Search Results (89)

Background/Objectives: Relationships between sleep quality, anxiety and depression are well-documented across the lifespan. Here we investigated relationships between sleep, mental health and markers of obesity and cardiovascular health in Higher Education students (young adults, 18–28 years) using repeated cross-sectional sampling. Methods: Students (n = 486) participated at one of four timepoints across 2020–2023. The PSQI (sleep quality), GAD7 (anxiety) and PHQ8 (depression) were completed online. Measurements of obesity (Body Mass Index (BMI), body fat percent (BF%) and waist–hip ratio (WHR)) and cardiovascular function (heart rate (HR), diastolic and systolic blood pressure (DP and SP)) were determined. Changes over time, differences between sexes, and correlations between parameters were examined. Results: All measures were stable over the 4-year period. GAD7 (p < 0.0001) and PHQ8 (p = 0.0014) scores were significantly higher in females than males. There were significant, moderate to strong correlations between PSQI, GAD7 and PHQ8 scores for both sexes (r = 0.34–0.71). Only 18.1% of females and 23% of males reported both good quality sleep and no or low levels of anxiety and depression. Significant sex-specific differences were observed across markers of obesity and cardiovascular function (for BF%, WHR, HR and SP—all p ≤ 0.01), which showed weak to moderate correlations with sleep and mental health. Impaired sleep latency (C2) was identified as a potential key contributing factor. Conclusions: These observations provide evidence of multiple established, interlinked chronic challenges affecting sleep, mental and physical health in students. Identification of a key role for impaired sleep latency provides a foundation for targeted intervention, focusing upon improving sleep initiation, to improve mental health outcomes. Full article

Atrial fibrillation (AF) is the supraventricular tachy-arrhythmia most commonly detected in the general population, with significant sex-related differences in epidemiology, pathophysiology, and treatment outcomes. Emerging evidence highlights the role of sex hormones—particularly estrogen and testosterone—in modulating left atrial electrophysiologic substrate, structural remodeling, inflammation, and thromboembolic risk. Hormonal fluctuations across different lifespan influence AF onset, progression, and therapeutic response, yet current management approaches largely overlook such determinants. This narrative review integrates data from basic, translational, and clinical research to examine hormonal effects on atrial substrate, disease progression, and differential results of treatments, including stroke prevention, pharmacological options, and transcatheter ablation. It also explores the potential of hormone-targeted interventions, antifibrotic therapies, and precision strategies tailored to hormonal status. Addressing these mechanisms could optimize patient-specific management, improve outcomes and guide future clinical practice recommendations. Advancing toward sex-specific, hormone-informed AF care requires further mechanistic studies, hormonal profiling, and sex-stratified clinical trials. Full article

Objective: This study investigated the prevalence of arterial stiffness among individuals diagnosed with myeloproliferative neoplasms (MPNs), specifically essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF). Methods: We performed a cross-sectional study at Chiang-Mai University Hospital, Thailand, defining arterial stiffness as a mean cardio-ankle vascular index (CAVI) ≥8.0. Patients were compared to age-, sex-, and Thai cardiovascular (CV) risk score-matched controls with CV risk factors. Additional outcomes included the 10-year CV risk in MPN patients, estimated by the Thai CV risk score, and the correlation between plasma C-reactive protein (CRP) levels and CAVI. Results: Eighty participants were included (50 with PV, 24 with ET, 6 with PMF; median age: 63.5 years). Arterial stiffness was present in 63.8% of MPN patients overall, with respective rates for ET, PV, and PMF being 70.8%, 60.0%, and 66.7% (p = 0.655). When compared to matched non-MPN controls with CV risk, prevalence of arterial stiffness did not differ significantly (65.2% vs. 60.9%, p = 0.539). The median estimated 10-year CV risk for patients with MPNs was 13.6% (range 0.7–30.0). No significant association was observed between CRP levels and mean CAVI (R = 0.208, p = 0.073). Conclusions: Arterial stiffness was detected in 63.8% of individuals with MPNs, a prevalence like that of matched non-MPN patients with CV risk factors. Full article

