Search Results (300)

Cardiovascular disease (CVD) is increasingly recognized as a significant comorbidity in people living with HIV (PWH), contributing to increased morbidity and mortality. Epidemiological studies indicate that PWH have a 1.2–2-fold higher risk of myocardial infarction (MI) and other CVD events compared to HIV-negative individuals. While the mechanisms underlying HIV-associated CVD are not fully understood, they are likely to include a combination of cardiovascular-related adverse effects of HIV medications, vascular dysfunction caused by HIV-induced monocyte activation, and cytokine secretion, in addition to existing comorbidities and lifestyle choices. This comprehensive review examines the complex relationship between HIV infection and CVD, highlighting key pathophysiological mechanisms such as chronic immune activation, inflammation, endothelial dysfunction, and the role of antiretroviral therapy (ART) in promoting cardiovascular risk. Alongside conventional risk factors such as smoking, hypertension, and dyslipidemia, HIV-specific elements, especially metabolic abnormalities associated with ART, significantly contribute to the development of CVD. Prevention strategies are crucial, focusing on the early identification and management of cardiovascular risk factors as well as optimizing ART regimens to minimize adverse metabolic effects. Clinical guidelines now recommend routine cardiovascular risk assessment in PWH, emphasizing aggressive management tailored to their unique health profiles. However, challenges exist in fully understanding the cardiovascular outcomes in this population. Future research directions include exploring the role of inflammation-modulating therapies and refining sustainable prevention strategies to mitigate the growing burden of CVD in PWH. Full article

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. This increases the demand for real-world evidence to complement findings from randomized controlled trials. The German IQVIA Disease Analyzer (DA) database, which is populated with anonymized electronic medical records from general practitioners and specialists, has become an increasingly valuable source for cardiovascular research. Over the past two decades, and especially between 2020 and 2025, numerous epidemiological studies have used this database to explore associations between cardiovascular risk factors, comorbidities, therapeutic patterns, and cardiovascular outcomes in large, broadly representative outpatient populations. This review synthesizes evidence from 13 selected DA-based studies examining atrial fibrillation, heart failure, cardiometabolic disease, lipid management, non-alcoholic fatty liver disease (NAFLD)–related cardiovascular risks, cerebrovascular complications, COVID-19-associated vascular events, and modifiable behavioral and anthropometric factors. These studies were selected based on predefined criteria including cardiovascular relevance, methodological rigor, large sample size, and representativeness of key disease domains across the 2000–2025 period. Eligible studies were identified through targeted searches of peer-reviewed literature using the German IQVIA Disease Analyzer database and were selected to reflect major cardiovascular disease domains, risk factors, and therapeutic areas. Across disease domains, the reviewed studies consistently demonstrate the DA database’s capacity to identify reproducible associations between cardiometabolic risk factors, comorbidities, and cardiovascular outcomes in routine outpatient care. While causal inference is not possible, the database enables the identification of clinically meaningful associations that inform hypothesis generation, help quantify disease burden, and highlight gaps in prevention or treatment. The database’s strengths include large sample sizes (often exceeding 100,000 patients), long follow-up periods, and high external validity, while limitations relate to coding accuracy, residual confounding, and the absence of detailed clinical measures. Collectively, the evidence underscores the importance of the DA database as a crucial platform for real-world cardiovascular research. Full article

