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Cerebrovascular events are linked to ankylosing spondylitis. Accelerated atherosclerosis and endothelial dysfunction against a backdrop of inflammation have been widely blamed for the increased cerebrovascular risk in ankylosing spondylitis. The absence of a comprehensive review encouraged us to consider the link between ankylosing spondylitis and cerebrovascular diseases. Web of Science, PubMed, Medline, Scopus, and EMBASE were searched to identify studies published from 2000 to June 10, 2023. All observational and cohort studies reporting myocardial infarction or stroke and considering classic cerebrovascular risk in ankylosing spondylitis patients and healthy controls were included. Most of the included studies reported that the risk of cerebrovascular disorders was greater in ankylosing spondylitis than in the general population. Also, most studies showed that for both sexes, the prevalence of cardiovascular illnesses rose with age, and this trend was consistent across all subgroups of cardiovascular disorders. Also, most studies reported that the rate of cerebrovascular accidents in ankylosing spondylitis patients was higher than in control groups. Some studies reported that the risk of developing an ischemic stroke was higher in young patients with ankylosing spondylitis, while others did not. Our systematic analysis found that most studies agreed that ankylosing spondylitis patients had a higher risk of cerebrovascular diseases than the general population. Still, this increased risk was influenced by several factors that need further research exploration. [ABSTRACT FROM AUTHOR]

Background: Vascular dementia (VaD) is a prevalent neurodegenerative disease characterized by cognitive impairment due to cerebrovascular factors, affecting a significant portion of the aging population and highlighting the critical need to understand specific targets and mechanisms for effective prevention and treatment strategies. We aimed to identify pathways and crucial genes involved in the progression of VaD through bioinformatics analysis and subsequently validate these findings. Methods: We conducted differential expression analysis, Weighted Gene Co-expression Network Analysis (WGCNA), Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, and Protein-Protein Interaction (PPI) analysis. We utilized pheochromocytoma 12 (PC12) cells to create an in vitro oxygen-glucose deprivation (OGD) model. We investigated the impact of overexpression and interference of adrenoceptor alpha 1D (ADRA1D) on OGD PC12 cells using TdT-mediated dUTP nick-end labeling (TUNEL), reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot (WB), and Fluo-3-pentaacetoxymethyl ester (Fluo-3 AM) analysis. Results: We found 187 differentially expressed genes (DEGs) in the red module that were strongly associated with VaD and were primarily enriched in vasoconstric-tion, G protein-coupled amine receptor activity, and neuroactive ligand-receptor interaction, mitogen-activated protein kinase (MAPK) signaling pathway, and cell adhesion. Among these pathways, we identified ADRA1D as a gene shared by vasoconstriction, G protein-coupled amine receptor activity, and neuroactive ligand-receptor interaction. The TUNEL assay revealed a significant decrease in PC12 cell apoptosis with ADRA1D overexpression (p<0.01) and a significant increase in apoptosis upon silencing ADRA1D (p < 0.01). RT-qPCR and WB analysis revealed elevated ADRA1D expression (p < 0.001) and decreased phospholipase C beta (PLCß) and inositol 1,4,5-trisphosphate receptor (IP3R) expression (p < 0.05) with ADRA1D overexpression. Moreover, the Fluo-3 AM assessment indicated significantly lower intracellular Ca2+ levels with ADRA1D overexpression (p < 0.001). Conversely, interference with ADRA1D yielded opposite results. Conclusion: Our study provides a new perspective on the pathogenic mechanisms of VaD and potential avenues for therapeutic intervention. The results highlight the role of ADRA1D in modulating cellular responses to OGD and VaD, suggesting its potential as a target for VaD treatment. [ABSTRACT FROM AUTHOR]

Background The COVID-19 pandemic caused changes in daily life and disrupted hospital performance and the provision of medical services, especially in the organ transplant departments. Objective This study aims to compare the frequency of organ donation and transplantation before and after the COVID-19 outbreak in the transplant centers of northern Iran. Methods This cross-sectional study was conducted on 75 donors with brain death from 2018 to 2021 in Rasht. Demographic data, underlying diseases, history of smoking and drug use, causes of brain death, type of donated organ, number of donated organs per patient, type of transplanted organ, and the location of transplantation (in or out of the province) were recorded. Then, these factors were compared between two time periods: Before the pandemic (from July 2018 to February 2020) and during the pandemic (from February 2020 to August 2021). The recorded data was analyzed in SPSS software, version 21. The significance level was set at 0.05. Results The mean age of donors during the pandemic was significantly higher than that of patients before the pandemic (P<0.001). The most common cause of brain death in donors before the pandemic was trauma; after the pandemic, cerebrovascular causes were more common (P=0.01). The frequency of organ donation and the mean number of donated organs per donor during the pandemic were significantly lower than before the pandemic (P<0.001). Conclusion The COVID-19 pandemic has significant impact on the process of organ donation and transplantation in northern Iran. [ABSTRACT FROM AUTHOR]

Background: Turkmens are an ethnic group mainly living in northeastern Iran. Despite previous studies on coronary artery bypass surgery (CABG) outcomes among different ethnicities, the effect of Turkmen ethnicity on outcomes of CABG surgery is still unknown. We aimed to assess the association between Turkmen ethnicity and postoperative outcomes following CABG. Methods: We used the CABG data from two heart centers in northeastern Iran between 2007 and 2016. We included adult patients undergoing CABG surgery. The study outcomes were in-hospital major adverse cardiac and cerebrovascular events (MACCEs), consisting of myocardial infarction (MI), stroke, and cardiovascular death, and postoperative outcomes, including postoperative arrhythmia, acute atrial fibrillation (AF), major bleeding, and acute renal failure (ARF). Results: Over the course of one decade, 3632 patients, with an average age (standard deviation) of 59.0 (9.8) years, were studied. Of these, 3,331 patients were of non-Turkmen ethnicity, and 301 patients were Turkmens. According to adjusted analysis, ethnicity was not associated with MACCEs (OR: 1.15, 95 % CI: 0.61, 2.16; P = 0.663), postoperative arrhythmia (OR: 1.10, 95% CI: 0.78, 1.54; P = 0.588), acute AF (OR: 1.17, 95 % CI: 0.83, 1.66; P = 0.359), major bleeding (OR: 1.21, 95 % CI: 0.55, 2.67; P = 0.636), or ARF (OR: 2.60, 95 % CI: 0.60, 11.75, P = 0.224). Conclusion: This study found that despite ethnic disparity and preoperative differences, Turkmen ethnicity was not associated with in-hospital MACCEs, AF, major bleeding, or ARF after coronary artery bypass. [ABSTRACT FROM AUTHOR]

Sneddon's syndrome is a rare condition characterized by the presence of neurocutaneous lesions, including reticular livedo and an increase in thrombotic risk, and it is associated with a greater risk of cerebrovascular disease. It is diagnosed through a skin biopsy and neurological manifestations. In this study, we present a clinical report of a 39-year-old nurse exposed to shift and night work in an intensive care unit. She was diagnosed with Sneddon's syndrome, whose workplace had to be readapted, considering the complications and restrictions of her condition and aiming her protection and healthcare promotion. Night work can exacerbate cerebral and cardiovascular events due to its impact on metabolism, blood pressure profile, and hormone concentrations. Therefore, given a syndrome characterized by an increased thrombotic risk associated with cerebrovascular events, the restriction of night work is imperative. The occupational physician is responsible for intervening in the workplace and preventing long-term consequences for employees. [ABSTRACT FROM AUTHOR]

Background: Although Chagas cardiomyopathy is related to thromboembolic stroke, data on risk factors for cerebrovascular events in Chagas disease is limited. Thus, we assessed the relationship between left ventricular (LV) impairment and cerebrovascular events and sources of thromboembolism in patients with Chagas cardiomyopathy. Methods: This retrospective cohort included patients with chronic Chagas cardiomyopathy who underwent cardiovascular magnetic resonance (CMR). CMR was performed with a 1.5 T scanner to provide LV volumes, mass, ejection fraction (LVEF), and myocardial fibrosis. The primary outcome was a composite of incident ischemic cerebrovascular events (stroke or transient ischemic attack—TIA) and potential thromboembolic sources (atrial fibrillation (AF), atrial flutter, or intracavitary thrombus) during the follow-up. Results: A total of 113 patients were included. Median age was 56 years (IQR: 45–67), and 58 (51%) were women. The median LVEF was 53% (IQR: 41–62). LV aneurysms and LV fibrosis were present in 38 (34%) and 76 (67%) individuals, respectively. The median follow-up time was 6.9 years, with 29 events: 11 cerebrovascular events, 16 had AF or atrial flutter, and two had LV apical thrombosis. In the multivariable model, only lower LVEF remained significantly associated with the outcomes (HR: 0.96, 95% CI: 0.93–0.99). Patients with reduced LVEF lower than 40% had a much higher risk of cerebrovascular events and thromboembolic sources (HR: 3.16 95% CI: 1.38–7.25) than those with normal LVEF. The combined incidence rate of the combined events in chronic Chagas cardiomyopathy patients with reduced LVEF was 13.9 new cases per 100 persons-year. Conclusions: LV systolic dysfunction is an independent predictor of adverse cerebrovascular events and potential sources of thromboembolism in patients with chronic Chagas cardiomyopathy. [ABSTRACT FROM AUTHOR]