Background: While hyperuricemia has been widely studied in cardiovascular and renal diseases, the prognostic impact of low serum uric acid (UA) remains unclear. Emerging evidence suggests hypouricemia may be linked to increased mortality and adverse outcomes. This study aimed to assess the relationship between low UA levels and poor outcomes, including mortality and intensive care unit (ICU) admission, in hospitalized patients. Methods: This retrospective cohort study included 1679 hospitalized patients (744 females, 935 males) from the Internal Medicine Clinic. Patients were categorized into normal and low UA groups based on sex-specific thresholds (male: <3.4 mg/dL, female: <2.4 mg/dL). The primary outcome was in-hospital mortality; secondary outcomes were ICU admission and discharge status. Logistic regression models adjusted for age, chronic kidney disease (CKD), hypertension (HT), and coronary artery disease (CAD). A Prognostic Uric Acid Score (PUAS) was developed using significant predictors and evaluated by Receiver Operating Characteristic (ROC) analysis. Results: Low UA levels were significantly associated with higher ICU admission and mortality (p = 0.012). Multivariate analysis identified age (OR: 1.032), low UA (OR: 2.285), and CKD (OR: 1.571) as predictors of poor prognosis. PUAS showed moderate performance (AUC: 0.664), with a cutoff score of 3.5 optimizing sensitivity and specificity. Conclusions: Low UA levels independently predict mortality and poor prognosis in hospitalized patients. These findings support routine UA monitoring and suggest hypouricemia may be a useful prognostic biomarker. Further studies are needed to understand clinical implications and guide UA-targeted interventions. Full article

Background and Objectives: The autonomic nervous system (ANS) orchestrates adaptation to stress; however, its reactivity is influenced by demographic, anthropometric, and psychosocial factors. While arterial stiffness and central adiposity are established cardiovascular risk markers, less is known about how maladaptive coping strategies, cumulative life stress, and quality of life influence short-term autonomic regulation. This study examined the age- and sex-specific associations between anthropometry, maladaptive coping, life stress, quality of life, and ANS adaptation in adults. Materials and Methods: In this cross-sectional study, 122 healthy adults aged 21–78 years underwent a standardized lay–stand–lay (LSL) protocol with pulse wave analysis. Hemodynamic outcomes included pulse wave velocity (PWVao), augmentation indices (AIxA and AIxB), and aortic blood pressures (SBPao and PPao). Anthropometric measures comprised BMI, waist and hip circumference, waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR). Psychosocial assessments included the Young Hypercompensation Inventory (maladaptive coping), Holmes–Rahe Life Events Inventory (life stress), and EQ-5D-3L (quality of life). Associations were analyzed using mixed-effects models adjusted for covariates, with false discovery rate correction. Results: Age was the strongest determinant of autonomic reactivity: older adults showed greater recovery of augmentation indices and central pressures after orthostatic challenge. Sex differences were evident, with women displaying consistently higher augmentation indices and men showing greater PWV responses. Central adiposity (WHR, WHtR, and waist circumference) predicted blunted augmentation index reactivity, while hip circumference was protective. BMI-defined obesity showed weaker associations. Maladaptive coping, life stress burden, and quality of life were not significantly associated with ANS indices after correction for multiple comparisons. Conclusions: ANS adaptation to postural stress is largely determined by age, sex, and visceral adiposity, whereas psychosocial measures showed limited influence in this healthy adult sample. These findings highlight the demographic and anthropometric determinants of cardiovascular adaptability, suggesting that psychosocial influences may primarily act through long-term behavioral and neuroendocrine pathways. Full article