The quality of high-density lipoproteins (HDLs) is characterized by lipid and protein composition, oxidation and glycation extent, and particle size, while the quantity of HDL-C is just the cholesterol amount in HDL. The inverse association between HDL-C and cardiovascular disease (CVD) and hypertension has been well established; however, the U-shaped mortality risk observed from HDL-C underscores that HDL quality and function are equally important. The present cross-sectional study assessed the correlations of serum lipid and glucose profiles, and low-density lipoprotein (LDL) and HDL characteristics, with blood pressure (BP) distribution in ordinary middle-aged Korean participants (n = 50; mean age 47.0 ± 11.7 years; males: n = 25, 49.2.0 ± 11.7 years; females: n = 25, 44.8 ± 11.5 years), with particular focus on HDL quality and its antioxidant capacity. This study observed that serum elevated triglyceride (TG) and glucose levels were directly proportional to elevated systolic BP (SBP) and diastolic BP (DBP), whereas serum total cholesterol (TC), LDL-C, and HDL-C were not correlated with BP. However, HDL-C/TC (%) was negatively associated with SBP (p = 0.036), while TG/HDL-C and glucose/HDL-C ratios were positively associated with both SBP and DBP, suggesting that TG and glucose proportions relative to HDL-C are probable predictors of hypertension. Elevations of TG, oxidation, and glycation in LDL were positively associated with elevations of BP, whereas LDL particle size was negatively correlated with BP. Similarly, elevations of TG and glycation in HDL₂ and HDL₃ were positively correlated with elevations of BP, while the particle size of HDL₂ was negatively correlated with BP. The heightened HDL₂-associated paraoxonase (PON) activity and ferric ion reduction ability (FRA) negatively correlated with LDL oxidation and particle size, whereas elevated HDL₃-associated PON and FRA activities were inversely related to LDL glycation. An enhanced glycation in HDL₂ was negatively correlated with HDL₂-associated PON activity and FRA, while an increase in HDL₂ particle size was only dependent on the associated PON activity but not on FRA. In conclusion, observational outcomes demonstrated that improved HDL quality and functionality (characterized by large particle size, reduced glycation, and higher FRA and PON activities) were inversely correlated with LDL oxidation, glycation, particle shrinkage, and the risk of hypertension. Full article

Background: Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide and are strongly influenced by dietary habits. Beyond caloric intake, nutrients act as molecular signals that regulate cardiac metabolism, mitochondrial function, inflammation, and epigenetic remodeling. Objectives: This review aims to synthesize current evidence on how dietary patterns and specific nutritional interventions regulate cardiac metabolism and function through interconnected molecular and epigenetic mechanisms, highlighting their relevance for cardiovascular disease prevention. Methods: A narrative review of the literature was conducted using PubMed, Scopus, and Web of Science, focusing on studies published between 2006 and 2025. Experimental, translational, and clinical studies addressing diet-induced modulation of cardiac metabolic pathways, oxidative and inflammatory signaling, epigenetic regulation, and gut microbiota-derived metabolites were included. Results: The analyzed literature consistently shows that unbalanced diets rich in saturated fats and refined carbohydrates impair cardiac metabolic flexibility by disrupting key nutrient-sensing pathways, including AMP-activated protein kinase (AMPK), proliferator-activated receptor alpha (PPARα), mammalian target of rapamycin (mTOR), and sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (SIRT1/PGC-1α), leading to mitochondrial dysfunction, oxidative stress, chronic inflammation, and maladaptive remodeling. In contrast, cardioprotective dietary patterns, such as caloric restriction (CR), intermittent fasting (IF), and Mediterranean and plant-based diets, enhance mitochondrial efficiency, redox balance, and metabolic adaptability. These effects are mediated by coordinated activation of AMPK-SIRT1 signaling, suppression of mTOR over-activation, modulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2) pathways, and favorable epigenetic remodeling involving DNA methylation, histone modifications, and non-coding RNAs. Emerging evidence also highlights the central role of gut microbiota-derived metabolites, particularly short-chain fatty acids, in linking diet to epigenetic and metabolic regulation of cardiac function. Conclusions: Diet quality emerges as a key determinant of cardiac metabolic health, acting through integrated molecular, epigenetic, and microbiota-mediated mechanisms. Targeted nutritional strategies can induce long-lasting cardioprotective metabolic and epigenetic adaptations, supporting the concept of diet as a modifiable molecular intervention. These findings provide a mechanistic rationale for integrating personalized nutrition into cardiovascular prevention and precision cardiology, complementing standard pharmacological therapies. Full article

