Direct oral anticoagulants (DOACs) have become the mainstay of stroke prevention in patients with atrial fibrillation (AF). Decision to anticoagulate frail and post-stroke patients with AF may be challenging and complex. This study aimed to compare the outcomes of complex older patients with acute ischaemic stroke and AF who were treated with and without oral anticoagulants for secondary stroke prevention.

This is a retrospective observational study of all older persons (≥65 years) admitted to the geriatric medicine ward in our university hospital with acute ischaemic stroke and AF from January 2016 - December 2021. The inclusion criteria in our study were patients discharged alive from hospital post-ischaemic stroke with AF. Exclusion criteria were those who died as inpatient, those undergoing end-of-life care or with very severe frailty which are contraindication to anticoagulation. Comparison was done between patients who were anticoagulated and patients who were eligible for anticoagulation but were not anticoagulated for various reasons.

There were 539 patients with ischaemic stroke, of whom 110 (21%) had AF. Among them, 29 patients were excluded due to death during hospitalization (19), end-of-life (4), and very severe frailty (6). While 65 (80%, mean age 84.1 ± SD 6.3) were discharged on anticoagulation, 16 (20%, mean age 88.3 ± SD 4.3, p=0.388) were discharged without anticoagulation. The median clinical frailty score was six in both groups. Among the anticoagulated, 59 (91%) were commenced on DOACs and six (9%) were on warfarin. The main reasons recorded for not commencing anticoagulants in eligible patients were patient/family did not agree to start (8), high bleeding risk (7), and poor social support (1). Mortality was significantly higher in the non-anticoagulated group (n=10, 63%) compared to the anticoagulated group (n=22, 32%) (p=0.036).

Although frail older persons are perceived to have a poorer benefit/risk ratio when anticoagulated, our study demonstrated lower mortality in post-stroke anticoagulated complex older AF patients compared to those who were not anticoagulated. However, given the small numbers of participants in our study, further studies are required to determine characteristics of patients who may have better outcomes or lower risk of adverse events on anticoagulants. These findings also underscore the pressing need for a standardized, frailty-prescribing and monitoring protocol to maximise benefit and minimise risks of adverse outcomes.

This study aims to evaluate the cardiovascular disease risk and related factors among incarcerated individuals in a closed prison.

Cardiovascular diseases represent a leading cause of global mortality, among incarcerated individuals facing heightened risks attributable to environmental and lifestyle factors.

This cross-sectional study was conducted with foreign-nationed inmates aged 40-69 at Maltepe No. 3 L-Type Closed Prison in Istanbul, Türkiye, using World Health Organization (WHO) risk assessment tools. Data has been collected from January to March 2023 through in-person interviews, anthropometric assessments, and laboratory tests.

Of the 366 participants, all of them were male, mean age was 47.4 years (±6.2), as ethnic origin 74.6% were Asian. The median cardiovascular risk score was 6% (range: 1-52%), 74.6% classified as low-risk, 21.0% as moderate-risk, and 4.4% as high or very high-risk. Significant predictors of elevated cardiovascular risk included advanced age (p < 0.001), smoking (p < 0.001), systolic/diastolic hypertension (p < 0.001), and abdominal obesity (p = 0.005). Individuals exhibiting high-risk profiles showed increased levels of total cholesterol, LDL-C, HbA1c, and fasting blood glucose (p < 0.001). No correlation was found between incarceration duration and cardiovascular risk.

This study emphasises the importance of individual health evaluation including BMI and cardiovascular risk assessment and implementing preventive measures, such as smoking cessation, healthy diet and exercise programmes to protect low-and moderate-risk individuals and to lower the high risk as normal population. These preventive health services can be provided in primary care centres located in prison settlement.