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Increasing evidence indicates that sex differences significantly influence the development, progression, and outcomes of CVDs. Recent advances have highlighted the central role of mitochondria, not only as cellular energy hubs but also as key regulators of oxidative stress, inflammation, and apoptosis, in mediating sex-specific cardiovascular responses. This review explores sexual dimorphism in cardiovascular disease, focusing on the interplay between mitochondrial function and sex hormones in cardiovascular tissues. We summarize current evidence on the molecular, hormonal, and cellular mechanisms contributing to sex-based disparities in cardiovascular outcomes. Preclinical studies suggest that female cardiac mitochondria may exhibit greater antioxidant capacity and produce fewer reactive oxygen species than male mitochondria, contributing to enhanced cardioprotection. Estrogen has been shown to influence mitochondrial bioenergetics and gene expression, affecting vascular tone, inflammation, and cardiac remodelling, whereas the role of testosterone remains less well defined. Additionally, sex-specific mitochondrial signalling responses have been reported under cardiac stress conditions, which may underlie differences in disease presentation and progression. A better understanding of how sex modulates mitochondrial function could improve risk stratification and support the development of personalized prevention and treatment strategies. Further research is needed to translate these mechanistic insights into clinical practice. Full article

Background: This novel study addresses the question of whether schizophrenia is associated with an increased risk of cardiovascular diseases (CVDs) by controlling for metabolic syndrome-related conditions through propensity score matching, using real-world primary care data from Germany. Methods: This retrospective cohort study analyzed 12,527 patients aged 18 or older with schizophrenia from 1209 general practices (GPs) in Germany between 2005 and 2023 from the IQVIA Disease Analyzer database. Patients were matched 1:5 with individuals without schizophrenia based on sex, age, index year, consultation frequency, and chronic conditions. CVDs cumulative incidence was assessed using Kaplan–Meier curves and hazard ratios (HRs) were calculated using univariable Cox regression analysis. Results: Over a 10-year follow-up, schizophrenia was associated with a higher risk of heart failure (HR: 1.33, 95% CI: 1.20–1.48) and a lower risk of atrial fibrillation and flutter (HR: 0.77, 95% CI: 0.67–0.89). No significant associations were observed for acute myocardial infarction (HR: 0.97, 95% CI: 0.76–1.25), angina pectoris (HR: 0.78, 95% CI: 0.63–0.96), or chronic ischaemic heart disease (HR: 0.91, 95% CI: 0.82–1.02). Stratified analyses showed that schizophrenia was most strongly associated with heart failure in women aged 41–50 years (HR: 3.34, 95% CI: 2.11–5.31), followed by women aged 61–70 years (HR: 1.88, 95% CI: 1.45–2.44) and men aged 51–60 years (HR: 1.81, 95% CI: 1.34–2.45). Conclusions: This study highlights significant differences in the 10-year cumulative incidence of CVDs between individuals with and without schizophrenia. While patients with schizophrenia appear less likely to be diagnosed with milder or asymptomatic CVDs, they are at increased risk for severe outcomes. The study’s findings underscore the need for sex-specific and symptom-sensitive public health strategies to improve early detection and prevention of CVDs in patients with schizophrenia. Full article

Introduction: Diverticular disease is common in Western countries, and the frequency of emergency operations for acute left-sided complicated diverticulitis (ALCD) has increased over the past 15 years. Methods: A total of 49 patients aged over 80 years and 125 younger patients who underwent emergency surgery for ALCD between October 2018 and June 2025 were analyzed. Demographics and postoperative outcomes were compared between the groups. Multivariate logistic regression was used to assess the association between age and postoperative morbidity and mortality. A separate regression model was used to identify risk factors for postoperative mortality and morbidity, specifically in elderly patients. Results: Significant differences between the two groups were found in sex distribution (p < 0.001), cardiovascular comorbidities (p < 0.001), chronic renal insufficiency (CRI) (p < 0.001), ASA score (p < 0.001), ALCD severity according to the modified Hinchey classification (p = 0.006), Mannheim Peritonitis Index (MPI) (p = 0.021), postoperative complications (p < 0.001), and 90-day mortality rates (p < 0.001). Advanced age was a significant predictor of 90-day postoperative mortality and morbidity. In the elderly subgroup, an ASA score ≥ 3, MPI > 25, CRI, and COPD were identified as independent predictors of 90-day postoperative mortality and morbidity. Conclusions: Advanced age is an independent risk factor for 90-day postoperative mortality and morbidity following emergency surgery for ALCD. In patients over 80 years, an ASA score ≥ 3, CRI, COPD, and MPI ≥ 25 are associated with a poorer prognosis. Full article