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, with heart failure (HF) representing a major contributor to hospitalizations, healthcare costs, and death. Effective management of HF is hindered by the limitations of current biomarkers and diagnostic tools. Conventional biomarkers, such as natriuretic peptides, primarily reflect downstream hemodynamic stress and often lack specificity, particularly in HF with preserved ejection fraction or multiple comorbidities. While imaging provides valuable structural and functional information, it is resource-intensive, costly, and unsuitable for frequent longitudinal monitoring. As a result, these conventional approaches are inadequate to capture the dynamic and heterogeneous nature of HF pathophysiology. Circulating cell-free nucleic acids (cfNAs), including cell-free DNA (cfDNA) and RNA (cfRNA), have emerged as promising noninvasive liquid biopsy biomarkers capable of providing real-time insight into upstream pathological events, such as cardiomyocyte injury, immune activation, inflammation, and maladaptive remodeling. Importantly, cfNAs also act as active mediators of CVD pathology. When released under stress or injury, cfNAs interact with pattern recognition receptors (PRRs) that trigger sterile inflammation, cardiovascular cell dysfunction, and adverse cardiac remodeling. This review summarizes the origins, mechanistic roles, and clinical significance of cfNAs in HF and related CVD, highlighting their dual roles as diagnostic biomarkers and mechanistic effectors of disease. Finally, we discuss emerging cfNA-targeted therapeutic strategies, challenges, and future opportunities for precision medicine in HF and HF-associated CVD. Full article

Adherence to exercise-based cardiac rehabilitation (CR) is essential for preventing and managing cardiovascular disease (CVD). Participation in CR reduces all-cause mortality by 27% and cardiac deaths by 31% and lowers rehospitalization rates while also improving functional capacity and quality of life. However, many patients do not start, complete, or maintain CR, resulting in reduced functional abilities, a higher risk of recurring events, and poorer long-term outcomes. This narrative review summarizes patterns of adherence to exercise and CR in CVD, with a specific focus on sex- and gender-related differences in referral, participation, and completion. We synthesize evidence on biological, psychological, and social barriers that limit engagement and describe emerging strategies, such as technology-enabled and home-based programs, multidisciplinary care, and family-centered models, to enhance adherence. Finally, we propose a practical, gender-aware framework for CR design and delivery that can be adjusted and evaluated across diverse healthcare settings to guide clinical practice and future research. Full article

Background/Objectives: This study explored the epidemiology of Status Epilepticus (SE) in Kazakhstan. Methods: Utilizing data from the National Health System from 2014 to 2023, we investigated the age-standardized incidence rate (ASIR) of SE. The authors employed restricted mean survival time (RMST) models to evaluate how sex, older age, epilepsy, history of cerebrovascular diseases (CVD), central nervous system (CNS) infections, brain tumors, and cancer affected survival during 30 days through the fifth year following hospital admission for SE. Results: This study included 14,010 patients. The ASIR per 100,000 increased threefold, from 4.15 (95% CI: 3.85; 4.46) in 2014 to 12.12 (95% CI: 11.64; 17.59) in 2023, with a sharp increase during the COVID-19 pandemic. The 30-day and 5-year mortality were 2.10% and 8.85%, respectively. The RMST identified that all-cause mortality was driven by elderly age, brain tumors, and cancer, where the difference in survival increased from one day at baseline to over a year by the fifth year. The effects of CVD, CNS infections, and sex on survival were substantially lower. However, epilepsy was associated with a better prognosis. Conclusions: We observed an incremental increase in the SE incidence over a decade. Our findings warrant actions to resolve issues related to rescue medicines to improve SE outcomes in both country and region. It may be a priority for elderly patients and those with systemic tumors. Further research is needed to understand the role of epilepsy in SE epidemiology, with emphasis on design-related biases. Full article

