In clinical practice, the diagnosis of hypertension is based on non-invasive upper-arm cuff blood pressure (BP) measurement. Most measurements are performed seated, although evidence indicates that supine BP may provide additional information. This review summarises recent findings on the influence of body posture on BP readings and cardiovascular (CV) risk prediction across office, ambulatory, and home BP monitoring (OBPM, ABPM, HBPM), their clinical implications and future research directions.

In OBPM, patients with supine-only hypertension demonstrated CV risk comparable to patients with hypertensive BP in both positions, and a higher risk than seated-only hypertensives. Supine hypertension was particularly predictive in individuals under 65 years of age. In ABPM, the strongest predictors of CV events are nocturnal hypertension and abnormal dipping patterns, particularly when patients are truly asleep, whereas supine nocturnal HBPM has been less extensively investigated. Current clinical practice remains primarily based on seated BP measurements. Recent trials have highlighted that supine OBPM may provide additional predictive power in the assessment of CV risk. These findings offer a partial explanation for the residual high predictive value of nocturnal BP values which can be derived from ABPM or specialised HBPM devices that goes beyond the correlation of breathing related sleep disorders Research should focus on homogenising supine risk data into composite risk scores combining seated and supine BP while new outcome studies should consider including supine BP measurement. Future guideline committees should consider recommending the structured clinical application of supine BP, given its demonstrated prognostic benefits.

Globally, stroke is a common cause of death and disability. More than 80% of strokes are reported to be preventable through effective management of modifiable risk factors. Text messages can encourage changes in health behaviour. The Love Your Brain project involves the development and evaluation of a digital health platform for stroke prevention in Australia. In this study, we aimed to develop a text message system and content for this digital platform.

The first phase involved reviewing a repository of existing health promotion messages from prior research on stroke. The second phase included co-designing the content and delivery of the messaging system with community members (n = 12) and health knowledge experts (n = 10) through 16 focus groups. New messages were then developed and formatted. These messages were reviewed by subject matter experts, then adjusted for reading age ≤ Grade 10. The final phase included the development of the messaging platform.

Among 1500+ pre-existing messages reviewed for suitability, ≈10% were adapted for primary prevention. Focus group participants reported that receiving messages on weekdays was preferred and 'having a choice' was beneficial. No consensus was reached regarding message frequency. Weblinks and shorteners were felt to be untrustworthy by participants; therefore, a Love Your Brain website using one hyperlink was developed. New messages were co-designed and personalised with greetings and sign-offs to increase engagement. All messages were revised by at least three of eight experts. After editing, 98% were readable at ≤ Grade 10 reading age and 79% at ≤ Grade 8. A REDCap message platform was built to enable personalisation at any time regarding the selection of 'healthy choices' relevant to participants' risk factors and preferences for the number of messages per week.

Integrating prior research and co-design enriched the text message platform, including content and delivery. This system can be adapted for other conditions and cultural needs to deliver relevant health information.

People with lived experience of stroke including family/caregivers. and members of the public, actively participated in the co-design focus groups. The Love Your Brain Management Committee includes people with lived experience of stroke who work in partnership with researchers and clinicians to provide oversight of all stages of the study and the preparation of this manuscript.

We employed a robust genetic approach to provide a better understanding of whether Gastroesophageal reflux disease (GERD) contributes to coronary artery disease (CAD) risk from a genetic perspective.

Multivariable Mendelian Randomization (MVMR) was applied to explore causal links between GERD and CAD using genetic instruments derived from genome-wide association studies (GWAS). The MVMR models were adjusted for key metabolic confounders, including low-density lipoprotein cholesterol (LDL-C), body mass index (BMI), systolic blood pressure (SBP), and glycated hemoglobin (HbA1c). Genetic correlations were estimated using linkage disequilibrium score regression. Cross-trait meta-analyses, Heritability Estimation from Summary Statistics (ρ-HESS) and colocalization analyses were performed to identify pleiotropic genes and shared genetic loci, elucidating the genetic relationship between GERD and CAD.

