Extending women's health-span is a key challenge for the medical community. Although women live longer than men, they face a higher burden of chronic diseases, such as cardiovascular diseases (CVDs) and disabilities. Endogenous estrogens appear to benefit cardiovascular health, and their marked decline at menopause is associated with increased cardiovascular risk; conversely, poor cardiovascular health may hasten menopause onset. Systemic menopause hormone therapy (MHT) begun early-ideally soon after symptom onset and at most within 10 years of the final menstrual period-alleviates climacteric symptoms and is associated with long-term benefits. This joint position paper between the International Federation of Gynecology and Obstetrics (FIGO) and the World Heart Federation (WHF) aims at supporting both gynecologists and cardiologists in providing a tailored and evidence-based counseling on systemic MHT use to women with increased CVD risk or established ischemic heart disease (IHD). Women with CVD risk factors require thorough risk stratification to tailor MHT type, dose, and route. For those at high thromboembolic risk, transdermal estrogen, with micronized progesterone or dydrogesterone when needed, is considered the safest regimen. Women with established IHD may receive systemic MHT for symptom relief, provided risks and benefits are carefully reviewed. Transdermal low-dose estrogen, alone or with micronized progesterone or dydrogesterone, is the best choice. All primary and secondary prevention measures, including statins, should be continued. Managing the most complex cases warrants the adoption of a multidisciplinary approach between cardiologists, gynecologists, internists and primary care providers to offer the best possible care.

Mitral regurgitation affects 2% of the population globally, with a widely increasing prevalence. Although mitral regurgitation is most commonly corrected by open surgery, there has been a recent shift toward less invasive transcatheter approaches, including both transcatheter edge-to-edge repair (TEER) and transcatheter mitral valve replacement (TMVR).

A comprehensive literature search was conducted using four databases: PubMed, Cochrane Library, Virtual Health Library (VHL), and Web of Science (WOS), following the PRISMA guidelines. Relevant observational studies were assessed for reporting using STROBE guidelines, whereas case reports were assessed using CARE guidelines. Independent reviewers evaluated studies based on eligibility criteria and analyzed relevant studies.

Postoperative complications observed in patients undergoing either technique (TMVR or TEER) included acute kidney injury, stroke, access site complications, and postoperative bleeding. These complications were generally more frequent in patients after TMVR. Myocardial infarction, prosthesis malposition, and valve migration were reported exclusively after TMVR, whereas ischemic cardiomyopathy was associated with TEER. Regarding hemodynamic outcomes, TMVR patients were associated with greater MR reduction to ≤ 1, frequently observed complete MR resolution, near-laminar blood flow, and marked improvement in left ventricular function (assessed using LVEDVI and LVESVI). TMVR was associated with significantly higher 30-day mortality, whereas pooled 1-year mortality did not differ significantly between TMVR and TEER.

Although TEER remains the safer option in appropriately selected patients, TMVR offers greater efficacy in MR resolution at the cost of higher procedural risk. However, findings should be interpreted with caution, given that patient selection between TMVR and TEER patients may influence observed outcomes.

Sleep disruption and irregular work schedules are increasingly recognized as behavioral risk factors for premature cardiovascular disease. Their associations with coronary plaque complexity and CT-derived functional ischemia in young adults remain underexplored.

To investigate the association of multidimensional sleep phenotype, shift-related occupation, and coronary plaque complexity as well as CT-derived functional ischemia in adults aged ≤40 years, adjusting for clinical confounders.

This retrospective study included 3,983 young adults who underwent coronary CT angiography (CCTA). Sleep phenotype was assessed using a multidimensional score incorporating sleep duration, timing, regularity, quality, and sleep-related symptoms. Occupations were classified as shift-related or non-shift. Coronary plaque characteristics, including stenosis severity, minimum lumen area, lesion length, diffuse disease, occlusion, coronary artery calcium score, and CT-derived fractional flow reserve (CT-FFR), were analyzed. Multivariable logistic regression, adjusted for age, sex, BMI, smoking, hypertension, diabetes, dyslipidemia, and shift-related occupation, assessed associations with CT-FFR ≤ 0.80.

