Atherosclerosis (AS), a chronic inflammatory disease driven by lipid accumulation and immune dysregulation, predisposes to acute cardiovascular events via plaque rupture and thrombosis. The molecular mechanisms linking immune microenvironment imbalance to plaque instability remain incompletely defined. Utilizing the GSE100927 dataset (69 AS patients vs 35 controls), we identified differentially expressed genes (DEGs) and constructed co-expression networks via weighted gene co-expression network analysis. Hub genes were intersected with DEGs to determine core genes. Immune cell infiltration was quantified using Cell-type Identification By Estimating Relative Subsets Of RNA Transcripts, and correlations between core genes and immune subsets were assessed. Diagnostic potential was evaluated by receiver operating characteristic (ROC) analysis. We identified 2596 DEGs (1575 up-/1021 downregulated) in AS tissues. Weighted gene co-expression network analysis revealed 3 disease-associated modules, yielding 54 hub genes. Intersection with DEGs identified 12 core genes, including HLA-G, HLA-A, HLA-C, and beta-2-microglobulin (B2M). These genes were enriched in "major histocompatibility complex class Ib-mediated antigen presentation" and significantly upregulated in AS (P < .001). Immune profiling showed elevated M0 macrophages and reduced resting CD4+ memory T cells in AS (P < .0001). Expression of HLA-G, HLA-A, HLA-C, and B2M positively correlated with M0 macrophages and negatively with CD4+ T cells (P < .001). ROC analysis within the GSE100927 dataset demonstrated high diagnostic accuracy for distinguishing AS samples from controls (HLA-G/A/C area under the ROC curve = 0.94; B2M area under the ROC curve = 0.87). HLA-G, HLA-A, HLA-C, and B2M modulate macrophage and T cell functions, driving immune dysregulation in AS. This immune imbalance is associated with plaque instability and may contribute to thrombosis risk, highlighting the potential of these molecules as diagnostic biomarkers and therapeutic targets.

Ischemic stroke (IS) exhibits notable sex-related differences, indicating a potentially important role for sex hormones such as sex hormone-binding globulin (SHBG), estradiol, and testosterone. This study employed 2-sample Mendelian randomization (MR) to investigate the causal relationships between these sex hormones and the risk of IS and its subtypes. Genetic instrumental variables for SHBG, estradiol, and testosterone were obtained from the IEU OpenGWAS database. These instruments were analyzed to assess their causal effects on IS and its subtypes using MR methods. Sensitivity analyses were performed using several complementary MR approaches. SHBG was inversely associated with the risk of IS (OR = 0.92; 95% CI = 0.87-0.97; P = .007) and with the small-artery occlusion subtype (OR = 0.84; 95% CI = 0.75-0.94; P = .002), whereas no associations were observed for the large-artery atherosclerosis or cardioembolism subtypes. No causal effects of estradiol or testosterone on IS were identified. Our findings suggest that higher SHBG levels may reduce the risk of IS and could represent a potential therapeutic target. Further studies are needed to elucidate the mechanisms by which SHBG may confer protection against IS.

Chronic total coronary occlusion (CTO) is a critical condition associated with poor outcomes in patients with coronary artery disease. Anion gap, a readily available laboratory marker, has been linked to various clinical outcomes, but its relationship with mortality in CTO patients is not well established. This study aimed to investigate the association between anion gap and 28-day all-cause mortality in patients with CTO admitted to the intensive care unit (ICU). We conducted a retrospective cohort study using data from the medical information mart for intensive care, version IV database (version 3.1), spanning from 2008 to 2019. Patients with CTO admitted to the ICU were included, and those with missing anion gap data or non-first-time ICU admissions were excluded. We used univariate and multivariate Cox regression models to evaluate the impact of anion gap on 28-day all-cause mortality. Adjustments were made for various clinical and laboratory parameters. A total of 830 patients were included in the analysis. The mean age was 69.4 years, and 76.5% were male. Anion gap was significantly associated with 28-day all-cause mortality in both univariate (hazard ratio [HR] 1.09, 95% confidence interval [CI] 1.05-1.13, P < .001) and multivariate analyses (HR 1.15, 95% CI 1.10-1.20, P < .001). The risk increased across quartiles, with the highest risk observed in the highest quartile (Q4, HR 21.22, 95% CI 2.78-161.93, P = .003). Subgroup analysis revealed significant interactions with gender and heart failure. Anion gap is a significant predictor of 28-day all-cause mortality in patients with CTO admitted to the ICU. Our findings suggest that monitoring anion gap could be clinically useful for risk stratification in this patient population. Further studies are needed to confirm these results and explore potential mechanisms.