Genetically predicted GERD was found to be causally linked with CAD (rg = 0.38, P = 2.37E-52), independent of metabolic risk factors, including LDL-C, BMI, SBP, and HbA1c (odds ratio: 1.24, 95% CI: 1.02-1.52, p < 0.05). Cross-trait meta-analyses identified eight novel pleiotropic single nucleotide polymorphisms, four of which were independent of metabolic confounders, including rs11764337 in MAD1L1, rs2240326 in RBM5, rs9615905 in FAM19A5, and rs9837341 in BSN. ρ-HESS and colocalization analysis further revealed shared genetic loci for GERD and CAD, specifically rs4643373 in IGF2BP1 (located in chr17: 45876022-47517400 and posterior probability for H4 > 0.75).

GERD is identified as an independent risk factor for CAD. The discovery of shared genetic loci provides novel insights into the genetic mechanisms underlying GERD and CAD, with IGF2BP1 emerging as a potential therapeutic target for intervention.

While the physical implications of acute myocardial infarction (AMI) have been extensively studied, its psychological aspects, particularly post-traumatic growth (PTG) and post-traumatic stress disorder (PTSD) have gained increasing attention. This retrospective cohort study aimed to investigate the correlations between age, PTG, and PTSD in the context of AMI.

A total of 250 cases of patients with AMI were included in the study, sourced from the coronary care unit of Hanzhong Central Hospital and followed up in the outpatient department from January 2017 to June 2023. The data collection for this study was conducted from July 2023 to August 2023. Patients were divided into two groups based on their age at the time of AMI: 148 patients in the Younger group (≤45 years) and 102 patients in the Older group (>45 years). The patients were assessed for PTSD using the PTSD Checklist-Civilian Version (PCL-C) and for PTG using the Posttraumatic Growth Inventory (PTGI). Statistical analysis was conducted to examine the correlations and associations between age and PTG and PTSD symptoms.

The findings revealed significant age-related variations in PTSD symptomatology and PTG following AMI. Older adults exhibited higher re-experience (p < 0.001), lower hyperarousal (p = 0.023), and lower avoidance/numbing (p = 0.037) symptoms compared to younger adults, along with decreased scores in PTG domains such as relating to others (p < 0.001), appreciation of life (p < 0.001), spiritual change (p < 0.001), and personal strength (p < 0.001). The correlation analysis further demonstrated that age was significantly positively correlated with re-experience (r = 0.366, p < 0.001) and negatively correlated with avoidance/numbing (r = -0.129, p = 0.041), hyperarousal (r = -0.154, p = 0.015), relating to others (r = -0.393, p < 0.001), appreciation of life (r = -0.256, p < 0.001), spiritual change (r = -0.285, p < 0.001), and personal strength (r = -0.460, p < 0.001). Linear regression analysis showed that for every year increase in age, the beta coefficient for re-experience was 0.369 (Standard Error (SE) = 0.051, t = 7.18, p < 0.001, 95% Confidence Interval (CI) [0.266, 0.466]), indicating a significant positive association. Conversely, age had significant negative associations with avoidance/numbing (β = -0.131, SE = 0.061, t = -2.11, p = 0.036, 95% CI [-0.249, -0.009]), hyperarousal (β = -0.158, SE = 0.067, t = -2.30, p = 0.022, 95% CI [-0.286, -0.022]), relating to others (β = -0.391, SE = 0.047, t = -8.36, p < 0.001, 95% CI [-0.485, -0.301]), appreciation of life (β = -0.263, SE = 0.058, t = -4.41, p < 0.001, 95% CI [-0.370, -0.142]), spiritual change (β = -0.282, SE = 0.054, t = -5.28, p < 0.001, 95% CI [-0.391, -0.179]), and personal strength (β = -0.464, SE = 0.049, t = -9.39, p < 0.001, 95% CI [-0.556, -0.364]).

The study underscores the importance of adopting a multidimensional approach to patient care following AMI, tailored interventions to address the specific needs of younger and older adults, and the need for age-specific psychological assessment and intervention strategies in the management of patients recovering from AMI.

As a neurovascular disorder, migraine currently lacks well-established macroscopic biomarkers detectable by magnetic resonance angiography (MRA). While the basilar artery (BA) has been implicated in migraine pathophysiology, this relationship remains poorly characterized. This study investigates whether BA morphological parameters could serve as diagnostic biomarkers for migraine and predictive markers for disease progression.

This study included 41 healthy controls (HCs), 41 episodic migraine (EM) patients, and 95 chronic migraine (CM) patients who completed both MRI examinations and standardized questionnaires. Using established diagnostic criteria for vertebrobasilar dolichoectasia (VBD), we quantified the diameter, length, and height of the BA bifurcation. Furthermore, we measured the superior cerebellar artery (SUCA) outlet angle and basilar artery lateral displacement (BALD). These BA-derived metrics were subsequently incorporated into multivariable logistic regression models to assess their predictive value for migraine chronification.