Alterations in tissue microstructure in normal-appearing white matter (NAWM), specifically measured by diffusion tensor imaging (DTI) fractional anisotropy (FA), have been associated with cognitive outcomes following stroke. The purpose of this study was to comprehensively compare conventional DTI measures of tissue microstructure in NAWM to diverse vascular brain lesions in people with cerebrovascular disease (CVD) and to examine associations between FA in NAWM and cerebrovascular risk factors. DTI metrics including fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (AD), and radial diffusivity (RD) were measured in cerebral tissues and cerebrovascular anomalies from 152 people with CVD participating in the Ontario Neurodegenerative Disease Research Initiative (ONDRI). Ten cerebral tissue types were segmented including NAWM, and vascular lesions including stroke, periventricular and deep white matter hyperintensities, periventricular and deep lacunar infarcts, and perivascular spaces (PVS) using T1-weighted, proton density-weighted, T2-weighted, and fluid attenuated inversion recovery MRI scans. Mean DTI metrics were measured in each tissue region using a previously developed DTI processing pipeline and compared between tissues using multivariate analysis of covariance. Associations between FA in NAWM and several CVD risk factors were also examined. DTI metrics in vascular lesions differed significantly from healthy tissue. Specifically, all tissue types had significantly different MD values, while FA was also found to be different in most tissue types. FA in NAWM was inversely related to hypertension and modified Rankin scale (mRS). This study demonstrated the differences between conventional DTI metrics, FA, MD, AD, and RD, in cerebral vascular lesions and healthy tissue types. Therefore, incorporating DTI to characterize the integrity of the tissue microstructure could help to define the extent and severity of various brain vascular anomalies. The association between FA within NAWM and clinical evaluation of hypertension and disability provides further evidence that white matter microstructural integrity is impacted by cerebrovascular function. [ABSTRACT FROM AUTHOR]

Background: Among the primary environmental issues affecting global health, air pollution is considered the leading cause of concern. Globally, around 800,000 deaths were attributed to air pollution according to WHO. Evidence suggests that there has been a strong association of air pollution with stroke. Approximately, 25% of stroke mortality was due to air pollution according to a study in 2013. Objective: The aim of this review was to analyze the association between stroke, intracerebral hemorrhage, and subarachnoid hemorrhage and air pollution and its burden globally with a special focus on South Asia along with its association with the COVID-19 pandemic. Results: There is growing research data linking air pollution to cardiovascular disorders including stroke. Short-term and long-term air pollution exposures have been shown to increase stroke incidence in epidemiological data. Air pollution, both gaseous and particle, show a strong and tight temporal relationship with stroke hospitalizations and death. The link between ICH and SAH to air pollution is less strong and less well studied as compared to ischemic stroke. Stroke and air pollution both are highly prevalent in South Asia. It is possible that the high prevalence of stroke in south Asia may be linked to the high frequency of air pollution in addition to other conventional risk factors. Decreased stroke admissions and mortality and reduced cardiovascular mortality reported during coronavirus disease 2019 (COVID) lockdown may be attributable to decreased levels of air pollution. Conclusion: Even though air pollution poses a significant threat to human health, a great number of countries still fail to achieve internationally agreed air quality standards. Air pollution should be recognized among the most significant controllable risk factors for cardiovascular and cerebrovascular disease prevention and treatment. [ABSTRACT FROM AUTHOR]

Objective. The objective of this study was to examine the correlation between blood glucose and serum insulin with acute cerebrovascular disease. Methods. A total of 1548 patients with acute cerebrovascular illness and 364 patients with a normal physical examination who were admitted to our hospital (endocrinology department) between January 2017 and July 2020 were recruited. Patients with acute cerebrovascular illness were included in the experimental group, while healthy individuals after physical examinations were included in the control group. All patients' blood glucose and serum insulin levels were measured, and the association of blood glucose and serum insulin with acute cerebrovascular illness was investigated. Results. Acute cerebrovascular disease is associated with significantly higher blood glucose and serum insulin levels versus healthy status (P < 0.05). Blood glucose and serum insulin levels were observed to be significantly higher in the hemorrhagic stroke group than in the ischemic stroke or mild hemorrhagic group (P < 0.05). Severe ischemic strokes were associated with significantly higher blood glucose levels versus mild ischemic strokes (P < 0.05). There were no significant differences in serum insulin levels between the severe ischemic stroke group and the mild ischemic stroke group (P > 0.05). Conclusion. A rise in blood glucose and serum insulin levels is associated with the incidence and prognosis of acute cerebrovascular disease, and it is positively correlated with the severity of the acute cerebrovascular disease. [ABSTRACT FROM AUTHOR]

Psoriatic arthritis (PsA), an inflammatory seronegative spondyloarthropathy is the most common co-morbidity of psoriasis (PsO), in almost 30% of cases. Delayed diagnosis and treatment of PsA may result in irreversible joint damage, significant morbidity, impaired quality of life, and several cardiometabolic and cerebrovascular co-morbidities. Dermatologists are uniquely privileged to be able to diagnose latent PsA at an early stage, as almost 80% of these patients present with pre-existing cutaneous PsO. This review provides a detailed overview of PsA along with its salient clinical features, classification criteria, screening tools, simple physical examination maneuvers, imaging findings, and therapeutic options to acquaint dermatologists and other clinicians with this morbid musculoskeletal disorder. We hope to generate awareness about this condition among dermatologists to enable proactive screening of all PsO patients for early diagnosis, initiation of appropriate treatment, and prompt referral to a rheumatologist; thus, helping to arrest PsA disease progression, irreversible joint damage, and subsequent permanent disability. [ABSTRACT FROM AUTHOR]

Simple Summary: Previous studies have shown that the occurrence of cerebrovascular-specific diseases was common in cancer patients. However, the association between colorectal cancer and cerebrovascular-specific diseases remains to be fully elucidated. In this large-population cohort study, we found that the mortality of cerebrovascular-specific diseases mortality in colorectal cancer patients was significantly higher than the general US population. In addition, we investigated several potential predictors of cerebrovascular-specific diseases mortality in colorectal cancer. This study may be useful for the prevention, risk stratification and therapeutic optimization of cerebrovascular-specific diseases in colorectal cancer patients. Background: Colorectal cancer (CRC) is one of the most prevalent diseases and the second leading cause of death worldwide. However, the relationship between CRC and cerebrovascular-specific mortality (CVSM) remains elusive, and less is known about the influencing factors associated with CVSM in CRC. Here, we aimed to analyze the incidence as well as the risk factors of CVSM in CRC. Methods: Patients with a primary CRC diagnosed between 1973 and 2015 were identified from the Surveillance Epidemiology and End Results database, with follow-up data available until 31 December 2016. Conditional standardized mortality ratios were calculated to compare the incidence of CVSM between CRC patients and the general U.S. population. Univariate and multivariate survival analyses with a competing risk model were used to interrogate the risk factors for CVSM. Results: A total of 563,298 CRC individuals were included. The CVSM in CRC patients was significantly higher than the general population in all age subgroups. Among the competing causes of death in patients, the cumulative mortality caused by cerebrovascular-specific diseases steadily increased during the study period. While age, surgery, other/unknown race and tumors located at the transverse colon positively influenced CVSM on both univariate and multivariate analyses, male patients and those who had radiotherapy, chemotherapy, a more recent year (2001–2015) of diagnosis, a grade II or III CRC, rectal cancer, or multiple primary or distant tumors experienced a lower risk of CVSM. Interpretation: Our data suggest a potential role for CRC in the incidence of CVSM and also identify several significant predictors of CVSM that may be helpful for risk stratification and the therapeutic optimization of cerebrovascular-specific diseases in CRC patients. [ABSTRACT FROM AUTHOR]

Background/Aims: Obstructive sleep apnea (OSA) is characterized by repeated episodes of complete or partial obstruction of the upper airways, leading to chronic intermittent hypoxia (IH). OSA patients are considered at high cerebrovascular risk and may also present cognitive impairment. One hypothesis explored is that disturbances may be linked to blood-brain barrier (BBB) dysfunction. The BBB is a protective barrier separating the brain from blood flow. The BBB limits the paracellular pathway through tight and adherens junctions, and the transcellular passage by efflux pumps (ABC transporters). The aims of this study were to evaluate the impact of IH and sustained hypoxia (SH) on a validated in vitro BBB model and to investigate the factors expressed under both conditions. Methods: Exposure of endothelial cells (HBEC-5i) in our in vitro model of BBB to hypoxia was performed using IH cycles: 1% O2-35 min/18% O2-25 min for 6 cycles or 6 h of SH at 1% O2. After exposure, we studied the cytotoxicity and the level of ROS in our cells. We measured the apparent BBB permeability using sodium fluorescein, FITCdextran and TEER measurement. Whole cell ELISA were performed to evaluate the expression of tight junctions, ABC transporters, HIF-1a and Nrf2. The functionality of ABC transporters was evaluated with accumulation studies. Immunofluorescence assays were also conducted to illustrate the whole cell ELISAs. Results: Our study showed that 6 h of IH or SH induced a BBB disruption marked by a significant decrease in junction protein expressions (claudin-5, VE-cadherin, ZO-1) and an increase in permeability. We also observed an upregulation in P-gp protein expression and functionality and a downregulation in BCRP. Hypoxia induced production of ROS, Nrf2 and HIF-1a. They were expressed in both sustained and intermittent conditions, but the expression and the activity of P-gp and BCRP were different. Conclusion: Understanding these mechanisms seems essential in order to propose new therapeutic strategies for patients with OSA. [ABSTRACT FROM AUTHOR]