The non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) is a novel lipid marker for cardiovascular disease. While previous studies have suggested a link between dyslipidemia and hypertension in various populations, the association between NHHR and hypertension in the older Chinese population remains unclear. This study aimed to investigate the association between NHHR and hypertension in a middle-aged and older Chinese population using data from the China Health and Retirement Longitudinal Study (CHARLS). We conducted a cross-sectional study using data from the China Health and Retirement Longitudinal Study 2015 database. NHHR was calculated as the ratio of non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol. Multivariable logistic regression models and penalized spline analysis were employed to investigate the association between NHHR and hypertension. Additionally, subgroup and sensitivity analyses were performed to assess the robustness of the findings. A total of 8342 participants (median age 67 years [interquartile range = 63-72]; 49.6% male, 50.4% female) were included in the analysis. NHHR was positively associated with prevalent hypertension. In the continuous analysis, the odds ratio for hypertension increased with each unit increment in NHHR across all multivariable-adjusted models. In the categorical model, the P value for the trend in the fully adjusted model was .097. A penalized spline analysis revealed a nonlinear association between NHHR and hypertension (P < .001). The association remained robust in subgroup and sensitivity analyses. This study found a significant association between NHHR and hypertension among older Chinese adults. The nonlinear relationship suggests a complex interplay that warrants further investigation. Prospective studies are needed to confirm these findings and clarify the temporal relationship between NHHR and hypertension.

Elevated serum uric acid is strongly associated with metabolic abnormalities and an increased risk of cardiovascular diseases. Endothelial dysfunction is considered a critical link in metabolic abnormalities. The Endothelial Activation and Stress Index (EASIX), a composite laboratory-based index, has not been systematically examined for its association with serum uric acid levels and endothelial function. This study utilized data from the 2007-2018 National Health and Nutrition Examination Survey (NHANES) with a cross-sectional design to assess the relationship between the EASIX index and serum uric acid levels. Multivariable linear regression analysis was conducted to evaluate their independent association, while restricted cubic splines (RCS) and piecewise regression models were employed to explore nonlinear dose-response trends. Subgroup and sensitivity analyses were performed to validate the robustness of the results. This study included 7602 participants, comprising those with normal and elevated serum uric acid levels. Regression analysis revealed a significant positive correlation between the EASIX index and serum uric acid levels after full adjustment for covariates (β = 0.26, 95% CI: 0.06-0.46). Quartile trend analysis demonstrated that serum uric acid levels increased with rising EASIX. RCS analysis revealed a nonlinear relationship, with serum uric acid levels plateauing at an EASIX value of approximately 1.31, suggesting a "threshold saturation" effect. Subgroup analyses confirmed consistent results across different demographic characteristics and disease statuses, and sensitivity analyses further validated the robustness of the findings. Among US adults, EASIX was positively and nonlinearly associated with serum uric acid levels. Exploratory analysis further suggested that higher EASIX quartiles were associated with increased odds of hyperuricemia. These findings indicate that EASIX may reflect systemic endothelial stress and metabolic burden related to uric acid variation. Further prospective and externally validated studies are needed to determine its clinical utility.

Isolated persistent left superior vena cava (IPLSVC) is an extremely rare congenital malformation with a low overall prevalence in the general population. Most patients present without typical clinical manifestations, leading to a relatively high rate of missed diagnoses in clinical practice. Owing to abnormal venous drainage, IPLSVC is frequently complicated with lesions of the cardiac conduction system, which may further induce arrhythmias.

A 37-year-old asymptomatic male patient accidentally discovered IPLSVC through chest echocardiography and computed tomography (CT) scans during a routine physical examination. The patient has no history of cyanosis, breathing difficulties, chest pain, or family history of heart disease.

Transthoracic echocardiography showed coronary sinus dilatation, and chest CT confirmed the absence of the right superior vena cava and the confluence of the right innominate vein into the left superior vena cava. Combined with imaging findings and clinical manifestations, the patient was diagnosed with IPLSVC.

Complete echocardiography and chest CT were performed to confirm the diagnosis, inform the patient of relevant procedural risks, recommend regular follow-up examinations and ambulatory electrocardiogram monitoring, and retain imaging data for subsequent diagnosis and treatment.

The patient experienced no discomfort during follow-up. Regular reexaminations and long-term cardiac monitoring were recommended.

Although IPLSVC patients are often asymptomatic in the early stages, it may increase the risk of central venous access, cardiothoracic surgery, and pacemaker implantation. Noninvasive echocardiography can provide a basis for early diagnosis of asymptomatic patients and has certain clinical significance. This case helps clinicians further understand IPLSVC in asymptomatic patients, confirms the screening value of routine cardiac ultrasound, and provides practical references for the diagnosis, follow-up, and clinical management of similar cases.

