Current neurovascular research最新文献

Objective: This study aims to identify risk factors for symptomatic intracerebral hemorrhage (ICH) in patients with old cerebral infarction.

Methods: A retrospective cohort study was conducted at Jining First People's Hospital between January 2022 and May 2024, including 287 individuals with a history of prior cerebral infarction. Study participants were classified into two groups based on the presence of symptomatic hemorrhage: those with ICH (n = 96) and those without ICH (n = 191). Logistic regression analysis was employed to identify risk factors associated with cerebral hemorrhage occurring after cerebral infarction in this population.

Results: The incidence of ICH among individuals with prior cerebral infarction was 33.48% (96/287 cases). Univariate regression analysis revealed significant differences between the ICH and the non-ICH groups in alcohol consumption, hypertension, hyperlipidemia, statin therapy, antiplatelet therapy, systolic blood pressure, diastolic blood pressure, glycosylated hemoglobin, platelet-to-lymphocyte ratio, and cerebral microbleeds (CMBs). Multivariate logistic regression analysis revealed that CMB, alcohol consumption, hyperlipidemia, and statin treatment were independent predictors of ICH in individuals with prior cerebral infarction. Additionally, CMB severity was significantly positively correlated with ICH occurrence.

Conclusion: The development of ICH in individuals with prior cerebral infarction is influenced by multiple factors. Effective management of CMBs, control of hyperlipidemia, alcohol abstinence, and careful adjustment of statin therapy are critical for preventing ICH. CMB severity emerges as a particularly strong predictor of ICH risk.

Introduction: Acute ischemic stroke (AIS) is linked to dysregulated immuneinflammatory responses. The platelet-to-high-density lipoprotein cholesterol ratio (PHR) and fibrinogen-to-high-density lipoprotein cholesterol ratio (FHR) have emerged as potential systemic inflammation biomarkers. This study evaluated the association among PHR, FHR, and 6- month functional outcomes in patients with large-vessel occlusion-related AIS (AIS-LVO) treated with endovascular therapy (EVT).

Methods: This single-center retrospective study included AIS-LVO patients undergoing EVT at Beijing Chaoyang Hospital (Jan 2023-May 2024). Demographic, clinical, and preoperative laboratory data were collected, and 6-month outcomes were assessed using the modified Rankin Scale (mRS). Multivariate logistic regression and operating characteristic curves (ROC) analyses were used to evaluate the predictive value of PHR and FHR, with subgroup analyses performed across clinical strata.; Results: A total of 46.76% (123/263) of patients had unfavorable outcomes at the 6-month follow- up. Multivariate analysis revealed that higher preoperative PHR (adjusted odds ratio [aOR] = 1.015; 95% confidence interval [CI], 1.009-1.020; P < 0.001) and FHR (aOR = 1.007; 95% CI, 1.004-1.010; P < 0.001) were independent risk factors for poor functional outcomes at 6 months post-EVT.

Discussion: Findings align with prior links between inflammatory biomarkers and AIS prognosis, extending to EVT-treated AIS-LVO. The utility of PHR/FHR may reflect integration of the prothrombotic-anti-inflammatory pathway, with limitations, including a single-center design and a lack of dynamic inflammatory monitoring.

Conclusion: PHR (PHR AUC=0.727, 95% CI: 0.667-0.788) and FHR (AUC=0.716, 95% CI: 0.655-0.777) independently predict 6-month outcomes, with elevated levels linked to poor prognosis. These markers may reflect synergistic roles in post-stroke inflammation and thrombosis, offering potential for integration into individualized prognostic models to guide early intervention.

Introduction: The impact of integrated glycemic indices on acute ischemic stroke (AIS) prognosis remains unclear. This study assessed the correlation between the stress hyperglycemia ratio (SHR) and the glucose-to-albumin ratio (GAR), mediated by the systemic inflammatory response index (SIRI), and their effects on the 90-day prognosis of AIS patients.

Methods: Between January 2017 and November 2023, 5,313 AIS patients were registered in the Nanjing Stroke Registry. The links are as follows: SHR, GAR, and neurological deficits after AIS were statistically evaluated via univariate logistic regression analysis (ULRA) and multivariate logistic regression analysis (MLRA). Subgroup analyses were conducted to confirm the stability of the outcome. Finally, a mediation analysis of the SIRI was undertaken to investigate the relationship between hyperglycemia status and the outcomes of AIS.

Results: Depending on the modified Rankin scale (mRS) score, there were 815 patients with a poor outcome and 4,498 patients with a better outcome during the mean 90-day follow-up period. ULRA and MLRA revealed that SHR and GAR were strongly related to adverse stroke outcomes after adjusting for covariates. The SHR (Model III: OR = 1.12, 95% CI, (1.03-1.22), p = 0.006). GAR (Model III: OR = 1.22, 95% CI, 1.12-1.34, p < 0.001). SIRI mediated 28.4% (SHR) and 17.2% (GAR) of these effects.