Recent epidemiological studies have revealed a correlation between atypical features and worse functional outcomes in Parkinson's disease (PD) patients with cerebrovascular disease (CVD). We aimed to evaluate the brain hemodynamics of PD patients with risk factors for CVD using Doppler ultrasonography. In this prospective pilot study, we randomly included 27 outpatients diagnosed with PD. Transcranial color-coded sonography (TCCS) examinations were performed, obtaining measurements of middle cerebral artery mean flow velocities (Vm), the resistance index (RI), and the pulsatility index (PI). The breath-holding index (BHI) was used to assess cerebrovascular reactivity (cVR). Standardized functional scales (UPDRS III, Hoehn & Yahr scale, and MoCA) were administered. The patients were divided into two groups: those with two or more vascular risk factors (PDvasc) and those with fewer than two vascular risk factors (PDnvasc). Patients in the PDvasc group showed higher PI (1.00 vs. 0.85; p = 0.020), RI (0.59 vs. 0.5; p = 0.05), H&Y mean (2.4 vs. 1.4; p = 0.036), higher frequency of altered cVR (90.9% vs. 25.0%; p = 0.001), and lower BHI (0.46 vs. 1.01; p = 0.027). We also divided the patients in other two groups: one with patients with classical and another with akinetic-rigid PD clinical type. Patients with the akinetic-rigid type of PD had significantly higher RI (0.60 vs. 0.51; p = 0.03), PI (0.99 vs. 0.77; p = 0.03), higher frequency of altered cVR (80% vs. 35%; p = 0.02), and lower BHI (0.48 vs. 0.96; p = 0.05) than patients with classic-type PD. We concluded that TCCS displays impaired cerebrovascular reactivity and a more severe disease pattern in Parkinsonian patients with two or more risk factors for CVD and in the akinetic-rigid type. Doppler ultrasonography may be a useful tool in a clinical setting to investigate PD patients. [ABSTRACT FROM AUTHOR]

Recent evidence indicates that our understanding of the relationship between cardiac function and ischemic stroke remains incomplete. The Cardiovascular Health Study enrolled community-dwelling adults ≥ 65 years old. We included participants with speckle-tracking data from digitized baseline study echocardiograms. Exposures were left atrial reservoir strain (primary), left ventricular longitudinal strain, left ventricular early diastolic strain rate, septal e' velocity, and lateral e' velocity. The primary outcome was incident ischemic stroke. Cox proportional hazards models were adjusted for demographics, image quality, and risk factors including left ventricular ejection fraction and incident atrial fibrillation. Among 4,000 participants in our analysis, lower (worse) left atrial reservoir strain was associated with incident ischemic stroke (HR per SD absolute decrease, 1.14; 95% CI 1.04–25). All secondary exposure variables were significantly associated with the outcome. Left atrial reservoir strain was associated with cardioembolic stroke (HR per SD absolute decrease, 1.42; 95% CI 1.21–1.67) and cardioembolic stroke related to incident atrial fibrillation (HR per SD absolute decrease, 1.60; 1.32–1.95). Myocardial dysfunction that can ultimately lead to stroke may be identifiable at an early stage. This highlights opportunities to identify cerebrovascular risk earlier and improve stroke prevention via therapies for early myocardial dysfunction. [ABSTRACT FROM AUTHOR]

Sickle cell disease (SCD) is a group of hemoglobinopathies that vary in severity, the most severe form, homozygous sickle cell anemia, is more commonly associated with neurologic complications. These are attributed to the vaso-occlusion and micro obstruction in the circulation of the central nervous system. The incidence of various neurologic complications in SCD ranges from 6% to 30% in various series. The commonly reported in literature include silent cerebral infarction (SCI), ischemic stroke, transient ischemic attacks (TIAs), headaches, seizures and neurocognitive impairment. However, hemorrhagic complications like subarachnoid hemorrhage (SAH), hemorrhagic stroke, extradural and subdural hematomas, especially in absence of trauma are rarely thought of. We report three uncommon spontaneous hemorrhagic manifestations of sickle cell anemia -- one case of parenchymal (intracerebral) bleed who presented with acute onset of parkinsonism and two cases of extradural hematoma (EDH) of which one patient had recurrent EDH at the same site which is hitherto not reported in the literature. [ABSTRACT FROM AUTHOR]

Background: The aim of our study was to evaluate the risk for comorbid cardio- and cerebrovascular diseases in the working-aged migraine population of Finland.Methods: A total of 1505 cases who reported diagnosed migraine and 3010 controls from a cohort of 11,596 cases in the Finnish Health and Social Support Study were included. The study material was linked with two registers. ICD diagnoses I63 for ischemic stroke (IS), I21 - I22 for acute myocardial infarction (AMI), and G43 for transient ischemic attack (TIA) among study participants were drawn from the national Finnish Care Register for Health Care at the follow-up in 2012. Reimbursed triptan prescriptions were drawn from the national Social Security Institution (SII) data. The self-reported vascular risk factors were hypertension, high cholesterol values, any diabetes, myocardial infarction, stroke, and TIA. Odds Ratios (OR) with 95% confidence (95% CI) intervals were assessed for diagnosed stroke, myocardial infarction, and TIA.Results: Migraineurs were mostly female (82%) and ≥ 54 years old (62%). Triptans were reimbursed among 34.7% of migraineurs. A self-reported hypertension (21%), high serum cholesterol (38%), and any diabetes (7%) were more common among migraineurs vs controls (p < 0.05). There was no risk for AMI. The risk for TIA (OR 3.20, 95% CI 1.45-7.05) and IS (2.57, 95% CI 1.28-5.17) among migraineurs vs controls remained high after adjustment for self-reported hypertension, obesity, and smoking. The risk was higher among women in two groups ≥54 years (3.25, 95% CI 1.35-7.84 and 5.0, 95% CI 1.94-12.89, respectively). The average age for IS in migraine was 57.5 years and for TIA 58.2 years among women, and 52.8 years and 50.3 years among men, respectively.Conclusion: Cardiovascular risk should be screened in the aging migraine population, and hormonal and other migraine-related risk factors should be considered, especially among women. Efficacious attack treatment with triptans should be offered to migraine patients who do not show contraindications. [ABSTRACT FROM AUTHOR]

The incidence and risk factors associated with radiation-induced leukoencephalopathy (RIL) in long-term survivors of high-grade glioma (HGG) are still poorly investigated. We performed a retrospective research in our institutional database for patients with supratentorial HGG treated with focal radiotherapy, having a progression-free overall survival > 30 months and available germline DNA. We reviewed MRI scans for signs of leukoencephalopathy on T2/FLAIR sequences, and medical records for information on cerebrovascular risk factors and neurological symptoms. We investigated a panel of candidate single nucleotide polymorphisms (SNPs) to assess genetic risk. Eighty-one HGG patients (18 grade IV and 63 grade III, 50M/31F) were included in the study. The median age at the time of radiotherapy was 48 years old (range 18–69). The median follow-up after the completion of radiotherapy was 79 months. A total of 44 patients (44/81, 54.3%) developed RIL during follow-up. Twenty-nine of the 44 patients developed consistent symptoms such as subcortical dementia (n = 28), gait disturbances (n = 12), and urinary incontinence (n = 9). The cumulative incidence of RIL was 21% at 12 months, 42% at 36 months, and 48% at 60 months. Age > 60 years, smoking, and the germline SNP rs2120825 (PPARg locus) were associated with an increased risk of RIL. Our study identified potential risk factors for the development of RIL (age, smoking, and the germline SNP rs2120825) and established the rationale for testing PPARg agonists in the prevention and management of late-delayed radiation-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Introduction: Introduction: dysphagia is common in patients with cerebrovascular disease (CVD), with an incidence reported to be 35 %-50 %. Dysphagia can result in malnutrition, dehydration, and death, and negatively affects anxiety levels. Objectives: this study aimed to evaluate the effects of recommended nutritional treatment (NT) on nutritional status and anxiety levels in patients with dysphagia based on clinical and fiber-optic endoscopic evaluation of swallowing (FEES) tests. Methods: seventy-five patients over the age of 50 who were diagnosed with CVD, hospitalized at the Mersin City Research and Training Hospital, Neurology Clinic, from October 2019 to January 2020 were followed up for the study. The FEES test was performed to diagnose dysphagia in CVD patients. Anthropometric measurements of the patients were taken to calculate their body mass index (BMI) values. To determine a patient's daily energy and food intake, 24-h food recalls were taken, and the Nutritional Risk Screening 2002 (NRS 2002) test was used to identify patients at risk of malnutrition. State (SAI)-Trait Anxiety Inventories (TAI) were used to determine instant and general anxiety levels. After patient evaluations NT was provided. All evaluations were repeated 8 weeks after NT. Our study was carried out based on a longitudinal design since we worked with the same units at two different time points. Results: post-NT SAI scores were significantly lower than pre-NT scores (p < 0.05). A moderate correlation was found between pre- and post-NT SAI scores and daily energy and fluid intake status, and between TAI scores and daily energy, fat, and fluid intake amounts (p < 0.05). Post-NT SAI scores significantly decreased with both NRS 2002 and BMI values (p < 0.05). Conclusions: this study highlights the importance of NT in improving rehabilitation outcomes of patients with dysphagia. Since exercises such as postural techniques or maneuvers, and muscle strengthening to reduce swallowing difficulties are an important part of NT for dysphagia, a multidisciplinary study is required for the management of dysphagia, and further studies are needed on this subject. [ABSTRACT FROM AUTHOR]