Background/Objectives: Cardiac sarcoidosis (CS) is a granulomatous inflammatory cardiomyopathy with heterogeneous presentations, from palpitations to heart failure and sudden cardiac arrest. Despite advances in imaging and immunosuppressive (IS) therapy, relapse patterns and long-term outcomes remain poorly defined. This study aimed to characterize relapse and identify predictors of relapse and major adverse cardiac events (MACE) in a real-world CS cohort. Methods: This retrospective single-center study included 25 adults diagnosed with CS at Geneva University Hospitals between 2016 and 2024, classified per the 2024 American Heart Association diagnostic criteria. Relapse was defined as clinical, arrhythmic, or imaging deterioration requiring treatment escalation. MACE included cardiovascular hospitalization, device therapy, left ventricular assist device, heart transplant, or death. Statistical methods included Kaplan–Meier analysis with log-rank tests and multivariable Cox regression adjusted for age and sex. Results: Relapse occurred in 13 patients (56%), frequently subclinical (61.5%) and detected incidentally on routine PET-CT during IS tapering. In the multivariate model, predictors of relapse included right ventricular FDG uptake (aHR 13.1; 95% CI 1.3–133.7; p = 0.03) and second-line immunosuppression duration ≤24 months (aHR 20.1; 95% CI 1.1–363.8; p = 0.04). Relapse-free patients were more often maintained on dual or triple IS therapy (71.4% vs. 15.4%; p = 0.02) and low-dose prednisone (<10 mg/day) (57.1% vs. 7.7%; p = 0.03). Conclusions: Relapse is common in CS, often subclinical, and associated with PET-CT findings and premature IS tapering. Maintenance therapy may reduce risk. Multimodal imaging remains critical for disease monitoring, though tracers with higher specificity are needed. Further research should refine relapse definitions and support personalized treatment strategies. Full article

Obesity has traditionally been considered a major risk factor for numerous metabolic disorders and diseases. However, a subset of individuals with obesity, classified as having “metabolically healthy obesity” (MHO), display relatively normal metabolic parameters despite excess adiposity. This review critically examines the current knowledge surrounding MHO, including its various definitions, prevalence, clinical characteristics, contributing factors, and long-term outcomes. While MHO carries lower health risks compared to metabolically unhealthy obesity (MUO), evidence consistently demonstrates increased disease risk compared to metabolically healthy normal-weight individuals, particularly for type 2 diabetes, cardiovascular disease, chronic kidney disease, and certain cancers. MHO prevalence ranges from 10 to 30% among individuals with obesity globally, varying by sex, age, BMI, and ethnicity. Multiple factors contribute to the MHO phenotype, including beneficial adipose tissue distribution patterns, enhanced adipocyte function, favorable genetic profiles, and lifestyle factors. Recent single-cell transcriptomic analyses have identified specific cell populations, particularly mesothelial cells, as key drivers of metabolic health in visceral adipose tissue. The discovery of persistent epigenetic memory of obesity provides molecular evidence for why MHO often represents a transient state, with many individuals progressing to MUO over time. Emerging evidence also reveals differential therapeutic responses to GLP-1 receptor agonists between MHO and MUO phenotypes, highlighting the need for precision medicine approaches. The concept of MHO has important clinical implications for risk stratification and personalized treatment approaches. This review synthesizes current evidence while highlighting knowledge gaps and future research directions in this rapidly evolving field. Full article