Poor sleep phenotype was associated with more severe stenosis, smaller lumen area, longer lesions, and higher prevalences of diffuse disease, occlusion, and CT-FFR ≤ 0.80. In multivariable analysis, sleep phenotype remained independently associated with CT-FFR ≤ 0.80 after adjusting for clinical covariates and shift-related occupation. Shift-related occupation further modified this association, with a stronger relationship observed among shift workers.

In young adults, poorer sleep phenotype was accompanied by more complex coronary plaque features and was independently associated with a higher likelihood of CT-FFR-defined functional ischemia after adjustment for clinical covariates.

Poor sleep and irregular working hours may affect heart health, but their relationship with early coronary artery disease in young adults is not well understood. We studied 3,983 adults aged 40 years or younger who underwent coronary CT scans. Participants with poorer sleep patterns were more likely to have longer and more severe coronary artery narrowing, more widespread plaque, and reduced blood flow to the heart. These associations remained after accounting for established cardiovascular risk factors. The relationship between poor sleep and impaired coronary blood flow was particularly strong among people working night shifts or other irregular schedules. Although this observational study cannot prove that poor sleep directly causes coronary disease, the findings suggest that sleep habits and work schedules may help identify young adults who could benefit from earlier cardiovascular risk assessment and preventive support.

Central adiposity is a key determinant of hypertension, yet most studies rely on single-time-point measures or include individuals with diabetes, potentially confounding associations. The relationship between long-term body roundness index (BRI) trajectories and incident hypertension in non-diabetic populations remains unclear.

We conducted a longitudinal analysis of non-diabetic middle-aged and older adults from the China Health and Retirement Longitudinal Study (CHARLS), with external validation using the English Longitudinal Study of Ageing (ELSA). In CHARLS, BRI measurements from Waves 1-3 (2011-2016) were used to construct trajectories, and incident hypertension was assessed at Wave 4 (2018-2020). In ELSA, trajectories were constructed using BRI measurements from Waves 2, 4, and 6 (2004-2013), and incident hypertension was assessed at Wave 8 (2016-2017). Associations were examined using multivariable logistic regression, with subgroup and sensitivity analyses. Machine learning models were additionally developed for multivariable hypertension risk prediction.

Three BRI trajectories were identified in both cohorts: low-level inverted U-shaped, moderate-level inverted U-shaped, and high-level increasing trajectories. Higher BRI trajectories were associated with a graded increase in incident hypertension risk in CHARLS. Compared with the low-level inverted U-shaped trajectory, the adjusted odds ratios (95% confidence intervals) were 1.40 (1.13-1.73) for the moderate-level inverted U-shaped trajectory and 1.76 (1.21-2.56) for the high-level increasing trajectory. Directionally consistent findings were observed in ELSA, particularly for the high-level increasing trajectory. Findings remained robust in subgroup and sensitivity analyses. Machine learning analyses showed that BRI trajectory provided complementary predictive information when combined with clinical and biomarker variables.

Longitudinal BRI patterns were associated with incident hypertension in non-diabetic adults. Repeated assessment of BRI may provide complementary information for identifying individuals at elevated hypertension risk, although its causal and clinical implications require further investigation.

This study examined the mediating role of self-efficacy in the relationship between social integration and self-disgust among patients with stroke, with the aim of informing the development of targeted interventions.

In this cross-sectional study, a total of 207 patients with stroke completed a general demographic questionnaire, the Stroke Rehabilitation Self-Efficacy Assessment Scale, the Social Network Scale, and a self-disgust assessment tool. Pearson's correlation analyses were performed to examine the relationships among self-efficacy, social integration, and self-disgust. Mediation analysis was then conducted, with the significance of indirect effects evaluated using the bootstrap method.

Median (interquartile range) scores for self-disgust, social integration, and self-efficacy were 40 (36, 45), 3 (2, 5), and 70 (67, 77) respectively. Correlation analysis indicated that self-disgust was significantly negatively correlated with social integration (p < 0.01), and with self-efficacy (p < 0.01). Additionally, social integration was significantly positively correlated with self-efficacy (p < 0.01). Mediation analysis demonstrated that self-efficacy exerted a significant indirect effect on the relationship between social integration and self-disgust (effect = -0.475), with the indirect pathway through self-efficacy was associated with 43.42% of the total observed effect.