Stroke is a leading cause of disability and mortality all over the world. Due to an aging population, the incidence of stroke is rising significantly, which has led to devastating consequences for patients. In addition to traditional risk factors such as age, hypertension, hyperlipidemia, diabetes and atrial fibrillation, sleep disorders, as independent modifiable risk factors for stroke, have been highlighted increasingly. In this review, we provide an overview of common types of current sleep disturbances in cerebrovascular diseases, including insomnia, hypersomnia, breathing-related sleep disorders, and parasomnias. Moreover, evidence-based clinical therapeutic strategies and pitfalls of specific sleep disorders after stroke are discussed. We also review the neurobiological mechanisms of these treatments as well as their effects on stroke. Since depression after stroke is so prevalent and closely related to sleep disorders, treatments of post-stroke depression are also briefly mentioned in this review article. [ABSTRACT FROM AUTHOR]

Optimal ferritin level in hemodialysis patients between Japan and other countries is controversial. Long-term side effects of iron supplementation in these patients remain unclear. We aimed to elucidate whether past hyperferritinemia in hemodialysis patients was associated with high risk of death and cerebrovascular and cardiovascular diseases (CCVDs). This small retrospective cohort study included approximately 44 patients unintentionally supplemented with excessive intravenous iron. A significantly higher risk of CCVDs was observed in patients with initial serum ferritin levels ≥1000 ng/mL than in the remaining patients. High ferritin levels slowly decreased to <300 ng/mL in a median of 24.2 (10.5–46.5) months without treatment. However, compared with the remaining patients, only patients whose ferritin levels did not decrease to <300 ng/mL steadily had a significantly higher risk of all-cause death (hazard ratio, 9.6). Long-term hyperferritinemia due to intravenous iron therapy is a risk factor for death in maintenance hemodialysis patients. For a prolonged better prognosis, intravenous iron should be carefully administered so as to avoid hyperferritinemia in patients with hemodialysis. [ABSTRACT FROM AUTHOR]

Objective Chronic pain (CP) may increase the risk for major adverse cardiac and cerebrovascular events (MACCEs); however, this issue is still unclear in the Asian population. We conducted this study to delineate it. Design From the Taiwan National Health Insurance Research Database, we identified 17,614 participants (<65 years) with CP and matched them by age and sex at a 1:2 ratio to participants without CP, who made up the comparison cohort. Several causes of CP and its underlying comorbidities were also analyzed. Outcome Measure A comparison of MACCE occurring in the two cohorts was performed via follow-up until 2015. Results The mean age (SD) was 50.2 (11.5) years and 50.4 (11.7) years in participants with and without CP, respectively. In both cohorts, the percentage of female participants was 55.5%. Common causes of CP were spinal disorders (23.9%), osteoarthritis (12.4%), headaches (11.0%), gout (10.2%), malignancy (6.2%), and osteoporosis (4.5%). After adjusting for hypertension, diabetes, chronic obstructive pulmonary disease, renal diseases, hyperlipidemia, liver diseases, dementia, and depression, participants with CP had a higher risk for MACCE than those without CP (adjusted hazard ratio [AHR] = 1.3, 95% confidence interval [CI] = 1.3 − 1.4). After conducting subgroup analyses, an increased risk was also found for all-cause mortality (AHR = 1.4, 95% CI = 1.1 − 1.8), acute myocardial infarction (AHR = 1.2, 95% CI = 1.0 − 1.4), and stroke (AHR = 1.3, 95% CI = 1.3 − 1.4). Conclusions CP is associated with increased occurrence of MACCE. Early detection and interventions for CP are suggested. [ABSTRACT FROM AUTHOR]

Hypertension is the most common cardiovascular disease in China, which can seriously affect the heart, brain, kidney and other vital organs of the human body, and is the main cause of cardiovascular and cerebrovascular diseases and even death. Chronic hypertension can lead to remodeling of the right atrium, mainly due to factors such as pressure and volume overload of the right atrium and overactivation of neuroendocrine factors. It mainly includes cardiac remodeling and myocardial tissue remodeling. The purpose of this study was to observe the ultrastructure of myocardial cells in the right atrium of spontaneous hypertension rats. In this study, 10 12-week-old SHR rats were selected as the experimental group (SHR group), and WKY rats of the same age and sex were selected as the control group (WKY group, n = 10). Blood pressure was measured at the beginning and end of the 18-week trial. A section of the rat right atrium was taken for staining, and the percentage of the vascular wall area, the vascular lumen area (LA), and the vascular wall area of the heart wall were calculated by using the computer-assisted imaging system. The results showed that WKY's blood pressure remained at the normal level (106.65±6.55) mmHg. The blood pressure of SHR group increased from 8 weeks of age, and the systolic blood pressure of SHR8, SHR16 and SHR24 groups were (121.4±5.60), (204.7±5.60) and (226.45±6.60) mmHg, respectively, which were significantly higher than the WKY group of the same week (P < 0.05). In 30-week old SHR rats, the intima of the myocardial wall arterioles were significantly thickened and lumen decreased. This mechanism may be related to the imbalance between proliferation and apoptosis of medium smooth muscle cells. This paper introduces the characteristics of myocardial arteriole remodeling in SHR, which provides a basis for the study of hypertension and its vascular remodeling as well as the prevention and treatment of target organ damage. [ABSTRACT FROM AUTHOR]

Background: It is still unknown that whether co-existing intracranial stenosis and extracranial carotid vulnerable plaques have higher predictive value for subsequent vascular events. This study aimed to determine the relationship between co-existing extracranial carotid vulnerable plaques and intracranial stenosis and subsequent vascular events utilizing cardiovascular magnetic resonance (CMR) vessel wall imaging. Methods: Patients who had recent cerebrovascular symptoms in anterior circulation (< 2 weeks) were consecutively enrolled and underwent multi-contrast CMR vessel wall imaging for extracranial carotid arteries and 3D time-of flight CMR angiography for intracranial arteries at baseline. After baseline examination, all patients were followed-up for at least 1 year to determined recurrence of vascular events. The co-existing cerebrovascular atherosclerosis was defined as presence of both intracranial artery stenosis and at least one the following measures of extracranial artery atherosclerosis: plaque, calcification, lipid-rich necrotic core (LRNC), or intraplaque hemorrhage. Univariate and multivariate Cox regressions were used to calculate the hazard ratio (HR) and corresponding 95% confidence interval (CI) of co-existing plaques in predicting subsequent vascular events. Results: In total, 150 patients (mean age: 61.8 ± 11.9 years; 109 males) were recruited. During the median follow-up time of 12.1 months, 41 (27.3%) patients experienced vascular events. Co-existing intracranial artery stenosis and extracranial carotid plaque (HR, 3.57; 95% CI, 1.63–7.82; P = 0.001) and co-existing intracranial artery stenosis and extracranial carotid LRNC (HR, 4.47; 95% CI, 2.15–9.27; P < 0.001) were significantly associated with subsequent vascular events, respectively. After adjusted for confounding factors and carotid stenosis, these associations remained statistically significant (HR, 5.12; 95% CI, 1.36–19.24; P = 0.016 and HR, 8.12; 95% CI, 2.41–27.31; P = 0.001, respectively). Conclusions: The co-existing cerebrovascular atherosclerotic diseases, particularly co-existing carotid lipid-rich necrotic core and intracranial stenosis, are independent predictors for subsequent vascular events. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MS), which includes metabolic disorders such as protein disorder, glucose disorder, lipid disorder, and carbohydrate disorder, has been growing rapidly around the world. Glycolipid disorders are a main type of metabolic syndrome and are characterized by abdominal obesity and abnormal metabolic disorders of lipid, glucose, and carbohydrate utilization, which can cause cardiovascular and cerebrovascular diseases. Glycolipid disorders are closely related to intestinal flora and its metabolites. However, studies about the biological mechanisms of the intestinal flora and its metabolites with glycolipid disorders have not been clear. When glycolipid disorders are treated with drugs, a challenging problem is side effects. Traditional Chinese medicine (TCM) and dietary supplements have fewer side effects to treat it. Numerous basic and clinical studies have confirmed that TCM decoctions, Chinese medicine monomers, or compounds can treat glycolipid disorders and reduce the incidence of cardiovascular disease. In this study, we reviewed the relationship between the intestinal flora and its metabolites in glycolipid metabolic disorders and the effect of TCM in treating glycolipid metabolic disorders through the intestinal flora and its metabolites. This review provides new perspectives and strategies for future glycolipid disorders research and treatment. [ABSTRACT FROM AUTHOR]