Lipid metabolism, coagulation, inflammation, and vascular integrity are closely interconnected biological systems. Although statins are primarily prescribed to reduce low-density lipoprotein cholesterol (LDL-C) and prevent atherosclerotic cardiovascular disease, increasing evidence indicates that these agents exert multiple pharmacological effects beyond lipid lowering, including modulation of endothelial function, platelet activation, tissue factor expression, thrombin generation, fibrinolysis, and thrombo-inflammation. These pleiotropic properties have generated growing interest in the potential role of statins as adjunctive modulators of thrombotic risk in patients receiving anticoagulant therapy. Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, is a major clinical setting in which anticoagulant treatment reduces recurrence and mortality but exposes patients to bleeding complications. Observational studies and registry-based analyses suggest that statin use may be associated with improved outcomes among anticoagulated patients with venous thromboembolism, particularly for all-cause mortality and early survival after pulmonary embolism. At the same time, emerging evidence suggests that very low LDL-C concentrations may be associated with increased bleeding risk during anticoagulation, raising important questions regarding the relationship between lipid availability, vascular stability, platelet function, and hemostatic balance. This review summarizes current pharmacological and clinical evidence linking lipid metabolism, statin therapy, anticoagulation, thrombosis, and bleeding. Particular attention is devoted to the mechanisms through which statins influence hemostatic pathways, the clinical evidence derived from venous thromboembolism cohorts, and the potential implications of LDL-C levels for personalized bleeding risk assessment. Future strategies that integrate lipid profiles, thrombotic and bleeding risk, and pharmacological modulation of coagulation may contribute to more individualized antithrombotic management.

This case report aims to illustrate the critical importance of a standardized diagnostic approach and genotype-specific therapy in hereditary transthyretin amyloid cardiomyopathy (ATTR-CM). It highlights the clinical challenge of diagnosing ATTR-CM amidst complex comorbidities and addresses the evidence gap regarding the long-term efficacy of tafamidis for the rare and aggressive p.Val40Ile (protein-level substitution of valine to isoleucine at codon 40) mutation.

A 72-year-old East Asian man with multiple comorbidities presented with refractory heart failure. Key clinical clues included the classic "red flag" of electrocardiogram (ECG)-echocardiogram discordance (low voltage with ventricular hypertrophy). Genetic testing identified the pathogenic p.Val40Ile transthyretin (TTR) mutation.

The diagnosis was confirmed non-invasively via cardiac magnetic resonance (CMR) and technetium-99m pyrophosphate scintigraphy. Following the initiation of tafamidis, the patient's symptoms significantly improved. Over a two-year follow-up period, he sustained clinical stability with a marked reduction in heart failure-related hospitalizations.

This report provides detailed case-based evidence supporting the long-term efficacy of tafamidis in stabilizing disease and improving prognosis for patients with ATTR-CM harboring the p.Val40Ile mutation. It underscores the value of timely diagnosis, genetic subtyping, and access to targeted therapy in altering the clinical course of this aggressive genotype.

Reverse cascade genetic screening, following initial lipid testing, is an effective strategy for the early diagnosis of familial hypercholesterolemia (FH) and related hereditary dyslipidemias. In this study, we present the results of a pilot project in Russia.

This was a hybrid retrospective-prospective cross-sectional study. Analysis of 1897 lipid screenings of children referred to the main pediatric centers in St. Petersburg, Russia, demonstrated that 60 (3.2%) met the Simon Broome criteria for FH, defined as total cholesterol (TC) ≥6.5 mmol/L or low-density lipoprotein cholesterol (LDL-C) ≥4 mmol/L. All families were invited to undergo genetic testing, regardless of their history, with 35 (58%) families participating in the second stage of the study. Targeted sequencing was performed for children, and Sanger sequencing was performed for variant validation in children and their family members.

Sixteen children were shown to have causal variants in dyslipidemia-associated genes, including fourteen (40% of 35 tested children) with hereditary dyslipidemias: twelve FH cases (linked to LDLR and APOB genetic variants), one dysbetalipoproteinemia case (APOE), and one sitosterolemia case (ABCG8). Two children were heterozygous for sitosterolemia variants (one case with ABCG5, one case with ABCG8). Family history of FH or atherosclerotic cardiovascular disease (ASCVD) was reported in only 50% of cases, regardless of whether a causal variant was present. TC and LDL-C were higher in the causal variant-positive subgroup. Receiver operating characteristic curve analysis revealed that LDL-C >4.8 mmol/L acted as a diagnostic indicator of disease causing variant with 84% accuracy, 93% sensitivity, and 73% specificity.