Conclusion: This study highlighted that SHR and GAR were positively correlated with adverse clinical and mortality outcomes in AIS patients at 90 days, partly mediated by the SIRI.

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Background: Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury.

Methods: The Oxygen-Glucose Deprivation/Re-oxygenation (OGD/R) model was employed in primary mouse astrocytes, and the Middle Cerebral Artery Occlusion (MCAO) model was established in mice to mimic ischemia-reperfusion-induced injury. Si-circ0001679, anti-miR- 216, and TLR4 ORF-clone were transfected either in cells or mice to study the molecular mechanisms during I/R-induced injury. Inflammation and oxidative stress were monitored after treatment.

Results: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress.

Conclusion: This study unveiled a novel regulatory axis of circ0001679-miR-216-TLR4 in I/Rinduced brain injury. Targeting circ0001679 may represent a promising therapeutic strategy for I/R-induced brain injury.

Background: Electroacupuncture (EA) exerts a protective role in Blood-brain Barrier (BBB) damage after ischemic stroke, but whether this effect involves the regulation of the pericytes in vitro is unclear.

Methods: The in vitro BBB models were established with brain microvascular endothelial cells (BMECs) and pericytes, and the co-cultured cells were randomly divided into three groups: the control group, oxygen-glucose deprivation/reoxygenation (OGD/R) group and EA group. OGD/R was performed to simulate cerebral ischemia-reperfusion in vitro. EA serum was prepared by EA treatment at the "Renzhong" (GV26) and "Baihui" (GV20) acupoints in middle cerebral artery occlusion/ reperfusion rats. Furthermore, the characteristics of BMECs and pericytes were identified with immunological staining. The cell morphology of the BBB model was observed using an inverted microscope. The function of BBB was measured with transendothelial electrical resistance (TEER) and sodium fluorescein, and the viability, apoptosis, and migration of pericytes were detected by cell counting kit-8, flow cytometry, and Transwell migration assay.

Results: BMECs were positive staining for Factor-VIII, and pericytes were positive staining for the α-SMA and NG2. EA serum improved cell morphology of the BBB model, increased TEER and decreased sodium fluorescein in OGD/R condition. Besides, EA serum alleviated pericytes apoptosis rate and migration number, and enhanced pericytes viability rate in OGD/R condition.

Conclusion: EA serum protects against BBB damage induced by OGD/R in vitro, and this protection might be achieved by attenuating pericytes apoptosis and migration, as well as enhancing pericytes viability. The findings provided new evidence for EA as a medical therapy for ischemic stroke.

Introduction: Early Brain Injury (EBI) significantly contributes to poor neurological outcomes and death following subarachnoid hemorrhage (SAH). The mechanisms underlying EBI post-SAH remain unclear. This study explores the relationship between serial cerebral blood flow (CBF) changes and neurological symptoms, as well as the mechanisms driving CBF changes in the ultra-early stages after experimental SAH in mice.

Methods: SAH was induced by endovascular perforation in male ddY mice. Mice were sacrificed at 6, 12, 24, and 48 h after behavioral tests using the modified neurological score and grid walking test, and CBF was measured via Laser Speckle Flow Imaging (LSFI). Neurofunctional evaluation, CBF analysis, and Western blotting were used to assess SAH-induced damage.

Results: Neurological symptoms were significantly worse at 12 h post-SAH compared to sham (9.5 ± 1.7 vs. 25.6 ± 0.63, respectively; p < 0.0001). CBF was significantly reduced at 12 h post- SAH compared to sham (35.34 ± 8.611 vs. 91.06 ± 12.45, respectively; p < 0.0001). Western blotting revealed significantly elevated thrombin and matrix metalloproteinase 9 levels 12 h post-SAH (p < 0.05).

Conclusion: Our results suggest that microthrombus formation peaked at 12 h post-SAH, potentially causing EBI and worsening neurological symptoms. Microthrombus formation in the ultraearly stages may represent a novel therapeutic target for managing EBI.

Introduction: Post-stroke dysphagia (PSD) is a common complication after acute stroke. It can be effectively alleviated by electroacupuncture (EA) stimulation at the Baihui acupoint; however, the underlying mechanism remains unclear.

Methods: Male ICR mice were used, and the suture occlusion method was employed to establish the middle cerebral artery occlusion (MCAO) mouse model. EA stimulation was applied to the Baihui acupoint for intervention. After treatment, the survival rate of the mice was assessed. Subsequently, a water swallow test was conducted to evaluate the degree of dysphagia in the mice. Additionally, neurological function was assessed through Garcia scoring and measurement of serum Ca²⁺-Mg²⁺-ATPase activity. Fur-thermore, MRI was utilized to evaluate the therapeutic effects of EA on cerebral infarction and edema rates. Then, the antioxidant activity of the EA intervention was assessed by measuring indicators of oxida-tive damage. Finally, the expressions of gamma- aminobutyric acid type B receptor subunit 1 (GAB-ABR1), N-methyl-D-aspartate receptor 1 (NMDAR1) were detected through WB, RT-qPCR, and immu-nofluorescence.