Mirabegron (Myrbetriq) is a ß3-adrenoreceptor agonist approved for treating overactive bladder syndrome in human patients. This drug can activate brown adipose tissue (BAT) in adult humans and rodents through the ß3-adrenoreceptor-mediated sympathetic activation. However, the effect of the mirabegron, approved by the US Food and Drug Administration, on atherosclerosis-related cardiovascular disease is unknown. Here, we show that the clinical dose of mirabegron-induced BAT activation and browning of white adipose tissue (WAT) exacerbate atherosclerotic plaque development. In apolipoprotein E-/- (ApoE-/-) and low-density lipoprotein (LDL) receptor-/- (Ldlr-/-) mice, oral administration of clinically relevant doses of mirabegron markedly accelerates atherosclerotic plaque growth and instability by a mechanism of increasing plasma levels of both LDL-cholesterol and very LDL-cholesterol remnants. Stimulation of atherosclerotic plaque development by mirabegron is dependent on thermogenesis-triggered lipolysis. Genetic deletion of the critical thermogenesis-dependent protein, uncoupling protein 1, completely abrogates the mirabegron-induced atherosclerosis. Together, our findings suggest that mirabegron may trigger cardiovascular and cerebrovascular diseases in patients who suffer from atherosclerosis. [ABSTRACT FROM AUTHOR]

Cerebrovascular diseases are the leading cause of mortality in Portugal, especially when related with extreme temperatures. This study highlights the impacts of the exposure-response relationship or lagged effect of low and high temperatures on cerebrovascular mortality, which can be important to reduce the health burden from cerebrovascular diseases. The purpose of this study was to assess the effects of weather on cerebrovascular mortality, measured by ambient temperature in the District of Lisbon, Portugal. A quasi-Poisson generalized additive model combined with a distributed lag non-linear model was applied to estimate the delayed effects of temperature on cerebrovascular mortality up to 30 days. With reference to minimum mortality temperature threshold of 22 °C, there was a severe risk (RR = 2.09, 95% CI 1.74, 2.51) of mortality for a 30-day-cumulative exposure to extreme cold temperatures of 7.3 °C (1st percentile). Similarly, the cumulative effect of a 30-day exposure to an extreme hot temperature of 30 °C (99th percentile) was 52% (RR = 1.65, 95% CI 1.37, 1.98) higher than same-day exposure. Over the 13 years of study, non-linear effects of temperature on mortality were identified, and the probability of dying from cerebrovascular disease in Lisbon was 7% higher in the winter than in the summer. The findings of this study provide a baseline for future public health prevention programs on weather-related mortality. [ABSTRACT FROM AUTHOR]

Traumatic atlantoaxial dislocation due to ligamentous and combined osseous injuries rarely occurs in adults. There are only few cases published in the literature. In this level 4 study, a cohort of nine consecutive patients suffering from traumatic atlantoaxial dislocation has been analyzed regarding morphology of injury, trauma mechanism, and outcome since 2007. Three types of those injuries have been found regarding direction of dislocation indicating the underlying ligamentous injuries as well as the accompanying grade of instability. Firstly, there was rotatory dislocation, if the alar ligaments were injured. Secondly, there occurred horizontal dislocation, when transverse atlantal ligament was damaged additionally. Thirdly, excessive ligamentous injury led to distraction of the atlantoaxial complex resulting in dissociation of the atlas against the axis. Additionally fractures of the atlas as well as of the odontoid process (type II or III according to Anderson/D'Alonzo) were diagnosed frequently. Atlantoaxial dislocation injuries, especially distraction injuries, offer a high risk for accompanied neurovascular disorders deserving reduction followed by surgical fixation. Only rotatory injuries leading to ligamentous damage solitarily can safely be successfully treated conservatively. Understanding of the injuries' morphology is essential, in order to set the correct diagnosis and to implicate the most advantageous treatment regime. [ABSTRACT FROM AUTHOR]

Introduction: Despite significant morbidity and mortality from stroke, patient delays to emergency department (ED) presentation following the onset of stroke symptoms are one of the main contraindications to treatment for acute ischemic stroke (AIS). Our objective was to identify patient and environmental factors associated with delayed presentations to the ED after onset of stroke symptoms. Methods: This was a pre-planned secondary analysis of data from a multicenter, retrospective observational study at three hospitals in Colorado. We included consecutive adult patients if they were admitted to the hospital from the ED, and the ED diagnosed or initiated treatment for AIS. Patients were excluded if they were transferred from another hospital. Primary outcome was delayed presentation to the ED (> 3.5 hours) following onset stroke symptoms. Results: Among 351 patients, 63% presented to the ED more than 3.5 hours after onset of stroke symptoms. Adjusted results show that patients who presented in the evening hours (odds ratio [OR] [0.45], 95% confidence interval [CI] [0.3-0.8]), as compared to daytime, were significantly less likely to have a delayed presentation. Speaking a language other than English (Spanish [OR 3.3, 95% CI 1.2-8.9] and "other" [OR 9.1, 95% CI 1.2-71.0]), having known cerebrovascular risk factors (>2 risk factors [OR 2.4, 95% CI 1.05-5.4] and 1-2 risk factors [OR 2.3, 95% CI 1.03-5.1], compared to zero risk factors), and presenting to a rural hospital (OR 2.2, 95% CI 1.2-4.2), compared to urban, were significantly associated with delayed presentation. Conclusion: Important patient and environmental factors are significantly associated with delayed ED presentations following the onset of stroke symptoms. Identifying how best to educate patients on stroke risk and recognition remains critically important. [ABSTRACT FROM AUTHOR]

Numerous vascular risk factors and vascular diseases contribute to cognitive impairment and dementia. Many studies and registries show an association of atrial fibrillation (AF) with cognitive impairment, cognitive decline, and dementia. This is true for vascular dementia and Alzheimer's disease. The assumed multifactorial mechanisms include ischemic stroke, both apparent and silent, cerebral microinfarcts, cerebral hemorrhage, and reduced cerebral blood flow. A number of retrospective observational and prospective studies support that anticoagulation in patients with AF may reduce the risk of cognitive decline and dementia. This holds for both vitamin K antagonists (e.g., warfarin) and direct oral anticoagulants. However, it still remains unproven if anticoagulation reduces cognitive decline and dementia in AF patients based on randomized trials. [ABSTRACT FROM AUTHOR]

Background. Infective endocarditis (IE) is a life-threatening disease. Its epidemiological profile has substantially changed in recent years although 1-year mortality is still high. Despite advances in medical therapy and surgical technique, there is still uncertainty on the best management and on the timing of surgical intervention. The objective of this review is to produce further insight into the short- and long-term outcomes of patients with IE, with a focus on those presenting cerebrovascular complications. [ABSTRACT FROM AUTHOR]

BACKGROUND: There is growing evidence that exposure to ultrafine particles (UFP; particles smaller than 100 nm) may play an underexplored role in the etiology of several illnesses, including cardiovascular disease (CVD). OBJECTIVES: We aimed o investigate the relationship between long-term exposure to ambient UFP and incident cardiovascular and cerebrovascular disease (CVA). As a secondary objective, we sought to compare effect estimates for UFP with those derived for other air pollutants, including estimates from two-pollutant models. METHODS: Using a prospective cohort of 33,831 Dutch residents, we studied the association between long-term exposure to UFP (predicted via land use regression) and incident disease using Cox proportional hazard models. Hazard ratios (HR) for UFP were compared to HRs for more routinely monitored air pollutants, including particulate matter with aerodynamic diameter =10 lm (PM10), PM with aerodynamic diameter =2:5 (PM2:5), and NO2. RESULTS: Long-term UFP exposure was associated with an increased risk for all incident CVD [HR=1:18 per 10,000 particles=cm3; 95% confidence interval (CI): 1.03, 1.34], myocardial infarction (MI) (HR=1:34; 95% CI: 1.00, 1.79), and heart failure (HR=1:76; 95% CI: 1.17, 2.66). Positive associations were also estimated for NO2 (HR for heart failure=1:22; 95% CI: 1.01, 1.48 per 20 lg=m3) and coarse PM (PMcoarse; HR for all CVD=1:21; 95% CI: 1.01, 1.45 per 10 lg=m3). CVD was not positively associated with PM2:5 (HR for all CVD=0:95; 95% CI: 0.75, 1.28 per 5 lg=m3). HRs for UFP and CVAs were positive, but not significant. In two-pollutant models (UFP+NO2 and UFP+PMcoarse), positive associations tended to remain for UFP, while HRs for PMcoarse and NO2 generally attenuated towards the null. CONCLUSIONS: These findings strengthen the evidence that UFP exposure plays an important role in cardiovascular health and that risks of ambient air pollution may have been underestimated based on conventional air pollution metrics. [ABSTRACT FROM AUTHOR]

Purpose: To determine whether ocular motor cranial nerve (CN) palsy raises the risk of subsequent stroke in the general population. Methods: We investigated the association between ocular motor CN palsy and occurrence of stroke using the National Health Insurance Service-National Sample Cohort database from 2002 to 2013. We included individuals aged ≥ 20 years on January 1st, 2004, and excluded those having any paralytic strabismus, disorders in binocular movement, diplopia and any cerebrovascular diseases before entering the cohort. Incident ocular motor CN palsy was identified by diagnostic codes for third, fourth, and sixth nerve palsies. To determine the effect of incident ocular motor CN palsy on the occurrence of subsequent stroke, we used time-varying covariate Cox regression models. Model 1 included only incident third, fourth, and sixth nerve palsies as a time-varying covariate. Model 2 included Model 1 and defined demographic information. Model 3 included Model 2, comorbidity, co-medication, and the Charlson index score. Results: Among 727,689 individuals in the cohort, 1,633 patients developed ocular motor CN palsy and 17,657 patients suffered stroke. Cox regression models showed that development of ocular motor CN palsy was associated with an increased risk of subsequent stroke (hazard ratio [HR] = 4.65; 95% confidence intervals [CIs], 3.74–5.80 in Model 1), and the results were consistent even after adjusting for demographic factors and confounders in Model 2 and 3. Men, older age, and individuals not living in Seoul/Incheon area were associated with an increased risk of stroke, while individuals with higher income were associated with decreased risk of stroke in both Model 2 and 3. Sensitivity analyses using propensity score-based matching produced similar results in all three Models (HR = 1.95; 95% CI, 1.55–2.46 in Model 1, HR = 1.91; 95% CI, 1.52–2.41 in Model 2, and HR = 1.63; 95% CI, 1.29–2.06 in Model 3). Conclusions: The occurrence of ocular motor CN palsy is a significant risk factor of subsequent stroke even after adjusting for demographic factors and confounders in the general population. Physicians may need to educate patients with ocular motor CN palsy regarding the higher risk of future stroke. [ABSTRACT FROM AUTHOR]

