Brain Circulation最新文献

Background: Chronic inflammation plays an essential role in the occurrence and progression of cardiometabolic diseases (CMDs). We aim to examine the association between a novel inflammatory biomarker Systemic Inflammatory Response Index (SIRI) and different cardiometabolic multimorbidity (CMM) statuses.

Methods: This was a cross-sectional study that includes general participants of the National Health and Nutrition Examination Survey database from 1999 to 2018. SIRI was calculated as neutrophil count × lymphocyte count/monocyte count. The CMDs were defined as a series of diseases including diabetes mellitus (DM), heart disease (HD), and stroke. We explored the association of SIRI with outcomes with weighted multivariable logistic regression models weighted restricted cubic spline. The diagnostic value of SIRI was evaluated using weighted receiver operating characteristic (ROC) curves.

Results: A total of 43,345 participants were enrolled with a mean age of 45.86 years. The weighted prevalence of CMD and CMM was 17.14% and 2.94%, respectively. Compared to those without CMD, the adjusted odds ratios (95% confidence interval) for each unit increase in SIRI were 1.14 (1.09-1.19) for DM, 1.13 (1.07-1.19) for HD, 1.11 (1.04-1.19) for stroke, 1.17 (1.12-1.22) for CMD, and 1.16 (1.10-1.23) for CMM, according to the weighted multivariable logistic regression. Elevated SIRI level was independently associated with increased CMM. There was no interaction found in subgroup analysis. According to the ROC analysis, SIRI had a superior diagnostic ability to neutrophil-lymphocyte ratio, platelet-lymphocyte ratio, and monocyte-lymphocyte ratio for CMD (area under the curve [AUC] =0.581) and CMM (AUC = 0.633).

Conclusions: Elevated level of SIRI was positively associated with the prevalence of DM, coronary artery disease, stroke, CMD, and CMM, suggesting that SIRI could be a potential noninvasive biomarker for CMD and CMM.

Background and aims: Cerebral aneurysms are a potentially life-threatening condition for humans. Due to the anatomical variability of different aneurysm types in human patients, animal models are indispensable for endovascular research. The aim of our study was to evaluate an endovascular aneurysm model in chronical experiments using 12 female Aachen minipigs.

Materials and methods: For aneurysm creation in external carotid and subclavian arteries, Amplatzer vascular plugs were used as occlusion devices, leaving simple stumps that serve as surrogate aneurysms. If necessary and anatomically possible, additional embolic materials, such as coils and liquid embolic agents were used.

Results: We created 42 aneurysms. Aneurysm creation was possible without complications in all cases. There was no spontaneous thrombosis of fabricated aneurysms. Complete perfusion arrest behind the fabricated aneurysm was challenging but achieved in 45% of cases. We were not able to identify significant factors that have an impact on the persisting perfusion of fabricated aneurysms on final imaging, particularly not the presence of side branches in the aneurysm lumen (P = 0.734) or volumes of the fabricated aneurysms (P = 0.620). Albeit not significant, the use of additional occlusive measures (coils, liquid embolic agents) and antithrombotic drugs (ASA, heparin and tirofiban) may be factors for persisting perfusion: Perfusion arrest behind the fabricated aneurysm was twice as high in animals treated with ASA and heparin compared to animals treated with ASA, heparin, and tirofiban (48% vs. 22%; P = 0.149).

Conclusion: Despite its limitations, including persistent perfusion and impaired predictability for long-term experiments, the endovascular aneurysm model shows potential to replace certain surgical models and offers broad applications in biomedical research and aneurysm therapy.

Background: Acetylcholinesterase inhibitors (AChEIs) are widely used in Alzheimer's disease (AD). This study aims to systematically review the literature about movement disorders (MDs) associated with AChEIs for AD, which include donepezil, galantamine, rivastigmine, tacrine, and ipidacrine.

Methodology: Two reviewers conducted a comprehensive review of relevant studies across six databases, without language restrictions, covering publications from 1992 to 2024.

Results: Overall, 74 studies containing 92 cases were found of MDs related to ACHEIs. The MDs found were Pisa syndrome in 33 patients, parkinsonism in 31, myoclonus in 11, dystonia in 10, dyskinesia in 6, and extrapyramidal symptoms in 1. Regarding the medications, the abnormal movements were associated with donepezil in 62 cases, rivastigmine in 15, galantamine in 10, and tacrine in 5. No case of ipidacrine-induced MD was found. Overall, the most commonly affected sex was the female, accounting for 61.9% of the cases. The mean and median age was 74.1 (standard deviation: 8.9) and 75 years (range: 49-93 years). The MD occurred within 6 months of the starting of AChEI in approximately 70% of the patients. Furthermore, the full recovery of the MD after the main management was noticed within 6 months in about 80% of the patients. About 86.3% of the individuals fully recovered after treatment, which included AChEI discontinuation, dose adjustment, and prescription of additional therapy.