Background/Objectives: Cardiovascular disease (CVD) and cerebrovascular disease (CeVD) remain leading causes of death in the United States, with Mississippi consistently reporting some of the nation’s highest mortality rates. Despite earlier national declines, recent evidence suggests stagnation or increases, particularly in high-burden regions. This study examined short-term trends in CVD and CeVD mortality in Mississippi between 2018 and 2022, stratified by age, sex, and race. Methods: Mortality data for adults aged ≥45 years were obtained from the Mississippi Statistically Automated Health Resource System (MSTAHRS). Age-adjusted mortality rates were calculated per 100,000 population and standardized to the 2000 U.S. population. Joinpoint regression was used to estimate annual percent change (APC) and average annual percent change (AAPC) with 95% confidence intervals (CIs). Analyses were stratified by sex, and within each racial group (White, Black, Other), mortality trends were further examined across age categories (45–54, 55–64, 65–74, 75–84, ≥85 years). Results: Cardiovascular mortality increased significantly among White women in midlife (ages 45–74), while “Other race” men in early midlife and “Other race” women in the oldest age group showed steep increases. Although Black adults did not experience significant changes over time, their mortality rates remained consistently higher than those of White adults. Conclusions: Progress in reducing cardiovascular and cerebrovascular mortality in Mississippi has reversed in several subgroups, particularly midlife White women and smaller racial populations. These findings mirror national stagnation and pandemic-related disruptions, highlighting the urgent need for equity-focused prevention, improved healthcare access, and targeted interventions addressing structural determinants of health. Full article

Cardiovascular disease (CVD) remains a leading cause of mortality worldwide, with myocardial infarction (MI) being a major contributor, particularly among individuals with obesity, a prevalent risk factor. Inflammation plays a key role in both MI and obesity, as well as in ischemia–reperfusion injury (I/R), the paradoxical cardiac injury response triggered by reperfusion. The complex cellular and molecular interplay between these risk factors in the context of MI remains incompletely understood. Preclinical research using murine models is crucial for studying disease mechanisms, identifying therapeutic targets, and advancing drug development. Despite promising preclinical findings, clinical translation of therapies targeting inflammation has been largely disappointing. A major shortcoming is the predominant use of healthy mice without comorbidities in studies of inflammation in MI. A deeper understanding of inflammatory signaling in mouse models of obesity and related metabolic disorders may help bridge the gap between preclinical research and successful clinical application. In this review, we focus on the specific role of inflammation in MI murine models with obesity and related metabolic disorders. We aim to provide a better understanding of the apparent variability in their cardiac injury phenotype, address the existing controversies in reported data, and highlight directions for future research. Full article

Background: Human papillomavirus (HPV) is a serious disease caused by a viral infection that can lead to various types of cancers in both women and men. Nearly all cases of cervical cancer (99.7%) develop as a result of an HPV infection, ranging from low to high grade, with a 5-year mortality rate ranging from 8 to 81% depending on the timeliness of diagnosis. Recent studies have further shown that HPV significantly increases the risk of cardiovascular disease, including coronary artery disease (CAD). However, the mechanism and impact of HPV on CVD from a proteomics and transcriptomics perspective are not well understood. Objectives: The purpose of this work is to provide the evidence framework for using machine learning to further advance knowledge on the interplay of HPV and CVD in relation to proteomic and transcriptomic changes. Key findings: In addition to existing known relationships between HPV and atherosclerosis and CAD, dilated cardiomyopathy (DCM) is identified as an important cardiovascular disease modified by HPV infections. A more comprehensive understanding of the cholesterol-modifying mechanisms underpinning HPV’s influence on CVD has been identified. Downstream ML has been used to selectively identify key proteins for subsequent bioinformatic mining across a range of public and in-house curated databases. Implications: By further understanding the mechanisms underlying HPV-induced cardiovascular pathogenesis, machine learning models can be developed in a more targeted manner, stratifying patients that will have an optimal response to emerging probiotic-based therapies. Full article