Elevated levels of FGF23 in individuals with chronic kidney disease (CKD) are associated with adverse health outcomes, such as increased mortality, large vessel disease, and reduced white matter volume, cardiovascular and cerebrovascular events. Apart from the well-known link between cardiovascular (CV) risk factors, especially diabetes and hypertension, and cerebrovascular damage, elevated FGF23 is also postulated to be associated with cerebrovascular damage independently of CKD. Elevated FGF23 predisposes to vascular calcification and is associated with vascular stiffness and endothelial dysfunction in the general population with normal renal function. These factors may lead to microangiopathic changes in the brain, cumulative ischemia, and eventually to the loss of white matter fibers. The relationship between FGF23 and brain integrity in individuals without CKD has hitherto not been investigated. In this study, we aimed to determine the association between FGF23, and white matter integrity in a cohort of 50 participants with varying degrees of CV risk burden, using high resolution structural human brain connectomes constructed from MRI diffusion images. We observed that increased FGF23 was associated with axonal loss in the frontal lobe, leading to a fragmentation of white matter network organization. This study provides the first description of the relationship between elevated levels of FGF23, white matter integrity, and brain health. We suggest a synergistic interaction of CV risk factors and FGF23 as a potentially novel determinant of brain health. [ABSTRACT FROM AUTHOR]

OBJECTIVES Postoperative atrial fibrillation (POAF) is a common complication after coronary artery bypass grafting. Although transient, POAF is linked to increased late mortality. We hypothesized that POAF increases late cerebrovascular (CeV) and composite cerebrovascular/cardiovascular/vascular (CV* = CeV + CV + Other-V) but not non-cardiovascular (Non-CV) mortality. METHODS We analysed 8807 non-salvage coronary artery bypass grafting patients (1994–2011). Fifteen-year and time-segmented (early, 0–1 year; intermediate, 1–6 years and late, 6–15 years) all-cause and cause-specific mortality were compared for POAF versus No-POAF patients. Corresponding POAF versus No-POAF adjusted hazard ratios [AHRs (95% confidence interval, CI)] were derived using the competing risk Cox regression. RESULTS POAF occurred in 1992 (23%) patients. Complications other than POAF occurred in 1875 (21%) patients but were more frequent among POAF patients (31% vs 18%; P  < 0.001). Overall mean follow-up was 9 ± 4 years. POAF patients had a higher 15-year unadjusted mortality (53% vs 39%; P  < 0.001) and were consequently associated with higher adjusted all-cause [AHR (95% CI) = 1.23 (1.14–1.33)] and composite cardiovascular [CV*: AHR (95% CI) = 1.15 (1.02–1.30)] mortality. The trends towards a higher 15-year CeV [AHR (95% CI) = 1.34 (0.94–1.91)] and Non-CV [AHR (95% CI) = 1.12 (0.99–1.26)] mortality were not significant. Time-segmented analyses showed that (i) POAF increased all-cause mortality early, and this persisted in the intermediate and late periods and (ii) CeV [AHR (95% CI) = 2.14 (1.14–4.04)] and CV* [AHR (95% CI) = 1.31 (1.06–1.62)] mortality rates were increased in the intermediate but not in the early or late periods. Non-CV mortality was similar in POAF and No-POAF for all time intervals. These findings were corroborated in propensity-matched sub-cohorts and in sensitivity analyses in patients free of any other complication. CONCLUSIONS POAF is associated with worse long-term survival principally driven by increased intermediate-term cerebrovascular and cardiovascular mortality, while Non-CV mortality was similar. [ABSTRACT FROM AUTHOR]

Hypertension and estrogen deficiency in women have been identified as significant risk factors for cerebrovascular diseases. Hypertension causes excessive vascular stretch and contributes to the initiation of cellular injury in blood vessels while estrogen has been demonstrated to exert beneficial protective effects on the vascular system. Although the specific biological outcomes exerted by either excessive stretch or estrogen exposure are well established, the combined biochemical effects of both stimuli remain unclear. Therefore, this study was conducted for quantitative proteomics study on human cerebral microvascular endothelial cells (HCMECs) subjected to 20% "pathological" cyclic stretch for a period of 18 hour in the presence or absence of 17β-estradiol by isobaric Taqs for Relative and Absolute Quantification. The results showed that only some proteins responded to 17β-estradiol (e.g., thioredoxin reductase-1), stretch (e.g., 14- 3-3 protein epsilon or acidic leucine-rich nuclear phosphoprotein 32 family member B) and interestingly, some proteins returned to control pre-treatment levels when exposed to both (e.g., d-dopachrome decarboxylase, thrombospondin-1). In addition, HCMECs that exposed only to estrogen had a very similar proteomic profile (i.e., up-regulation of structural, cellular adhesion and proliferation proteins) as to those exposed to estrogen with 20% stretching for 18 hour, suggesting that estrogen ablated the detrimental effects by the stretch alone. These findings sheds light on the molecular mechanisms by which the cerebrovascular protective actions of estrogen on HCMEC exposed to pathological levels of cyclic stretch which could provide a platform for future research in therapeutic approach. [ABSTRACT FROM AUTHOR]

Objectives: To examine the association between hepatitis C virus (HCV) infection, cardiovascular risk factors and cerebro-cardiovascular (CCV) disease.Methods: The source of data was the Egypt Health Issues Survey conducted in 2015. Participants were 11 256 individuals with complete HCV testing, age 25-59 years. Data on demographics, cardiovascular risk factors, CCV disease (myocardial infarction and/or cerebral stroke) and HCV infection were retrieved. Descriptive, bivariate, multivariable logistic regression and sensitivity analyses were performed to determine the independent association of past HCV exposure or chronic infection with diabetes, hypertension and CCV disease.Results: 3.9% of participants were antibody positive/RNA negative and considered to have past HCV exposure; 7.9% had detectable HCV-RNA and were considered to have chronic infection. Participants with negative antibodies and no history of liver disease (n = 9928) were the control group. In addition to the previously known risk factors, multivariable analyses revealed that diabetes was independently associated with past HCV exposure (OR = 1.71, 95% CI: 1.27-2.32) and HCV chronic infection (OR = 1.56, 95% CI: 1.23-1.97), whereas CCV disease was independently associated with past exposure (OR = 2.69, 95% CI: 1.62-4.46) and not with chronic infection. No evidence of an association between hypertension and either HCV status was found.Conclusion: The association of both past HCV exposure and chronic infection with diabetes and that of past HCV exposure with CCV disease may suggest targeting HCV-positive reactors for preventive and curative programmes addressing extrahepatic complications. [ABSTRACT FROM AUTHOR]

Background Endothelial dysfunction has been identified as an etiologic factor for osteonecrosis of the femoral head (ONFH) and major adverse cardiovascular and cerebrovascular events (defined as major cardiovascular disease [CVD] and cerebrovascular accident [CVA]). However, the incidence of major adverse cardiovascular and cerebrovascular events in patients with nontraumatic ONFH and any association between the two diagnoses remain unclear. Questions/purposes We compared a large cohort of patients with nontraumatic ONFH and a matched control group without this diagnosis and (1) examined the frequency and hazard ratio (HR) of major adverse cardiovascular and cerebrovascular events in both groups adjusted for age, sex, socioeconomic status, and associated comorbidities (which we defined as the adjusted HR), (2) determined whether any association of ONFH and major adverse cardiovascular and cerebrovascular events was stable after adjusting for confounding variables, and (3) compared the occurrence of major adverse cardiovascular and cerebrovascular events with time in both groups. Methods A population-based cohort with a 14-year dataset period (1997-2010) from the Taiwan National Health Insurance Research Database was used for this retrospective study. The database includes a greater than 99.5% Asian population randomly selected from more than 23 million citizens and foreigners residing in Taiwan for longer than 6 months. A total of 1562 patients with nontraumatic ONFH were identified from a population of one million patients in the database after excluding initially concomitant diagnoses of major CVD and CVA. The comparison group (n = 15,620) without ONFH was analyzed in a one-to-10 ratio by matching the study cohort based on age, sex, income, and urbanization. Results The patients with ONFH had a higher frequency of major adverse cardiovascular and cerebrovascular events than their counterparts without ONFH (19% versus 14%; p < 0.001). The patients with ONFH had 1.34- and 1.27-fold adjusted HRs for occurrence of major CVD and CVA as compared with the normal population (95% CI, 1.11-1.61, p = 0.002, and 95% CI, 1.09-1.47, p = 0.002, respectively). Sensitivity analysis showed a consistent association between ONFH and major adverse cardiovascular and cerebrovascular events after controlling for potentially relevant confounding variables such as hypertension and diabetes. After adjusting for potential confounders including surgery and medications, ONFH remained independently associated with major CVD (adjusted HR, 1.51, 95% CI 1.09-2.03, p = 0.026) and CVA (adjusted HR, 2.44, 95% CI 1.69-3.51, p < 0.001), apart from age older than 65 years and traditional atherosclerotic risk factors. The cumulative incidence of major adverse cardiovascular and cerebrovascular events also was higher in the ONFH group than the non-ONFH group (30.3% vs 23.1% at the end of followup, p < 0.001). Conclusions Patients with ONFH have a strong association with major adverse cardiovascular and cerebrovascular events as compared with the normal population, suggesting a potential common pathway involving endothelial dysfunction. In view of this association in the relatively young population with ONFH, it is important to closely monitor these patients, treat relevant comorbidities early, and investigate preventative measures for these major adverse events. [ABSTRACT FROM AUTHOR]

