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Endothelial dysfunction often precedes the development of cardiovascular diseases, including heart failure. The cardioprotective benefits of sodium-glucose cotransporter 2 inhibitors (SGLT2is) could be explained by their favorable impact on the endothelium. In this review, we summarize the current knowledge on the direct in vitro effects of SGLT2is on endothelial cells, as well as the systematic observations in preclinical models. Four putative mechanisms are explored: oxidative stress, nitric oxide (NO)-mediated pathways, inflammation, and endothelial cell survival and proliferation. Both in vitro and in vivo studies suggest that SGLT2is share a class effect on attenuating reactive oxygen species (ROS) and on enhancing the NO bioavailability by increasing endothelial nitric oxide synthase activity and by reducing NO scavenging by ROS. Moreover, SGLT2is significantly suppress inflammation by preventing endothelial expression of adhesion receptors and pro-inflammatory chemokines in vivo, indicating another class effect for endothelial protection. However, in vitro studies have not consistently shown regulation of adhesion molecule expression by SGLT2is. While SGLT2is improve endothelial cell survival under cell death-inducing stimuli, their impact on angiogenesis remains uncertain. Further experimental studies are required to accurately determine the interplay among these mechanisms in various cardiovascular complications, including heart failure and acute myocardial infarction.

Obesity-associated inflammation underlies much of cardiometabolic pathology, reflecting the convergence of chronic, low-grade systemic immune activation with region-specific maladaptation of adipose depots. Among these, epicardial adipose tissue (EAT)—a visceral fat layer contiguous with the myocardium and sharing its microvasculature—functions as a cardio-proximal immunometabolic interface that influences atrial fibrillation, heart failure with preserved ejection fraction, and coronary atherogenesis through paracrine crosstalk. These relationships extend beyond crude measures of adiposity, emphasizing the primacy of local inflammatory signaling, adipokine flux, and fibro-inflammatory remodeling at the EAT–myocardium interface. Of importance, substantial weight reduction only partially reverses obesity-imprinted transcriptional and epigenetic programs across subcutaneous, visceral, and epicardial depots, supporting the concept of an enduring adipose memory that sustains cardiovascular (CV) risk despite metabolic improvement. Accordingly, therapeutic strategies should move beyond weight-centric management toward mechanism-guided interventions. Resolution pharmacology—leveraging specialized pro-resolving mediators and their cognate G-protein-coupled receptors—offers a biologically plausible means to terminate inflammation and reprogram immune–stromal interactions within adipose and CV tissues. Although preclinical studies report favorable effects on vascular remodeling, myocardial injury, and arrhythmic vulnerability, clinical translation is constrained by pharmacokinetic liabilities of native mediators and by incomplete validation of biomarkers for target engagement. This review integrates mechanistic, depot-resolved, and therapeutic evidence to inform the design of next-generation anti-inflammatory strategies for obesity-related CV disease.

Purpose: Adolescence is a period of increased vulnerability to addictive behaviors, and Primary Health Care (PHC) plays a crucial role in prevention and intervention (e.g., through Screening, Brief Intervention, and Referral to Treatment), but professionals often face barriers, such as inadequate training and systemic challenges, particularly within the Greek context. Given the lack of data on their needs, this study aimed to investigate the levels of self-perceived knowledge/skills, attitudes regarding communication and readiness, perceived barriers, and educational expectations among PHC professionals in Greece. Method: A cross-sectional descriptive survey was conducted using an anonymous questionnaire with a convenience sample of 331 PHC professionals from 5 Health Regions. Results: Professionals recognized the high importance of effective communication (M = 4.31/5) but reported low preparedness (M = 2.65/5) and moderate confidence in knowledge, especially in screening tools/motivational interviewing (M = 2.25/5). Lack of training was the main barrier (87.6%). A strong positive correlation was found between knowledge and preparedness (rho = 0.68, p < 0.001), but not between age/experience and readiness (p > 0.05). Discussion: The study highlights a significant readiness gap and a substantial need for specialized training for PHC professionals in Greece, regardless of experience. Targeted interventions are required to enhance skills (especially in SBIRT/MI) and self-efficacy, alongside action to address systemic barriers.

Cardiovascular (CV) disease, chronic kidney disease, obesity, and diabetes mellitus have reached epidemic proportions over the past few decades. Accumulating evidence highlights the strong interconnection between these conditions, leading to the definition of a broader disease entity known as cardio-renal-metabolic (CRM) syndrome. This newly recognized clinical entity presents important challenges in identifying the optimal treatment strategy within a holistic, patient-centered framework. In line with this, sodium glucose cotransporter 2 inhibitors (SGLT2is), owing to their multifaceted pharmacological effects, have been suggested as possible treatment options in the management of CRM. SGLT2is exert their antihyperglycemic effects by impeding the renal reabsorption of sodium and glucose, causing glycosuria and natriuresis. Research has confirmed that their unique beneficial effects extend beyond glycemic control, reducing CV death and hospitalizations in patients with heart failure, and the incidence of kidney failure in dedicated kidney outcome studies—regardless of diabetes status. Furthermore, these agents contribute to weight loss and blood pressure reduction. Their benefits appear to stem from a combination of factors, which include reduced oxidative stress, lower levels of inflammation, regulated neurohormonal activation, improved endothelial function, and enhanced metabolic efficiency. This review aims to provide a comprehensive analysis of the pathophysiological mechanisms underlying the effects of SGLT2is in CRM syndrome, synthesize evidence from landmark clinical trials, evaluate current experimental and diagnostic approaches, and provide the emerging role of SGLT2is in the treatment of this new clinical entity.