No significant differences were found in BA diameter, BA length, BADE, or VBD when comparing either EM or CM groups with HCs. However, both BALD and SUCA outlet angles showed significant intergroup differences. There was a statistically significant difference in BADE between EM and CM. In the logistic regression, migraine was significantly associated with both BALD and SUCA outlet angles. In the multinomial logistic regression analysis, EM was significantly associated with SUCA outlet angle, while CM was significantly associated with both BALD and SUCA outlet angle.

Our data suggest that the reduced SUCA outlet angle may represent a risk factor for migraine and could potentially serve as an imaging biomarker. Additionally, BALD may constitute an independent risk factor for CM and could function as an MRA biomarker for migraine chronicity. Potential indicators related to the basilar artery may influence migraine attacks by affecting hemodynamic changes in migraine pathophysiology.

The first antiseizure medication (ASM) fails due to side effects or continued seizures in about half of cases. We used population-wide register data to assess whether patient demographics or comorbidities influenced likelihood of therapy revision in order to identify gaps in access to adequate epilepsy follow-up.

National registers identified all adults in Sweden with incident epilepsy between 2007 and 2019 and initial ASM monotherapy based on prescription data. Therapy revision was defined as changing medication or starting a second ASM. Cox proportional hazard models were used to evaluate clinical factors associated with therapy revision. Sensitivity analyses were restricted to patients surviving for 2 or 4 years, or to specific first monotherapies.

The final cohort included 44,185 individuals. Age (HR = 0.993, 95% CI: 0.992-0.993), cerebrovascular disease (HR = 0.81, 95% CI: 0.78-0.85), and dementia (HR = 0.63, 95% CI: 0.58-0.69) were associated with reduced likelihood of revising the first ASM. Women (HR = 1.14, 95% CI: 1.10-1.19), patients with brain infections (HR = 1.21, 95% CI: 1.08-1.35), and patients with brain tumors (HR = 1.31, 95% CI: 1.23-1.39) were more likely to revise their first treatment.

Older persons with epilepsy and those with cerebrovascular disease or dementia are less likely to change the first ASM, suggesting a disadvantage for older persons with epilepsy and those with brain morbidities associated with aging in current health care systems.

Stroke affects over 15 million people annually, with genetic factors significantly influencing risk and recovery. Understanding the complex interplay of factors contributing to stroke is crucial for developing effective prevention and treatment strategies.

This review aims to synthesize current evidence regarding the genetic underpinnings of both stroke risk and outcome, encompassing ischemic stroke, hemorrhagic stroke, and specific stroke subtypes. Genetic factors uniquely explain variability in stroke risk and treatment response beyond traditional factors like hypertension. We examine the roles of common genetic variants identified through genome-wide association studies (GWAS), the influence of rare, high-impact mutations implicated in monogenic stroke disorders, and the contribution of epigenetic modifications to stroke vulnerability and recovery. Furthermore, we explore the impact of genes involved in key pathways such as coagulation, inflammation, lipid metabolism, and cerebrovascular structure and function.

This review highlights the growing body of evidence associating specific genetic variants with increased stroke susceptibility, altered stroke severity, and differential responses to treatment. These findings have the potential to refine risk stratification strategies, identify novel therapeutic targets, and personalize stroke management based on individual genetic profiles.

Future research should focus on replicating findings across diverse populations, elucidating gene-environment interactions, and translating genetic discoveries into clinically actionable tools for stroke prevention and improved patient outcomes.

To investigate the characteristics of a video fluoroscopic swallowing study (VFSS) in patients with dysphagia caused by different parts of pontine infarction and to analyze the relationship between the severity of dysphagia and the parts of pontine infarction.

This study included 60 patients diagnosed with acute pontine infarction in the Department of Neurology and Rehabilitation Medicine of Handan Central Hospital from August 2022 to August 2023. Pontine infarction was divided into an upper pontine infarction group, middle pontine infarction group, and lower pontine infarction group according to the distribution characteristics of diffusion-weighted imaging (DWI). The VFSS evaluation results of patients with dysphagia brought on by infarction in different areas of the pons were calculated and analyzed to summarize the characteristics of dysphagia. The odified barium swallow impairment profile (MBSImP) was used to assess the severity of swallowing impairment in patients with pontine infarction at different locations.