Motivation: Obstructive sleep apnea (OSA) can impair cerebral vasoreactivity and is associated with an increased risk of cerebrovascular disease. Unfortunately, an easy-to-use, non-invasive, portable monitor of cerebral vasoreactivity does not exist. Therefore, we have evaluated the use of near-infrared diffuse correlation spectroscopy to measure the microvascular cerebral blood flow (CBF) response to a mild head-of-bed position change as a biomarker for the evaluation of cerebral vasoreactivity alteration due to chronic OSA. Furthermore, we have monitored the effect of two years of continuous positive airway pressure (CPAP) treatment on the cerebral vasoreactivity. Methodology: CBF was measured at different head-of-bed position changes (supine to 30° to supine) in sixty-eight patients with OSA grouped according to severity (forty moderate to severe, twenty-eight mild) and in fourteen control subjects without OSA. A subgroup (n = 13) with severe OSA was measured again after two years of CPAP treatment. Results: All patients and controls showed a similar CBF response after changing position from supine to 30° (p = 0.819), with a median (confidence interval) change of -17.5 (-10.3, -22.9)%. However, when being tilted back to the supine position, while the control group (p = 0.091) and the mild patients with OSA (p = 0.227) recovered to the initial baseline, patients with moderate and severe OSA did not recover to the baseline (9.8 (0.8, 12.9)%, p < 0.001) suggesting altered cerebral vasoreactivity. This alteration was correlated with OSA severity defined by the apnea-hypopnea index, and with mean nocturnal arterial oxygen saturation. The CBF response was normalized after two years of CPAP treatment upon follow-up measurements. Conclusion: In conclusion, microvascular CBF response to a head-of-bed challenge measured by diffuse correlation spectroscopy suggests that moderate and severe patients with OSA have altered cerebral vasoreactivity related to OSA severity. This may normalize after two years of CPAP treatment. [ABSTRACT FROM AUTHOR]

Carotid diseases are very important for the increase of total morbidity and mortality of the population affected by cerebrovascular diseases. The primary pathologic factor responsible for the diseases of the cerebrovascular system is atherosclerosis, and the measurement of the thickness of the intima-media complex (IMC) in the carotid artery extracranial segment represents a measurable indication of atherosclerosis. The thickness of the IMC of the carotid arteries is influenced by many factors such as local hemo-dynamics, wall stress, arterial hypertension, and other. The aim of our research was to confirm the influence of hypertension as a risk factor for the development of cerebrovascular diseases which influence the thickness of the intima-media complex of carotid arteries in asymptomatic and symptomatic observed patients concerning gender and age. The research was conducted in 100 patients of both sexes who were treated at outpatient department or while hospitalized at the Neurology Ward, with hypertension as the main risk for the development of the cerebrovascular diseases. The measurement of the IMC of the carotid arteries was conducted by the ultrasound examination, and the value of IMC>0,9 mm was taken as a border line between normal and pathologic findings. The research included 100 patients, out of which 36 were male, and 64 female patients. All patients had elevated values of blood pressure. In the male group, just 33.3% of the patients were affected by a hypertension disease only, while the remaining 66.7% had also suffered a cerebrovascular insult, and they had arterial hypertension as a risk factor in their anamnesis, as well. In the female group of 64 patients, 31.3% had a hypertension disease, 68.75% also suffered a cerebrovascular insult, as well as arterial hypertension. The measurement of the thickness of the IMC of the carotid arteries by the ultrasound method is important for the detection of the subclinical structural damage of the arterial walls and is a part of the algorithm for the assessment of the cerebrovascular risk in patients who suffer from the elevated blood pressure. There is a significant corre-lation among the thickness of the carotid IMC, hypertension disease, and cerebrovascular diseases. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a polygenic/complex disorder in which genomic, epigenomic, cerebrovascular,metabolic, and environmental factors converge to define a progressive neurodegenerative phenotype. Pharmacogenetics is a major determinant of therapeutic outcome in AD. Different categories of genes are potentially involved in the pharmacogenetic network responsible for drug efficacy and safety, including pathogenic, mechanistic, metabolic, transporter, and pleiotropic genes. However, most drugs exert pleiotropic effects that are promiscuously regulated for different gene products. Only 20% of the Caucasian population are extensive metabolizers for tetragenic haplotypes integrating CYP2D6-CYP2C19-CYP2C9-CYP3A4/5 variants. Patients harboring CYP-related poor (PM) and/or ultra-rapid (UM) geno-phenotypes display more irregular profiles in drug metabolism than extensive (EM) or intermediate (IM) metabolizers. Among 111 pentagenic (APOE-APOB-APOC3-CETP-LPL) haplotypes associated with lipid metabolism, carriers of the H26 haplotype (23-TT-CG-AG-CC) exhibit the lowest cholesterol levels, and patients with the H104 haplotype (44-CC-CC-AA-CC) are severely hypercholesterolemic. Furthermore, APOE, NOS3, ACE, AGT, and CYP variants influence the therapeutic response to hypotensive drugs in AD patients with hypertension. Consequently, the implementation of pharmacogenetic procedures may optimize therapeutics in AD patients under polypharmacy regimes for the treatment of concomitant vascular disorders. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a critical and rapidly growing global health problem. Neurological complications occur in almost all patients with severe CKD, potentially affecting all levels of the nervous system, from the central nervous system (CNS) through to the peripheral nervous system (PNS). Patients with CKD exhibit a high incidence of symptomatic and occult cerebrovascular diseases, associated tremendously high levels of inflammatory factors and homocysteine, as well as anemia, hypertension, and diabetes. As these risk factors overshadow aging and nonvascular factors, CKD patients represent a potential model of accelerated vascular cognitive impairment. In this article, the disease-related and treatment-related neurological complications of renal disorders will be reviewed. [ABSTRACT FROM AUTHOR]

The study included 125 patients aged 40 to 84 years, with multifocal vascular lesions. All patients were divided into three clinical groups, depending on the localization of vascular lesions with stenotic atherosclerosis. According to the correlation analysis, there is a direct correlation between the presence of clinical manifestations of cerebral insufficiency and the age of patients. In multifocal vascular lesions, chronic forms of cerebral ischemia (dyscirculatory encephalopathy) were recorded in 69.2% of patients who had a cerebral infarction, and in 87.0% of patients with TIA in the anamnesis. The most common concomitant pathology in patients with multifocal vascular disease is hypertension of various degrees and stages (92.8% of patients), type 2 diabetes (20.0%). In the study, a direct relationship was established between the degree of hypertension and the acute disorders of cerebral circulation. Infarctions of the brain in patients with multifocal vascular lesions occurred in 72.8%, mainly in the carotid basin, which is 3.2 times higher than the frequency of myocardial infarction in the vertebrobasilar basin. With simultaneous atherosclerotic lesions of the vessels of the brain, heart and lower limbs, there was no TIA as an independent form, but a clinical transition to a cerebral infarction was immediately noted. Repeated heart attacks took place in 28% of patients in the general group, mainly with simultaneous atherosclerotic lesions of the brain and heart vessels (31.0%) or all three basins (26.3%). In atherosclerotic lesions of the vascular basins of the brain and heart, CHD is manifested earlier (58.6%), and in the case of cerebral and lower extremity vessels, ischemia of the lower extremities (73.7%). The time interval between repeated cerebral infarctions was shorter in patients who continued to smoke 4.5 times. [ABSTRACT FROM AUTHOR]

Objective : Measurement of the degree of stenosis is not enough to decide on the treatment strategy for patients with carotid stenosis. Plaque morphology examination is needed for such a decision-making. Thus, we evaluated the usefulness of plaque magnetic resonance imaging (MRI) to decide on the modality of treatment for patients with carotid atherosclerotic plaques. Materials and Methods : Fifteen patients presenting with carotid stenosis between 2014 and 2016 were included. They underwent angiography for measurement of the degree of stenosis. Carotid plaques were visualized using MRI. Results : There were six (40%) stable and nine (60%) unstable plaques. Seven symptomatic patients (77.7%) had unstable lesions and two symptomatic patients (33.3%) had stable lesions (p = 0.096). There were six (40%) intraplaque hemorrhage (IPH) cases. There were six symptomatic patients (100%) in the IPH group and three symptomatic patients (33.3%) in the non-IPH group (p = 0.013). The mean stenosis degree was 58.9% in the IPH group and 70.4% in the non-IPH group (p = 0.094). Symptoms occurred irrespective of the degree of the stenosis in the IPH groups. In the IPH group, the recurrent ischemic cerebrovascular event rate was 33.3%. Particularly, the recurrent ischemic cerebrovascular event rate was 66.7% in the IPH group with mild stenosis treated with medications. Conclusion : IPH in plaque MRI is significantly associated with ischemic symptoms and has a high risk for subsequent ischemic cerebrovascular events irrespective of the degree of stenosis. Plaque MRI is a useful tool in predicting symptomatic risks for carotid stenosis irrespective of the degree of such stenosis. [ABSTRACT FROM AUTHOR]