Our results suggest that self-efficacy may partially mediate the relationship between social integration and self-disgust in patients with stroke. Interventions that enhance self-efficacy and promote social integration may reduce self-disgust and support rehabilitation outcomes.

Small artery occlusion stroke is often mild, but some patients need rehabilitation during acute hospitalization. We developed and internally validated an interpretable model to assist early in-hospital rehabilitation screening and triage and tested whether white matter hyperintensity burden and inflammatory-metabolic biomarkers improved prediction beyond routine clinical variables.

Consecutive adults with acute ischemic stroke classified as small artery occlusion were identified from a single-centre stroke registry and electronic health records. Early rehabilitation need was assessed within 48 h after admission by trained rehabilitation physicians using a structured protocol. The prespecified primary model used clinical variables. Extended models added modified Fazekas score, inflammatory metabolic biomarkers, or both. Eight regression and machine learning algorithms were compared. Internal validation used stratified tenfold cross validation with nested fivefold tuning. Performance was assessed using discrimination, precision recall, calibration, and decision curve analysis.

Among 411 patients, 155 had early rehabilitation need (37.7%). The clinical-variable model performed best, with an area under the receiver operating characteristic curve of 0.682 and an area under the precision recall curve of 0.591. Adding modified Fazekas score, inflammatory metabolic biomarkers, or both did not improve performance. Logistic regression performed comparably to complex algorithms. In the admission fixed-landmark sensitivity analysis, the clinical-variable model yielded an AUROC of 0.623, which decreased to 0.507 after variables directly reflecting acute neurological deficits were excluded. Leading predictors reflected neurological severity, early functional impairment, and care pathway characteristics.

Early rehabilitation need was common among patients with small-artery occlusion stroke during acute hospitalization. Routine clinical variables provided the dominant predictive information, whereas white matter hyperintensity burden and inflammatory-metabolic biomarkers added no stable incremental value.

Although patient activation and eHealth literacy are known to influence self-management in chronic diseases, evidence on whether eHealth literacy mediates this relationship in patients with coronary heart disease (CHD) remains limited. This study explored the associations between patient activation, eHealth literacy, self-efficacy and self-management in patients with CHD and aimed to examine both the direct and indirect associations of patient activation on self-efficacy and self-management through eHealth literacy.

A cross-sectional method was adopted and a convenience sample of 433 hospitalized patients with CHD was recruited. Data were collected using the Patient Activation Measure-13, the eHealth Literacy Scale and the Heart Health Self-Efficacy and Self-Management scale (which provides a composite outcome measure) and analyzed using Pearson correlation, stepwise regression and bootstrap methods.

The mean scores were 58.89 ± 18.87 for patient activation, 24.92 ± 8.94 for eHealth literacy and 60.70 ± 15.34 for the combined self-efficacy and self-management measure. Patient activation was moderately positively correlated with eHealth literacy (r = 0.51, p < 0.001) and the combined measure (r = 0.59, p < 0.001), and eHealth literacy showed a weak positive correlation with the combined measure (r = 0.37, p < 0.001). Patient activation was directly and positively associated with the combined measure (β = 0.533, p < 0.001), and eHealth literacy partially mediated this relationship (indirect effect = 0.043, 95% CI [0.002, 0.088], p = 0.043), accounting for 9% of the total effect. This relatively small indirect effect suggests a modest mediating role, indicating that the direct pathway from patient activation to self-efficacy and self-management is substantially more influential than the pathway through eHealth literacy in this population.

Patient activation, eHealth literacy, self-efficacy and self-management in patients with CHD were at moderate or moderately low levels. Higher levels of patient activation and eHealth literacy are associated with better self-efficacy and self-management, a pattern that may underlie improved self-management.