Compared with the upper and middle pontine infarction groups, the lower pontine infarction group was more prone to oropharyngeal swallowing disorder, and the incidence of lip closure, tongue control during bolus hold, oral residue, initiation of the pharyngeal swallow, laryngeal elevation, and tongue base retraction showed statistically significant differences among the three patient groups (p < 0.05). Compared with the suprapontine and middle infarct groups, the lower pontine infarct group had a higher MBSImP score in the oral and pharyngeal stages of swallowing disorders and a heavier degree of lip closure, tongue control during bolus hold, oral residue, initiation of the pharyngeal swallow, laryngeal elevation, and tongue base retraction, with statistical significance (p < 0.05).

Patients with subpontine infarction with dysphagia had relatively independent biological characteristics.

Atherosclerosis (AS) is a chronic inflammatory disease that primarily affects large and medium-sized arteries and serves as the major pathological basis for cardiovascular diseases such as coronary heart disease. During the progression of AS, macrophages play a crucial role in promoting inflammatory regulation. Sustained local inflammatory responses are triggered by the accumulation of macrophages in arterial walls, which either promote or inhibit the development of AS by modulating inflammatory progression, plaque stability, and the surrounding immune microenvironment. Therefore, therapeutic strategies targeting macrophages and eliminating pro-inflammatory features in the plaque microenvironment hold promise as novel approaches to slow the progression of AS. With the deepening understanding of the mechanisms underlying AS, numerous innovative nanotherapeutic systems for its diagnosis and treatment have been developed. Here, we review strategies for designing novel nanosystems to treat AS, including modifying targeting ligands and utilizing biomimetic nanoparticles to enhance drug accumulation in target lesions and improve bioavailability. Macrophage-targeted nanotherapeutic approaches aim to reduce plaque burden and inflammation by regulating macrophage apoptosis, autophagy, and inducing efferocytosis synergistically. Concurrently, the development of intelligent responsive nanoparticles based on the inflammatory microenvironment enables targeted elimination of inflammatory characteristics within plaque microenvironments. These strategies demonstrate significant potential for application in AS treatment.

Vascular contributions to cognitive impairment and dementia (VCID) are one of the leading causes of dementia, where reactive astrogliosis, blood-brain barrier (BBB) disruption, and white matter lesions (WML) are the key features. However, the molecular and cellular mechanisms underlying VCID are not well understood. Na-K-Cl cotransporter 1 (NKCC1) activation via its upstream regulatory kinase SPAK (STE20/SPS1-related proline/alanine-rich kinase) causes intracellular Na⁺ overload, hypertrophy, and astrogliosis, a cascade that has been implicated in VCID. In this study, we investigated whether treatment with the SPAK inhibitor ZT-1a at the symptomatic stage in a VCID mouse model is effective in reducing reactive astrogliosis and BBB breakdown, and in improving cerebral blood flow (CBF). VCID was induced in adult C57BL/6J mice using bilateral carotid artery stenosis (BCAS), and either Vehicle (Veh, DMSO) or ZT-1a was administered from weeks 4 to 8 post-BCAS. CBF was monitored by laser speckle imaging, and cognitive deficits were assessed using the Morris water maze test. BBB integrity, astrocytic endfeet coverage, and demyelination were assessed by immunofluorescence (IF) analysis. BCAS mice exhibited a biphasic reduction of CBF and cognitive impairments, parallel with a significant loss of myelin basic protein (MBP) in white matter tracts. Increased expression and phosphorylation of NKCC1 were detected in GFAP⁺ astrocytes and Iba1⁺ microglia/macrophage following BCAS. Reduced ZO-1, Claudin-5, and AQP4 expression in vessels and extravasation of serum albumin into the brain parenchyma in BCAS mice indicate the loss of BBB integrity. Importantly, ZT-1a treatment of the BCAS mice significantly improved CBF recovery and prevented the learning and memory deficit. These mice displayed reduced astrogliosis, microglial activation, MMP-2/9 expression, BBB damage, and axonal demyelination. Our results strongly suggest that hypoperfusion-induced SPAK-NKCC1 activation contributes to reactive astrogliosis, BBB disruption, CBF reduction, and cognitive impairment. The SPAK-NKCC1 complex represents a modifiable therapeutic target for counteracting VCID progression.