Reverse cascade genetic screening following selective lipid testing in children is an effective strategy to reveal new FH and other hereditary dyslipidemia cases, helping to mitigate future ASCVD risks and early mortality.

Health behavior adherence (HBA) is important for effective rehabilitation and secondary prevention after stroke. Young and middle-aged patients may face particular challenges in maintaining recommended health behaviors during hospitalization because of functional impairment, cognitive deficits, pain, and competing social or occupational responsibilities. However, factors associated with HBA in this population remain insufficiently characterized, and practical tools for the early identification of patients at risk of suboptimal adherence are limited. To identify factors associated with HBA in young and middle-aged patients with stroke during hospitalization and to develop a combined predictive model for the early identification of patients with non-high adherence.

A single-center retrospective observational study was conducted, including 298 young and middle-aged stroke patients hospitalized between January 2021 and June 2024. Patients were categorized into a high-adherence group and a non-high-adherence group based on the HBA Index. Differences in demographic and functional characteristics between the groups were compared. Correlation analysis and multivariate logistic regression were performed to identify independent factors affecting HBA. Receiver operating characteristic (ROC) curves were constructed to evaluate the predictive performance of individual indicators and the combined model.

Among the 298 patients, 143 (48.0%) were classified as non-high-adherence. The high-adherence group had significantly better functional and cognitive scores, including the Barthel Index (BI), Mini-Mental State Examination (MMSE), Fugl-Meyer Assessment (FMA), and Berg Balance Scale (BBS), and experienced less pain (all p < 0.001). Adherence was positively correlated with BI, MMSE, FMA, and BBS scores, and negatively correlated with Numeric Rating Scale (NRS) pain scores. In multivariate logistic regression analysis, MMSE, NRS, educational level, and first stroke status were independently associated with non-high adherence. In the final parsimonious multivariable logistic regression model, MMSE score, NRS score, educational level, and first-stroke status were independently associated with non-high adherence. The final four-predictor model demonstrated good discrimination.

A multidimensional combined predictive model demonstrated good discrimination performance and may help to identify patients at higher risk of non-high adherence.

Early neurological deterioration (END) after endovascular thrombectomy (EVT) may be accompanied by heterogeneous postprocedural imaging abnormalities. We investigated the association between short-course methylprednisolone and a study-defined early composite imaging abnormality after EVT.

This single-center retrospective analysis included 297 patients with acute ischemic stroke who developed END within 72 hours after EVT (96 treated with methylprednisolone and 201 not treated). The index time was defined as completion of the post-END treatment decision, and the first intravenous methylprednisolone dose marked the onset of exposure. The first evaluable scan obtained after END confirmation but before completion of the treatment decision was designated the index scan. All evaluable scans obtained after the index time through 72 hours after EVT were reviewed. For patients who met the primary composite outcome, the endpoint scan was the first scan showing a new abnormality or progression of a preexisting abnormality that met the specified progression criteria; for patients who did not meet the primary outcome, it was the last evaluable scan within 72 hours after EVT. Multivariate logistic regression, propensity-score analyses, a restricted analysis among patients with modified Thrombolysis in Cerebral Infarction (mTICI) grade 2b-3, and false discovery rate (FDR) correction were used.

The composite outcome occurred in 42 of 96 treated patients and 122 of 201 untreated patients (43.8% vs 60.7%; p = 0.006). After multivariate adjustment, short-course methylprednisolone was associated with lower odds of the composite outcome (adjusted odds ratio, 0.46; 95% confidence interval [CI], 0.27-0.80; p = 0.005). The results were directionally consistent among patients with mTICI grades 2b-3 (adjusted odds ratio, 0.48; 95% CI, 0.27-0.86; p = 0.013), whereas the estimate for mTICI grades 0-2a was imprecise (p = 0.699). The index-to-endpoint-scan interval, endpoint imaging modality, and post-index scan frequency were comparable between groups. After FDR correction across 17 exploratory outcomes, only new or worsening cerebral edema remained statistically significant (q = 0.034). Neither the 90-day 3-category modified Rankin Scale (mRS) distribution nor the comparison of mRS 0-2 remained statistically significant after correction. Safety estimates were imprecise.