A 7-year, 6-month-old, female neutered, Pug dog presented with lethargy, hyporexia, polydipsia, abdominal distension, and dyspnea. Point-of-care ultrasonography identified tricavitary effusions and cardiac tamponade. Pericardiocentesis yielded 83 mL of sanguineous scintillating fluid. Clinical examination, bloodwork, echocardiography, electrocardiography, thoracic and abdominal computed tomography scans, and pericardial fluid analysis including culture and sensitivity did not identify any cardiovascular, endocrine, neoplastic, or infectious causes of the pericardial effusion. Pericardial fluid analysis identified high cholesterol concentrations and numerous cholesterol crystals on cytology, supporting a diagnosis of cholesterol pericarditis. Subtotal pericardiectomy was performed 7 weeks later to address pericardial and pleural effusions. Histopathological pericardial biopsies identified pericarditis with no neoplastic tissue detected. A pleural port was placed 4 months later to manage recurrent pleural effusion. Elective euthanasia was performed 10 weeks later citing a compromised quality of life from increasingly frequent bouts of dyspnea. This is a case report of a dog with idiopathic cholesterol pericarditis presenting with cardiac tamponade.

Vitamin B12 and folate status were evaluated in adults with vasovagal syncope.No association was found between vitamin deficiency and vasovagal syncope overall.Lower vitamin B12 levels were observed in patients with frequent syncope.

Clinical evidence suggests an association between vitamin B12 deficiency and vasovagal syncope (VVS) in pediatric patients. This study investigated the association of vitamin B12 and folate deficiency with VVS in adults.

In this case-control study, adult patients with VVS who presented to the tertiary syncope unit for head-up tilt table testing comprised the case group. Age- and sex-matched individuals without syncope history from the population-based Tehran Cohort Study served as the control group. Exclusion criteria included but were not limited to the use of vitamin B supplements, carbamazepine, or phenobarbital, and sleeve gastrectomy. Serum vitamin B12, folate, and homocysteine levels were measured and compared.

From February 2020 through February 2021, 44 patients comprised the case group, matched with 44 controls (mean age, 37.9 years; 23 [52.3%] females in each group). No statistically significant difference existed between the groups in vitamin B12 or folate deficiency or serum levels. Serum vitamin B12 levels were significantly lower in patients with frequent VVS (≥3 lifetime episodes) than in patients with infrequent VVS (<3 lifetime episodes) (233.8 [80.7] vs 305.2 [118.1] pg/mL; P=0.042), and the association remained significant after adjustment for confounders (P=0.026).

No association existed between vitamin B12 or folate deficiency or serum levels and VVS. Frequent VVS was associated with lower serum vitamin B12 levels than infrequent VVS.

ST-segment elevation myocardial infarction (STEMI), a critical manifestation of coronary artery disease, involves complex molecular mechanisms potentially linked to brown adipocyte (BA) biology. This study aimed to identify BA-related key genes and elucidate their roles in STEMI progression. Transcriptomic data from peripheral blood mononuclear cells (PBMCs) of STEMI patients and stable coronary artery disease (CAD) controls were obtained from the GEO database (GSE59867, GSE62646). A 102-gene brown adipocyte-related gene (BARG) set was curated from published literature. Differentially expressed genes (DEGs) were identified using limma, and weighted gene co-expression network analysis (WGCNA) combined with single-sample gene set enrichment analysis (ssGSEA) was applied to detect BARG-associated module genes. The intersection of DEGs and module genes yielded 20 candidate genes, which were further refined using LASSO regression and SVM-RFE machine learning algorithms, identifying ASGR2, MCEMP1, and PPARG as key genes consistently upregulated in STEMI across both datasets. A nomogram model incorporating these three genes achieved an area under the ROC curve (AUC) of 0.973, demonstrating excellent diagnostic performance. Gene set enrichment analysis (GSEA) revealed convergent enrichment of all three key genes in neutrophil degranulation and Toll-like receptor signaling cascades. Immune infiltration profiling using CIBERSORT identified significant increases in monocytes alongside decreases in resting NK cells and eosinophils in STEMI, with all three key genes showing significant correlations with these immune cell populations. Molecular docking identified shinpterocarpin as a candidate compound targeting PPARG with a suggestive binding affinity (-5.8 kcal/mol), warranting further experimental validation. RT-qPCR in an independent preliminary clinical cohort (n = 5 per group) demonstrated upregulation of all three key genes in STEMI patients (p < 0.05), consistent with bioinformatic predictions. This study identifies ASGR2, MCEMP1, and PPARG as BA-associated key genes in STEMI PBMC profiles and highlights their potential immune-metabolic relevance.