Background/Objectives: To investigate the associations between educational attainment and 20-year cardiovascular disease (CVD) incidence, mortality, lifetime risk, and burden, and to explore the mediating role of healthy and sustainable dietary habits through a sex-specific lens. Methods: A total of 3042 CVD-free adults from the ATTICA Study were included at the 2001/2002 baseline. Educational level was treated as both continuous and ordinal variable. Adherence to the EAT–Lancet diet pattern (EAT-LDP) was assessed at baseline. Participants were followed for 20 years, with complete data on CVD outcomes available for 1988 individuals. Generalized structural equation and nested Cox regression models were used to estimate the direct and indirect effects between education attainment and 20-year CVD incidence. Moderation analysis was also conducted by incorporating interaction terms in Cox models. Results: An inverse educational gradient in CVD risk and burden was observed, particularly among females for lifetime risk estimates. Each additional year of education was associated with higher EAT-LDP adherence (β = 0.45, 95% CI: 0.40–0.50) and increased odds of physical activity (OR: 1.01, 95% CI: 1.00–1.01). These behaviors mediated part of the relationship between education and long-term CVD incidence. Among females, the cardioprotective role of EAT-LDP adherence was more evident at lower educational levels, suggesting potential effect modification. Conclusions: Educational disparities in long-term CVD outcomes are partly mediated by sustainable dietary habits. These findings highlight the need for gender-responsive and equity-focused strategies in cardiovascular prevention. Full article

The oral microbiota, long recognized for their role in local pathologies, are increasingly implicated in systemic disorders, particularly cardiovascular disease (CVD). This review focuses on emerging evidence linking oral dysbiosis to neuroglial activation and autonomic dysfunction as key mediators of cardiovascular pathology. Pathogen-associated molecular patterns, as well as gingipains and leukotoxin A from Porphyromonas gingivalis, Fusobacterium nucleatum, Treponema denticola, Aggregatibacter actinomycetemcomitans, etc., disrupt the blood–brain barrier, activate glial cells in autonomic centers, and amplify pro-inflammatory signaling. This glia driven sympathetic overactivity fosters hypertension, endothelial injury, and atherosclerosis. Crucially, sex hormones modulate these neuroimmune interactions, with estrogen and testosterone shaping microbial composition, glial reactivity, and cardiovascular outcomes in distinct ways. Female-specific factors such as early menarche, pregnancy, adverse pregnancy outcomes, and menopause exert profound influences on oral microbial ecology, systemic inflammation, and long-term CVD risk. By mapping this oral–brain–heart axis, this review highlights the dual role of oral microbial virulence factors and glial dynamics as mechanistic bridges linking periodontal disease to neurogenic cardiovascular regulation. Integrating salivary microbiome profiling with glial biomarkers [e.g., GFAP (Glial Fibrillary Acidic Protein) and sTREM2 (soluble Triggering Receptor Expressed on Myeloid cells 2)] offers promising avenues for sex-specific precision medicine. This framework not only reframes oral dysbiosis as a modifiable cardiovascular risk factor, but also charts a translational path toward gender tailored diagnostics and therapeutics to reduce the global CVD burden. Full article

Objectives: Sex-based disparities in COVID-19 outcomes are well-documented, with men experiencing greater acute severity and women showing increased vulnerability to post-viral syndromes. However, longitudinal immunometabolic trajectories in vaccinated individuals remain underexplored. In this study, sex-based differences in long-term metabolic, endocrine, renal, cardiovascular, and inflammatory responses were investigated among vaccinated individuals recovering from SARS-CoV-2 infection. Methods: This retrospective single-center cohort study included 426 adults (199 females, 227 males) with PCR-confirmed symptomatic COVID-19 and at least two vaccine doses. Serial assessments were conducted at baseline, 18-, 24-, and 30-month post-infection. Parameters included fasting glucose, HbA1c, lipid profile, thyroid function, renal markers, CRP, D-dimer, fibrinogen, troponin, and hematologic indices. Statistical analyses assessed longitudinal changes and sex-stratified correlations. Results: Fasting glucose and HbA1c levels significantly declined over time, more prominently in males. Glucose correlated with age and BMI only in females. Lipid levels remained largely unchanged, although males had higher baseline triglycerides. Females showed rising TSH levels and persistently lower free T3; males exhibited higher creatinine, urea, and troponin levels throughout. Inflammatory markers declined significantly in both sexes, with males displaying higher CRP and troponin, and females showing sustained fibrinogen elevation and a temporary lymphocyte surge. D-dimer was elevated in females at the 30-month point. Conclusions: Sex-specific physiological recovery patterns were evident among vaccinated COVID-19 survivors. Males exhibited earlier metabolic and cardiac alterations, while females had more persistent endocrine and inflammatory shifts. These findings underscore the need for sex-tailored long-term monitoring strategies prioritizing early metabolic and cardiac screening in men and prolonged immunoendocrine surveillance in women. Full article

