Scale (NIHSS) score fell from 7 to 0. Repeat brain scan showed infarcts in the right frontal and parietal lobes. He was found to have atrial fibrillation (AF) and advised anticoagulation. He opted for warfarin with dabigatran bridging which was started on day 2 of his hospital admission. His International Normalized Ratio (INR) exceeded 2 by day 6 of anticoagulation, at which time the bridging dabigatran was stopped, fixed-dose warfarin was continued, and he was discharged well. On subsequent reviews in the clinic, his INR was in the therapeutic range of 2.0-3.0. He had no bleeding or recurrent ischaemic events during follow-up. Patient B was a 78-year-old man with a hypertension, hyperlipidaemia, and diabetes mellitus. He was admitted after he developed difficulty talking and mild right-sided weakness. Clinically, he was alert but had expressive aphasia and mild right-sided upper limb weakness (NIHSS 6). The clinical diagnosis was of a left cortical stroke. The brain scan showed a left posterior frontal and parietal infarct. He was out of the time window for recanalization therapy and was treated conservatively. He was found to have AF and advised anticoagulation. He opted for warfarin with dabigatran bridging which was started on day 1 of his hospital admission. His INR was almost 2 by day 5 of anticoagulation, at which time the bridging dabigatran was stopped and fixed-dose warfarin continued. He declined daily blood taking - his INR 4 days later was in the therapeutic range of 2.0-3.0. He had no bleeding or recurrent ischaemic events. He underwent rehabilitation uneventfully and was discharged well.

Conclusions: The use of DOACs such as dabigatran as bridging therapy during optimization of OAC is feasible. Compared to heparin as bridging therapy, DOAC has the advantage of oral administration, lower cost, and possibly lower bleeding risks. This novel practice may be applicable in thrombosis in arterial and venous circulations, e.g., ischaemic stroke, deep venous thrombosis, pulmonary embolism.

Introduction: We aimed to determine whether relative hypotension, defined as a systolic blood pressure (SBP) threshold of <140 mm Hg or 160 mm Hg at the time of neuroimaging, was associated with rapid infarct progressor phenotype, as defined by a high hypoperfusion intensity ratio on MISTAR imaging software (DT6/DT2 >0.318) during anterior circulation large-vessel occlusion (LVO) acute ischaemic stroke (AIS).

Methods: In a retrospective cohort study, consecutive patients admitted to a metropolitan comprehensive stroke centre within South Australia between January 2017 and January 2024 with anterior circulation LVO AIS were included. LVO was defined as either carotid terminus or M1 occlusion. Univariable and multivariable logistic regressions were performed.

Results: A total of 477 patients were included (253 [53.0%] female), of whom 163 (34.2%) had an elevated hypoperfusion intensity ratio (HIR). Hypotension, as defined by either SBP of <160 mm Hg (odds ratio [OR]: 1.2, 95% CI: 0.8-1.8) or SBP of <140 mm Hg (OR 1.7, 95% CI 0.8-1.7), was not associated with elevated HIR. Insular cortex ischaemia (OR: 6.1, 95% CI: 1.7-38.9) and ischaemic heart disease (OR: 2.0, 95% CI: 1.3-3.1) were associated with elevated HIR. Smoking history (OR: 0.5, 95% CI: 0.3-0.9) and obesity (OR: 0.4, 95% CI: 0.2-0.8) were associated with lower HIR.

Conclusion: Relative hypotension was not significantly associated with rapid infarct progressor phenotype in anterior circulation LVO AIS. Insular cortex ischaemia and ischaemic heart disease were associated with rapid progression phenotype, whilst smoking history and obesity were associated with slower progression phenotype. Further mechanistic studies to elucidate how systemic comorbidities and regional brain vulnerability contribute to infarct evolution are needed.