Background: Chronic non-communicable diseases—chiefly chronic obstructive pulmonary disease (COPD), type 2 diabetes mellitus (T2DM), and cardiovascular diseases (CVDs)—remain the leading causes of morbidity and mortality worldwide. Despite the proliferation of telehealth programs, few longitudinal studies have rigorously evaluated theory-based, nurse-led digital education across multiple chronic conditions within a unified self-care framework. PROSELF (Promotion of Self-Care through Educational Interventions in Chronic Patients) addresses this gap. Methods: Promotion of Self-Care (PROSELF) is a prospective, longitudinal, multicenter, non-interventional study in community and primary-care settings in Southern Italy. A 12-month nurse-led digital educational intervention—grounded in the Middle-Range Theory of Self-Care of Chronic Illness—targets the three core self-care dimensions (maintenance, monitoring, and management) through individualized tele-education, asynchronous reinforcement, and structured follow-up at baseline, 3, 6, and 12 months. Validated self-care, quality-of-life, and social-support measures will be used. Data will be analyzed using repeated-measures and multivariate models to evaluate longitudinal changes in self-care, adherence, and related outcomes. Participation requires digitally informed consent. Results: The PROSELF study is expected to demonstrate the effectiveness of a 12-month, nurse-led digital educational program in improving adherence and self-care behaviors among patients with chronic diseases (COPD, diabetes, and cardiovascular disease). The intervention will leverage validated self-care assessment tools and tele-educational follow-up sessions. Conclusions: Findings from this study will inform the design of scalable, evidence-based, behaviorally informed models for digital chronic care delivery and nursing education. Full article

Background: Cardiovascular disease (CVD) in pregnancy is a major cause of maternal morbidity and mortality, accounting for nearly one-third of pregnancy-related deaths worldwide. Physiological adaptations—expanded plasma volume, increased cardiac output, and a prothrombotic state—represent a natural cardiovascular stress test that may precipitate decompensation or unmask subclinical disease. Aim: This review critically examines contemporary evidence and international guidelines on the management of pregnancy-related cardiovascular disorders, focusing on pathophysiological mechanisms, diagnostic challenges, and therapeutic controversies. Content: The discussion centers on three high-impact clinical domains: (1) peripartum and preexisting cardiomyopathies, emphasizing mechanisms, prognosis, and the role of bromocriptine; (2) anticoagulation management in women with mechanical prosthetic valves, balancing maternal safety and fetal protection; and (3) hypertensive disorders of pregnancy, highlighting recent evidence from the CHAP and WILL trials and their implications for long-term cardiovascular prevention. Comparative analysis of ESC 2025 and AHA 2020 recommendations reveals broad consensus but persistent discrepancies in anticoagulation targets, postpartum surveillance, and follow-up strategies. Perspectives: Endothelial dysfunction, angiogenic imbalance, and systemic inflammation emerge as shared mechanisms linking diverse pregnancy-related cardiovascular conditions. Strengthening multidisciplinary care through Pregnancy Heart Teams, integrating obstetric and cardiologic expertise, and establishing structured postpartum follow-up pathways are essential to improve outcomes. Full article

Cardiovascular diseases (CVDs) remain a leading cause of mortality worldwide. According to the WHO, every year, there is an increase in the rate of death globally due to CVDs, stroke, and myocardial infarction. Several risk factors contribute to the development of CVDs, one of which is hypoxia, defined as a reduction in oxygen levels. This major stressor affects aerobic species and plays a crucial role in the development of cardiovascular disease. Research has uncovered the “hypoxia-inducible factors (HIFs) switch” and investigated the onset, progression, acute and chronic effects, and adaptations of hypoxia, particularly at high altitudes. The hypoxia signalling pathways are closely linked to natural rhythms such as the circadian rhythm and hibernation. In addition to genetic and evolutionary factors, epigenetics also plays an important role in postnatal cardiovascular responses to hypoxia. Oxidized LDL-C initiates atherosclerosis amidst oxidative stress, inflammation, endothelial dysfunction, and vascular remodelling in CVD pathogenesis. Anti-inflammatory and antioxidant biomarkers are needed to identify individuals at risk of cardiovascular events and enhance risk prediction. Among these, C-reactive protein (CRP) is a recognized marker of vascular inflammation in coronary arteries. Elevated pro-atherogenic oxidized LDL (oxLDL) expression serves as an antioxidant marker, predicting coronary heart disease in apparently healthy men. Natural antioxidants and anti-inflammatory molecules protect the heart by reducing oxidative stress, enhancing vasodilation, and improving endothelial function. For instance, the flavonoid quercetin exerts antioxidant and anti-inflammatory effects primarily by activating the Nrf2/HO-1 signaling pathway, thereby enhancing cellular antioxidant defense and reducing reactive oxygen species. Carotenoids, such as astaxanthin, exhibit potent antioxidant activity by scavenging free radicals and preserving mitochondrial integrity. The alkaloid berberine mediates cardiovascular benefits through activation of AMO-activated protein kinase (AMPK) and inhibition of nuclear factor kappa B [NF-kB] signalling, improving lipid metabolism and suppressing inflammatory cytokines. Emerging evidence highlights microRNAs (miRNAs) as potential regulators of oxidative stress via endothelial nitric oxide synthase (eNOS) and silent mating-type information regulation 2 homolog (SIRT1). While the exact mechanisms remain unclear, their benefits are likely to include antioxidant and anti-inflammatory effects, notably reducing the susceptibility of low-density lipoproteins to oxidation. Additionally, the interactions between organs under hypoxia signalling underscore the need for a comprehensive regulatory framework that can support the identification of therapeutic targets, advance clinical research, and enhance treatments, including FDA-approved drugs and those in clinical trials. Promising natural products, including polysaccharides, alkaloids, saponins, flavonoids, and peptides, as well as traditional Indian medicines, have demonstrated anti-hypoxic properties. Their mechanisms of action include increasing haemoglobin, glycogen, and ATP levels, reducing oxidative stress and lipid peroxidation, preserving mitochondrial function, and regulating genes related to apoptosis. These findings emphasise the importance of anti-hypoxia research for the development of effective therapies to combat this critical health problem. A recent approach to controlling CVDs involves the use of antioxidant and anti-inflammatory therapeutics through low-dose dietary supplementation. Despite their effectiveness at low doses, further research on ROS, antioxidants, and nutrition, supported by large multicentre trials, is needed to optimize this strategy. Full article