Conclusions: The occurrence of tacrine-induced tremor indicated a potential predisposition to movement disorders associated with AChEI therapy. Based on the drug class side effect profile, it is possible that future studies may observe abnormal movements with other AChEIs.

Background: LINC01492 polymorphism has been implicated in the susceptibility of large artery atherosclerotic (LAA) stroke; however, a dearth of systematic research exists regarding this association in the Asian population at present.

Subjects and methods: This study enrolled Han Chinese patients with LAA stroke (n = 428) and age- and sex-matched controls (n = 434). We employed dominant, recessive, and codominant genetic models to analyze the distribution of alleles and genotypes for 14 tag single nucleotide polymorphisms (SNPs) in LINC01492. Furthermore, we quantified the transcript levels of LINC01492 as well as concentrations of inflammatory factors (interleukin [IL]-1β, IL-6, IL-8, IL-10, IL-18, tumor necrosis factor alpha, and CCL18). In addition, we explored the association between these SNPs and levels of inflammatory factors.

Results: The rs10990654 AA genotype of LINC01492 was markedly associated with a heightened risk of LAA stroke (odds ratio [OR] = 6.403, 95% confidence interval [CI] = 1.180-34.734, P = 0.031). Conversely, both the GG genotype of rs10990654 (OR = 0.614, 95% CI = 0.384-0.980, P = 0.041) and the GG genotype of rs16922693 (OR = 0.518, 95% CI = 0.313-0.857, P = 0.010) were identified as being linked to a reduced risk in this study population. In addition, the transcription level of LINC01492 was markedly reduced in patients compared to controls. Furthermore, significant variations were observed in IL-10 and IL-18 levels across genotypes at LINC01492 polymorphism loci among patients.

Conclusions: The genetic polymorphisms and transcript levels of LINC01492 exhibit an association with susceptibility to LAA stroke, and the available evidence suggests that this association may be mediated through IL-10 and IL-18.

Trial registration: The trial was registered with the Chinese Clinical Trial Registry (www.chictr.org.cn) under trial registration number ChiCTR2000032684.

In this review paper, we explore the complex relationship between sleep duration and stroke risk, outlining the association of both insufficient sleep and excessive sleep with an increased risk of cerebrovascular diseases. We explore a U-shaped relationship between sleep duration and cardiovascular outcomes, including stroke. Our review explores findings from cohort studies, meta-analyses, and Mendelian randomization studies, highlighting the nuanced findings and identifying gaps in the current literature. We discussed the direct and indirect effects of sleep duration on stroke risk, considering factors such as atherosclerosis, atrial fibrillation, hypertension, and hyperlipidemia. We also discuss the methodological challenges inherent in current studies, such as the reliance on self-reported sleep measures and the need for more objective and comprehensive assessments. The paper emphasizes the importance of recognizing individual variations in optimal sleep duration and the potential confounding effects of sleep quality and other sleep-related disorders on stroke risk. Furthermore, we explore the potential mechanisms by which sleep duration may influence endothelial function, oxidative stress, and vascular compliance, suggesting areas for future investigation. The paper makes a compelling case for the inclusion of sleep duration as a key factor in stroke prevention strategies, recommending that healthcare professionals proactively assess and manage sleep patterns to mitigate stroke risk.

Background: Thoracic aortic ischemia-reperfusion (I/R) injury occurs in clinical scenarios and can lead to damage in organs such as the spinal cord, kidneys, and intestines. Hypoxic postconditioning (HyP) has shown promise in reducing organ I/R injury, suggesting its potential applicability in thoracic aortic I/R injury. However, the pathological damage caused by thoracic aorta occlusion (TAO) to the heart and brain is not yet well understood. This study aims to investigate the protective effects of hypoxic conditioning (HyP) treatment on brain and cardiac tissues following TAO-induced I/R injury.