Vitamins A, D, E, K, B2, B12, and C play a key role in regulating metabolism and oxidative stress, significantly impacting cardiometabolic health. This review uniquely integrates mechanistic and epidemiological data to examine sex-specific differences in the bioavailability, metabolism, and physiological effects of these vitamins. By linking hormonal and genetic factors with oxidative stress modulation, lipid metabolism, and endothelial function, we outline how individualized vitamin intake strategies may help prevent cardiovascular and metabolic disorders. The paper also identifies natural dietary sources and optimal intake recommendations for each vitamin, emphasizing the importance of tailoring supplementation to sex-related needs. This sex-focused perspective provides a basis for developing personalized nutrition approaches to optimize cardiometabolic outcomes. Full article

Background: Armed conflicts impose complex logistical and behavioral challenges on healthcare systems, particularly in managing acute conditions such as ST-elevation myocardial infarction (STEMI) and ischemic stroke. Although both diagnoses require timely intervention, their clinical pathways differ significantly. Few studies have systematically compared their management during active warfare, particularly within the warzone. Methods: This retrospective cohort study was conducted at Soroka University Medical Center (SUMC), the sole tertiary hospital in southern Israel and the main referral center for cardiovascular and neurological emergencies in the region. We included all adult patients (≥18 years) admitted with new-onset STEMI or ischemic stroke during three-month periods of wartime (October–December 2023) and matched routine periods in 2021 and 2022. Patients with in-hospital events, inter-hospital transfers, or foreign citizenship were excluded. Data on demographics, comorbidities, arrival characteristics, treatment timelines, and outcomes were extracted from electronic medical records. Categorical variables were compared using Chi-squared or Fisher’s exact test, and continuous variables using t-tests or Mann–Whitney U tests, as appropriate. Multivariable logistic and linear regression models were adjusted for age, sex, Charlson Comorbidity Index (CCI), and mode of arrival. Interaction terms assessed whether wartime modified the associations differently for STEMI and stroke. Results: A total of 410 patients were included (193 with STEMI and 217 with stroke). Patients with STEMI were significantly more likely to arrive by self-transport during the war (38, 57.6% vs. 32, 25.2%, p < 0.001) and had higher rates of late arrival beyond 12 h (19, 28.8% vs. 13, 10.2%, p = 0.002). These findings support the conclusion that patients were more prone to delayed and unstructured presentations during a crisis. In contrast, patients with stroke showed a reduction of 354 min in symptom-to-door times during the war [median 246 (30–4320 range) vs. 600 min (12–2329 range), p = 0.026]. Regression models revealed longer delays for stroke vs. STEMI in routine settings [β = 543.07 min (239.68–846.47 95% CI), p < 0.001], along with significantly lower in-hospital (OR = 0.39, 95% CI= 0.15–0.97, p = 0.05) and 30-day mortality (OR = 0.43, 95% CI= 0.19–0.94, p = 0.04). However, these differences were no longer significant during wartime. Patients with STEMI showed a trend toward lower 180-day mortality during the war (OR = 0.33, 95% CI = 0.09–0.99; p = 0.07), although this difference did not reach statistical significance. Conclusions: During wartime, patients with stroke arrived earlier and in greater numbers, while patients with STEMI showed reduced admissions and delayed, self-initiated transport. Despite these shifts, treatment timelines and short-term outcomes were maintained. These diagnosis-specific patterns highlight the importance of reinforcing EMS access for STEMI and preserving centralized protocol-based coordination for stroke during crises. Full article