While pathophysiology underlying post-concussion symptom burden is unknown, data suggest that cerebrovascular dysfunction may be among the culprits. We sought to determine whether the degree of impairment in the ability of cerebrovasculature to buffer against changes in arterial gases (vasoreactivity) is associated with concussion symptoms. In 15 participants (19 ± 5 years, 1 week to 1 year post-injury) diagnosed with concussion, we assessed vasoreactivity from the slope of the linear relationship of beat-by-beat middle cerebral artery blood flow velocity (transcranial Doppler ultrasound) to end-tidal CO2 during progressive increases in end-tidal CO2 (air rebreathing). Symptom burden was assessed using the Post-Concussion Symptom Scale. Subsequently, we explored the relationship between vasoreactivity and the severity of post-concussion headache and cognitive difficulties by linear models. During rebreathing, CO2 increased from 32.6 ± 1.6 to 46.8 ± 1.8 mmHg and cerebrovascular conductance (i.e., flow velocity over pressure) increased from 0.48 ± 0.04 to 0.74 ± 0.06 cms−1 mmHg−1. There was a strong linear relationship between the increase in CO2 and in conductance ( R2 = 0.81 ± 0.05; p < 0.05). On average, cerebral vasoreactivity was 0.018 ± 0.003 cm−1 s−1 mmHg CO2−1. Although vasoreactivity tended to be somewhat higher in the asymptotic participants (0.019 ± 0.003 vs. 0.015 ± 0.005 cm−1 s−1 mmHg CO2−1), this difference was not statistically significant ( p = 0.48). Higher vasoreactivity was strongly associated with more severe headaches ( R2 = 0.57; p < 0.01) and worse cognitive symptoms ( R2 = 0.71; p < 0.01). Thus, cerebral vasoreactivity relates strongly to post-concussive headache and cognitive symptom burden. This has significant implications for understanding the pathophysiology underlying post-concussive symptom burden and for devising effective treatment options. [ABSTRACT FROM AUTHOR]

Background and objective: Changes in cerebral blood flow (CBF) immediately after cigarette smoking (CS) are still unclear. Our purpose was to evaluate the hemodynamic changes in each intracranial vessel after CS by using quantitative magnetic resonance angiography (MRA). Material and methods: Fifteen healthy male smokers less than 45 years old with more than 3 pack-year smoking history were enrolled in this study. The hemodynamic change in the vessels, represented by cerebral flow rate (CFR, ml/s) and flow velocity (FV, cm/s), was quantitatively measured in eleven vascular segments of the brain using phase-contrast MRA. Two sets of data at each vessel before and after CS were statistically analyzed by paired t-test. Three of 15 participants, as a control group, followed all the procedures but did not smoke. Results: Total CFR of the distal intracranial vessels (anterior, middle, and posterior cerebral arteries; ACA, MCA, and PCA) was significantly reduced after CS by 7.3% (847 vs. 785 ml/s, p = 0.024). Such flow changes were statistically more significant in the anterior circulation (ACA and MCA) compared to the posterior circulation (PCA). All distal intracranial vessels did not have significant FV change while peak systolic velocity and mean velocity dropped 7.4 and 4.3% and pulsatility index decreased 10.9% in the internal carotid artery. Regarding cross-sectional areas, all distal intracranial vessels showed diminished, and only MCA had a statistical significance (9.9 vs. 9.3 mm2, p = 0.016). Conclusions: There was a significant decrease of CFR after CS especially in the anterior circulation of twelve young male smokers. Considering the changes of FV and cross-sectional area all together, it can be suggested that cerebrovascular impedance increased after CS especially at the main trunk level of the distal intracranial vessels (ACA, MCA, and PCA). [ABSTRACT FROM AUTHOR]

Ischemic stroke appears the third leading cause of mortality and the first cause of disability in developing countries. The relationship between sleep disorders and cerebrovascular risk factors is well defined and there are different mechanisms in pathophysiology. Ischemic stroke affects many pathways, such as hypoxia, increased wakefulness reactions, decreased sleep quality, increased free oxygen radicals, inflammatory mechanisms activation, endothelial dysfunction, atherosclerosis, hypertension, and insulin resistance. Sleep disturbances contribute to stroke pathology through multiple direct or indirect mechanisms. Due to the fact that sleep disorders are among the changeable cerebrovascular risk factors, it is very important to raise awareness about the diagnosis, management and prevention of sleep disorders. [ABSTRACT FROM AUTHOR]

Tinnitus mostly results from central and peripheral auditory pathology. Chronic kidney disease (CKD) is a major risk factor for cerebrovascular disease. However, no studies have evaluated the association between tinnitus and CKD. The aim of this study is to investigate the risk of tinnitus in patients with CKD. This retrospective cohort study was conducted using Taiwan National Health Insurance Research Database from 2000 to 2010. We established a CKD group (n = 185,430) and a non-CKD comparison group (n = 556,290) to investigate the incidence of tinnitus. Cox proportional hazard regression analysis was used to evaluate the effects of CKD on tinnitus risk. The results showed CKD significantly increased the risk of tinnitus (adjusted hazard ratio, 3.02; 95% CI, 2.655–3.456, P<0.001). A subgroup analysis revealed the increase in risk of tinnitus is more in CKD patients with heart failure (adjusted hazard ratio, 9.975; 95% CI, 5.001–18.752) and diabetes mellitus (adjusted hazard ratio, 3.712; 95% CI, 2.856–5.007). Furthermore, compared to non-CKD patients, the risk of tinnitus was increased 4.586-fold (95% CI, 2.399–6.7) in CKD patients with dialysis and 2.461-fold (95% CI, 1.033–3.454) in CKD patients without dialysis. This study is the first to report that CKD is associated with an increased risk of tinnitus. Among CKD cohort, patients with dialysis are at a higher risk of tinnitus than those without dialysis. [ABSTRACT FROM AUTHOR]

The aim of the present study was to perform a meta-analysis of published data to determine the significance of clinical factors and exposures to the risk of perinatal arterial ischaemic stroke ( PAIS) and provide guidance for clinical diagnosis and treatment. A comprehensive literature search of the PubMed, Embase, MEDLINE and Cochrane Library databases for relevant observational studies (cohort/case−control) from March 1984 to March 2016 was undertaken. Two review authors independently examined the full text records to determine which studies met the inclusion criteria and evaluated risk factors for PAIS. Risk ratios, odds ratios and 95% confidence intervals were estimated. A total of 11 studies were included in the analyses. Intrapartum fever >38°C, pre-eclampsia, oligohydramnios, primiparity, forceps delivery, vacuum delivery, fetal heart rate abnormalities, abnormal cardiotocography tracing, cord abnormalities, birth asphyxia, emergency caesarean section, tight nuchal cord, meconium-stained amniotic fluid, umbilical arterial pH <7.10, Apgar score at 5 min <7, resuscitation at birth, hypoglycaemia, male gender and small for gestational age were identified as risk factors for PAIS. This systemic review and meta-analysis provides a preliminary evidence-based assessment of the risk factors for PAIS. Patients with any of the risk factors identified in this analysis should be given careful consideration to ensure the prevention of PAIS. Future studies focusing on the combined effects of multiple prenatal, perinatal and neonatal risk factors for PAIS are warranted. [ABSTRACT FROM AUTHOR]

Background: Patients who develop herpes zoster or herpes zoster ophthalmicus may be at risk for cerebrovascular and cardiac complications. We systematically reviewed the published literature to determine the association between herpes zoster and its subtypes with the occurrence of cerebrovascular and cardiac events. Methods/Results: Systematic searches of PubMed (MEDLINE), SCOPUS (Embase) and Google Scholar were performed in December 2016. Eligible studies were cohort, case-control, and self-controlled case-series examining the association between herpes zoster or subtypes of herpes zoster with the occurrence of cerebrovascular and cardiac events including stroke, transient ischemic attack, coronary heart disease, and myocardial infarction. Data on the occurrence of the examined events were abstracted. Odds ratios and their accompanying confidence intervals were estimated using random and fixed effects models with statistical heterogeneity estimated with the I2 statistic. Twelve studies examining 7.9 million patients up to 28 years after the onset of herpes zoster met our pre-defined eligibility criteria. Random and fixed effects meta-analyses showed that herpes zoster, type unspecified, and herpes zoster ophthalmicus were associated with a significantly increased risk of cerebrovascular events, without any evidence of statistical heterogeneity. Our meta-analysis also found a significantly increased risk of cardiac events associated with herpes zoster, type unspecified. Conclusions: Our results are consistent with the accumulating body of evidence that herpes zoster and herpes zoster ophthalmicus are significantly associated with cerebrovascular and cardiovascular events. [ABSTRACT FROM AUTHOR]