Materials and methods: Male C57BL/6 mice were used to construct the TAO model by blocking the thoracic aorta for 0.5 or 1 h, followed by 24 h of reperfusion. The mice were divided into five groups: sham, TAO (0.5 h), TAO (0.5 h) +HyP, TAO (1 h), and TAO (1 h) +HyP. Hematoxylin and eosin, Masson, and Sirius red staining were performed to assess morphological changes and collagen deposition in brain and heart tissues. Protein expression assays were conducted to quantify inflammation-related proteins in the serum.

Results: The results showed that TAO caused significant neuronal damage in the hippocampal regions (CA1, CA3, and DG) and myocardial cell damage with collagen deposition. HyP treatment significantly alleviated these damages, particularly with shorter ischemic durations (0.5 h). Specifically, in cardiac tissues, HyP treatment reduced myocardial injury and collagen deposition. In addition, HyP treatment modulated systemic inflammatory responses, as evidenced by the increased expression of anti-inflammatory proteins such as interleukin 13 (IL-13) and the decreased expression of pro-inflammatory proteins such as IL-6, IL-12p70, IL-17, and tumor necrosis factor-α.

Conclusion: HyP treatment significantly mitigates brain and cardiac tissue damage caused by TAO, especially with shorter ischemic durations. These findings highlight the potential clinical application of HyP treatment in reducing TAO-induced tissue damage and inflammation, offering a novel therapeutic option for patients with thoracic aortic I/R injury. Future studies should further investigate the mechanisms and optimal implementation protocols of HyP treatment to maximize its clinical value.

Posterior reversible encephalopathy syndrome (PRES) is a rare neurological disorder with no specific clinical symptoms in the early stage; thus, early imaging identification is of great importance. A 29-year-old pregnant woman at 37 weeks experienced sudden generalized seizures accompanied by impaired consciousness. Brain computed tomography, conducted around 3 h after the onset, revealed symmetric areas of decreased density in the basal ganglia, brainstem, and suboccipital cortex, along with cerebral swelling. Following treatment with positive inotrope, diuretics, antihypertensives, and dehydration therapy, the patient regained clear consciousness on the 2^nd day. On the 9^th day postonset, a follow-up contrast-enhanced magnetic resonance imaging (MRI) showed slightly elevated signals in the bilateral occipital lobes on the T2 fluid-attenuated inversion recovery sequence. A subsequent brain MRI on day 47 postonset indicated no significant abnormal changes. Neuroimaging is pivotal for PRES diagnosis, revealing typical signs of widespread vasogenic edema in the posterior brain white matter, affecting the occipital lobes, cerebellum, brainstem, thalamus, and basal ganglia. With timely treatment, these lesions can partially or completely resolve within days or weeks.

Background: The N2H3 model was evaluated for forecasting the 3-month outcomes for patients experiencing acute ischemic stroke who received intravenous thrombolysis (IVT), in our previous study. The present study aimed to validate the predictive ability of the N2H3 model and to compare its accuracy to the THRIVE-c and START models (both of which are widely employed for prognostic predictions following IVT).

Methods: Our study prospectively enrolled consecutive stroke patients who received IVT from 16 hospitals. Cases from one hospital were included in External Validation Dataset 1, whereas External Validation Dataset 2 included patients from the other 15 hospitals. The effectiveness of each model in distinguishing outcomes was assessed by calculating the area under the receiver operating characteristic curve (AUC-ROC). In addition, the overall performance of the N2H3 model was assessed through the scaled Brier score.

Results: Finally, 794 patients were included, of which 582 were included in External Validation Dataset 1 and 212 in External Validation Dataset 2. The N2H3 model's AUC-ROC for forecasting unfavorable outcomes at 3-months was 0.810 (95% confidence interval [CI]: 0.771-0.848) in the first dataset and 0.782 (95% CI: 0.699-0.863) in the second dataset. For the START model, the AUC-ROCs in the two validation datasets were 0.729 (95% CI: 0.685-0.772) and 0.731 (95% CI: 0.649-0.772), respectively. The THRIVE-c model showed AUC-ROCs of 0.726 (95% CI: 0.682-0.770) and 0.666 (95% CI: 0.573-0.759), respectively. The Brier scores of the N2H3 model were 0.153 and 0.147 in cohorts 1 and 2, respectively.

Conclusions: The N2H3 model exhibited good predictive ability in both external validation cohorts. Moreover, it demonstrated advantages over the THRIVE-c and is not inferior to the START nomogram in this regard.

Trial registration: Clinical Research of Intravenous Thrombolysis for Ischemic Stroke in Northeast of China (CRISTINA) (identifier: NCT05028868).