Short-course methylprednisolone was associated with lower odds of the study-defined early post-EVT composite imaging abnormality, primarily reflecting edema-related findings. This observational association did not establish functional benefit and requires prospective confirmation.

Heart failure (HF) is major and growing global health challenge, with lipid metabolism dysregulation recognized as a significant contributing factor. This review focuses on the emerging concept of the "metabolism-senescence axis", which plays a central role in disease development progression. Excess lipid metabolites, especially ceramides and diacylglycerols, contribute to cardiomyocyte injury through multiple mechanisms, including mitochondria dysfunction, promoting oxidative stress, and interfering with normal metabolic signals. The senescence-associated secretory phenotype (SASP) promotes a pro-senescent tissue microenvironment, thereby disrupting the normal metabolic balance and creating a vicious cycle that seriously affects heart structure and function. This review examines the molecular events underlying this process, including cellular injury, impaired fatty acid oxidation, oxidative stress, activation of the p53/p21 and p16INK4a/Rb, signaling pathways, and SASP-mediated metabolic dysfunction. We further discuss the rationale for combinatorial strategies targeting both metabolic dysfunction and cellular senescence, proposing that simultaneous intervention in these interconnected pathways may represent a promising therapeutic approach to delay the progression of HF and improve patient outcomes.

Ischemic stroke is a leading cause of mortality and long-term disability worldwide, with complex pathophysiological mechanisms and limited therapeutic options. The identification of key molecular targets that can effectively modulate the multifaceted pathological and reparative processes underlying ischemic stroke is urgently needed. Low-density lipoprotein receptor-related protein 1 (LRP1) is a multifunctional receptor widely expressed in the central nervous system (CNS), where it regulates lipid and bioenergetic metabolism, preserves blood‒brain barrier (BBB) function, modulates synaptic signaling, and supports neural stem/progenitor cell homeostasis. During cerebral ischemia, LRP1 undergoes a stage-dependent functional shift. In the acute phase, LRP1 promotes BBB disruption, tissue-type plasminogen activator (tPA)-associated hemorrhagic transformation, and early neuroinflammation, while also conferring neuroprotection by restraining inflammasome-mediated inflammatory responses and facilitating astrocyte-to-neuron mitochondrial transfer. In the recovery phase, LRP1 is involved in white matter injury and remodeling, including demyelination, remyelination, and white matter restoration. These effects are highly cell type-specific, reflecting distinct functions of LRP1 in endothelial cells, astrocytes, microglia, neutrophils, and oligodendrocyte-lineage cells. This context-dependent complexity underscores the need for a systematic review of the role of LRP1 in stroke. Here, we summarize the structural features and physiological functions of LRP1 in the CNS, discuss its roles and underlying mechanisms in ischemic stroke, and highlight the therapeutic potential and challenges of LRP1-targeted strategies for stroke intervention.

In Bangladesh, Cardiovascular diseases (CVDs) impose a significant healthcare and socioeconomic burden. Cardiac rehabilitation, a proven multidisciplinary approach, enhances the well-being of Cardiovascular disease (CVD) patients. However, there may be gaps in medical personnel's understanding of this vital intervention. This study, conducted at Bangladesh Medical University (BMU), Dhaka, Bangladesh a renowned cardiac care institution in Bangladesh, seeks to evaluate and improve medical professionals' knowledge, perceptions and attitudes regarding cardiac rehabilitation to enhance patient care and outcomes. The aim of this study was to identify the key factors influencing medical personnel's understanding of cardiac rehabilitation, including their training, experience and exposure to current guidelines. This cross-sectional observational study was conducted in the Department of Cardiology of Bangladesh Medical University (BMU), Dhaka, Bangladesh during the period from August 2022 to July 2023. In total 100 medical personnel included in the study. We found that the Mean±SD of age was 33.16±7.06 and the majority (80.0%) were female, followed by 20.0% who were male and 5.0% who were physicians. We also found that the majority of medical personnel have a positive understanding of cardiac rehabilitation. Cardiac rehabilitation (CR) is underutilized in Bangladesh, including among healthcare professionals. This study aims to enhance CR awareness and integration for better patient outcomes at Bangladesh Medical University, ultimately improving cardiovascular care in Bangladesh.