Evans syndrome is a rare autoimmune disorder characterised by concurrent or sequential autoimmune haemolytic anaemia and immune thrombocytopenia, often posing significant diagnostic and therapeutic challenges due to its relapsing nature and variable response to treatment. We report a patient with severe Evans syndrome who developed status epilepticus in the setting of intracranial haemorrhage secondary to profound treatment-refractory thrombocytopenia, illustrating the potential for life-threatening neurological complications when cytopenias are uncontrolled. Despite limited improvement with first-line therapies, the patient experienced haematologic recovery and clinical stabilisation following initiation of avatrombopag, a thrombopoietin receptor agonist. This case highlights the importance of early recognition of treatment refractoriness and supports the emerging role of avatrombopag as a valuable therapeutic option for persistent thrombocytopenia in Evans syndrome.

To develop a cardiovascular disease (CVD) risk prediction model with improved accuracy and interpretability by integrating diverse risk factors and applying Automated Machine Learning (AutoML), thereby enhancing clinical utility over conventional models.

This is a prospective cohort study. Data were obtained from the Multi-Ethnic Study of Atherosclerosis (MESA), including baseline and fifth follow-up visits, comprising 4713 participants. Exercise and dietary data were harmonized via Metabolic Equivalent of Task (MET) and Healthy Eating Index-2015 (HEI-2015), respectively. Predictor selection was performed using the Boruta algorithm alongside Random Forest (RF) error rate cross-validation. Logistic regression, four traditional machine learning algorithms, and H2O AutoML were each applied for model training and evaluation. Finally, the best-performing model was further interpreted using SHapley Additive exPlanations (SHAP).

A total of 21 predictors were selected, including age, sex, and Total Cholesterol (TC). Among the evaluated models, H2O AutoML outperformed other methods with an accuracy of 0.864, specificity of 0.892, precision of 0.610, F1 score of 0.670, and a Youden index of 0.635, achieving the highest AUC of 0.882 (0.846-0.918). SHAP analysis revealed the relative importance of predictors, with age, TC and Digit Symbol Score (DSS) ranking highest.

This study developed an AutoML-based CVD risk prediction model with superior discrimination and calibration, providing clinicians a practical tool for risk stratification. By enabling personalized prevention and early identification of high-risk individuals, this model has the potential to reduce CVD burden at the population level. Notably, DSS exhibited high importance and may represent a candidate risk marker.

To investigate the association between the frequency of adding salt to foods and incident osteoporosis and assess effect modification by genetic susceptibility.

Prospective cohort study.

UK Biobank, United Kingdom.

491,428 participants free of osteoporosis at baseline.

Frequency of adding salt to foods (excluding salt used in cooking) was assessed by questionnaire and categorized as never/rarely, sometimes, usually, or always. Multivariable Cox models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for incident osteoporosis and secondary cardiovascular outcomes.

During a median follow-up of 14.7 years, 15,953 osteoporosis cases were documented. Compared with the never/rarely group, fully adjusted HRs were 1.09 (95% CI 1.04-1.15) for usually and 1.32 (95% CI 1.24-1.41) for always (P for trend <0.001). The association was stronger in men, White participants, and those with higher BMI. In joint analyses, participants with high genetic risk who always added salt had the highest risk (HR 2.68, 95% CI 2.41-2.98). In the same cohort, always adding salt was also associated with higher cardiovascular mortality (HR 1.18, 95% CI 1.14-1.23) and cardiovascular events (HR 1.21, 95% CI 1.17-1.26).

A higher frequency of adding salt to foods was associated with a higher risk of incident osteoporosis. Together with the cardiovascular associations observed in this cohort, these findings suggest that adding salt to foods may be a modifiable behavior relevant to multiple age-related diseases.

To provide a practical, physiology-driven framework for advanced hemodynamic monitoring in patients with acute heart failure (AHF) and cardiogenic shock, highlighting and supporting clinicians in integrating monitoring tools into an individualized bedside approach.

Cardiogenic shock is increasingly recognized as a heterogeneous syndrome involving not only impaired cardiac output, but also systemic inflammation, vasoplegia, tissue hypoperfusion and multiorgan dysfunction. Recent studies have emphasized phenotype-based approaches for both diagnosis and treatment, integrating clinical evaluation, echocardiography, invasive hemodynamics and tissue perfusion markers. Machine learning derived phenotypes have further identified cardiorenal and cardiometabolic profiles associated with distinct prognostic implications. Critical care echocardiography has a central role for rapid diagnosis and serial reassessment, while transpulmonary thermodilution and pulmonary artery catheterization provide complementary information to echocardiography in refractory or complex cases.

Hemodynamic monitoring in AHF and cardiogenic shock should rely on individualized, multimodal and dynamic integration of clinical examination, biomarkers, echocardiography and invasive monitoring. The main goals are to define the underlying phenotype, assess congestion and tissue hypoperfusion, and evaluate treatment response. Echocardiography remains the cornerstone of bedside assessment, whereas invasive monitoring should be reserved for selected high-risk patients with persistent or complex shock.