Results: EA intervention effectively increased the survival rate of MCAO mice and alleviated their dysphagia. Additionally, the impaired neurological function of the mice was improved, and cerebral infarction and edema rates were reduced. Furthermore, EA alleviated oxidative stress in mice, reduced damage to neurons in the nucleus ambiguus, and upregulated GABABR1 while downregulating NMDAR1.

Discussion: Although we suggested that EA may exert therapeutic activity for PSD by maintaining the balance of NMDAR1 and GABABR1, this conclusion still requires further experimental validation.

Conclusion: EA stimulation of the Baihui acupoint was effective in treating PSD, which was related to its ability to improve damaged neurons, upregulate GABABR1, and downregulate NMDAR1. These findings provided a new insight into the mechanisms of EA treatment for PSD and serve as a theoretical basis for future clinical research.

Introduction: High On-Treatment Platelet Reactivity (HTPR) is frequently observed after carotid endarterectomy (CEA) or stenting (CAS), but its association with adverse events remains uncertain. This systematic review and meta-analysis evaluate the association between HTPR and recurrent vascular events in these patients.

Methods: EMBASE, PubMed, and Cochrane Library were searched for eligible studies from inception to July 1, 2024. Two independent reviewers screened the records, extracted data, and assessed the bias using predefined criteria. A meta-analysis was conducted using RevMan 5.4 software. The primary outcome was the risk of recurrent ischemic events in patients with HTPR. Secondary outcomes included the risk of hemorrhage and carotid restenosis.

Results: Eight studies involving 1,052 patients were included in the meta-analysis. This metaanalysis found that HTPR significantly increased the risk of adverse vascular events (OR = 2.41, 95% CI: 1.37-4.24), particularly in CAS patients (OR = 1.85, 95% CI: 1.14-2.98), but not in CEA patients (OR = 4.53, 95% CI: 0.52-39.12). Furthermore, HTPR was not significantly associated with an increased risk of bleeding (OR = 0.90, 95% CI: 0.24-3.37) or carotid restenosis (OR = 1.70, 95% CI: 0.38-7.55).

Discussion: This meta-analysis demonstrates that HTPR may increase the risk of recurrent ischemic events in CAS patients, supporting the clinical utility of platelet function monitoring in this population. However, no significant association was observed between HTPR and hemorrhage or restenosis. These findings should be interpreted cautiously due to study limitations, including small sample sizes and heterogeneity in platelet function assessment methodologies. Large-scale prospective studies with standardized protocols are warranted to validate these observations.

Conclusion: HTPR may be associated with an increased risk of recurrent ischemic events in patients undergoing CAS, highlighting the potential value of platelet function monitoring.

Introduction: Although ischemic stroke is associated with complex changes in the autonomic nervous system, the circadian patterns of heart rate (HR) and heart rate variability (HRV) in wake-up stroke (WUS) remain poorly understood. This study compared 24-hour heart rate and HRV patterns between patients with and without WUS.

Methods: This retrospective observational case-control study involved 104 patients with acute ischemic stroke (9 WUS, 95 non-WUS). HRV analysis was performed using a 14-day continuous electrocardiography patch monitor. Time- and frequency-domain HRV metrics were calculated, and 24-hour differences were assessed using generalized additive mixed models (GAMMs), adjusting for confounders.

Results: WUS patients had significantly higher HRs (80.60 ± 12.49 vs. 73.22 ± 14.49 beats per minute, P < 0.001) and lower HRV-measured by SDNN (28.06 ± 21.68 vs. 39.70 ± 25.73 milliseconds, P < 0.001), RMSSD (15.78 ± 12.49 vs. 22.16 ± 19.22 milliseconds, P < 0.001), and pNN50 (1.03% ± 2.78% vs. 2.61% ± 5.15%, P < 0.001)-than non-WUS patients. GAMMs indicated that patients with WUS experienced significant autonomic dysregulation, characterized by higher HRs, lower HRV, and altered circadian rhythms compared to those with non-WUS. These differences were particularly evident during the early morning hours.

Discussion: WUS patients exhibited distinct 24-hour HR and HRV profiles, characterized by higher HRs and reduced autonomic variability compared to non-WUS patients. These differences align with patterns typically associated with lower parasympathetic activity rather than elevated sympathetic tone.

Conclusion: WUS is associated with impaired autonomic regulation and disrupted circadian patterns of HR and HRV.