Cardiovascular disease (CVD) encompasses ischemic conditions of the heart, brain, and bodily tissues, primarily resulting from hyperlipidemia, atherosclerosis (AS), hypertension, and other related factors. CVD accounts for over 40% of global non-communicable disease mortality, making it the leading cause of death and a significant medical burden worldwide. AS, the principal pathological basis for most cardiovascular diseases, is characterized as a chronic, sterile inflammatory condition triggered by lipid overload and various other factors. In recent years, natural bioactive compounds have gained prominence in the treatment of human diseases. Among these, curcumin (Cur) has garnered considerable attention due to its anti-inflammatory, lipid-lowering, antihypertensive, and endothelial protective properties. This review examines traditional pharmacological approaches for treating AS, with particular emphasis on the critical mechanisms through which Cur exerts its therapeutic effects. Additionally, it introduces novel nanoformulations designed to address the inherent limitations of Cur, providing valuable insights for researchers investigating its application in AS therapy. Full article

Background: Cardiovascular disease (CVD) is the leading cause of mortality in peritoneal dialysis (PD) patients, with traditional risk factors failing to fully explain the accelerated atherosclerosis observed in this group. Hepcidin, a major regulator of iron metabolism and inflammation, has emerged as a potential contributor to vascular remodeling. Methods: We conducted a cross-sectional study of 82 PD patients to assess the relationship between serum hepcidin levels and carotid intima–media thickness (CIMT), a surrogate marker of subclinical atherosclerosis. Clinical, biochemical, and dialysis-related data were collected. Patients were stratified into tertiles by hepcidin levels, and correlation, regression, and ROC analyses were performed. Results: Serum hepcidin levels showed a strong positive correlation with CIMT (ρ = 0.788, p < 0.001). In multivariate linear regression, hepcidin (β = 0.0057, p = 0.012) and dialysis duration (β = 0.0018, p = 0.015) remained independent predictors of CIMT. ROC analysis demonstrated excellent discriminative ability of hepcidin for elevated CIMT (AUC = 0.922), which improved further with the inclusion of dialysis duration (AUC = 0.952). Conclusions: Serum hepcidin is a strong, independent predictor of subclinical atherosclerosis in PD patients. These findings suggest that iron dysregulation and inflammation may play a more prominent role than traditional cardiovascular risk factors in this population. Hepcidin may serve as a valuable biomarker for early vascular risk stratification and a potential therapeutic target. Full article