Ischemic heart disease remains the leading cause of death despite substantial advances in diagnosis, revascularization therapies, and risk-factor control. Beta-adrenergic receptor blockers (Beta-Blockers, BBs), long used to control heart rate, blood pressure, and reduce arrhythmic risk, may also confer cardioprotection through mechanisms beyond hemodynamic unloading. This review integrates an extensive range of preclinical, translational, and clinical studies to present a comprehensive overview of the cardioprotective effects of BBs in the context of myocardial ischemia and reperfusion injury. Mechanistic domains include modulation of redox homeostasis, attenuation of inflammation and neutrophil activation, preservation of mitochondrial integrity and anti-apoptotic signaling, improvement of endothelial function, and stabilization of calcium handling. Third-generation compounds, carvedilol and nebivolol, demonstrate additional antioxidant and vasodilatory benefits compared with first- and second-generation agents; however, no consistent class-wide effect exists across most pathways. The evidence base remains fragmented, often derived from agent- or context-specific studies in heterogeneous populations, with uncertainty surrounding optimal timing of intervention. By bridging mechanistic understanding with clinical outcomes, this review highlights the importance of standardized assessment of BB effects, the development of personalized treatment approaches, and the pursuit of future research to address ongoing translational gaps.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, associated with significant morbidity, mortality, and healthcare burden. Despite advances in AF management, challenges persist in early detection, risk stratification, and treatment optimization, necessitating innovative solutions. Artificial intelligence (AI) has emerged as a transformative tool in AF care, leveraging machine learning and deep learning algorithms to enhance diagnostic accuracy, improve risk prediction, and guide therapeutic interventions. AI-powered electrocardiographic screening has demonstrated the ability to detect asymptomatic AF, while wearable photoplethysmography-based technologies have expanded real-time rhythm monitoring beyond clinical settings. AI-driven predictive models integrate electronic health records and multimodal physiological data to refine AF risk stratification, stroke prediction, and anticoagulation decision making. In the realm of treatment, AI is revolutionizing individualized therapy and optimizing anticoagulation management and catheter ablation strategies. Notably, AI-enhanced electroanatomic mapping and real-time procedural guidance hold promise for improving ablation success rates and reducing AF recurrence. Despite these advancements, the clinical integration of AI in AF management remains an evolving field. Future research should focus on large-scale validation, model interpretability, and regulatory frameworks to ensure widespread adoption. This review explores the current and emerging applications of AI in AF, highlighting its potential to enhance precision medicine and patient outcomes.

Dietary sodium restriction is widely recommended in heart failure (HF) management; however, its benefits and risks remain a subject of ongoing debate. While moderate sodium reduction may improve symptoms and quality of life in selected patients, excessive restriction can trigger maladaptive neurohormonal activation, worsen renal function, and increase the risk of hyponatremia, malnutrition, and cachexia. Patient response is heterogeneous, influenced by clinical risk profile, salt sensitivity, comorbidities, and age, with some high-risk patients experiencing neutral or adverse outcomes. Additional challenges arise from hidden sodium in processed foods, medications, and meals, which complicate monitoring and adherence. Effective sodium management in HF therefore requires a nuanced, individualized approach that integrates risk stratification, dietary counseling, and public health measures targeting the food industry. Future research should refine patient selection criteria and establish optimal sodium targets to balance therapeutic efficacy with safety in real-world practice.

Diabetic atherosclerosis is a complex process that is characterized by diffuse and unstable lesions increasing 2–4-fold the risk of adverse cardiovascular (CV) events. Diabetic dyslipidemia has a predominant role in coronary artery disease (CAD) and has been the target of classical and emerging pharmaceutical agents with established or promising CV benefits. The aim of the present narrative review was to summarize the effects of classical and novel lipid-lowering pharmaceutical agents on lipid profile and CV outcomes in diabetic patients with established CAD or high risk of CAD. Statins remain the first-line treatment for all diabetic patients since they considerably ameliorate lipid parameters and non-lipid CV risk factors, leading to reduced CV morbidity and mortality. Complementary to statins, ezetimibe exerts lipid-lowering properties with modest but significant reductions in major adverse cardiovascular events (MACEs) and CV mortality. PCSK9 inhibitors considerably reduce LDL-C levels and lower MACEs in diabetic patients. On the other hand, fibrates may confer a very modest decline in MACE incidence, while the CV impact of omega-3 fatty acids is promising but remains questionable. Bempedoic acid and inclisiran have a potential therapeutic role in the management of diabetic dyslipidemia, but this is still not adequately documented. Given the heightened CV risk among individuals with diabetes, more decisive results would be of great importance in the utility of all these drugs.

Background: Novel and accessible biomarkers may add to the existing risk stratification schemes in patients with acute coronary syndrome (ACS). The platelet-to-lymphocyte ratio (PLR) and glucose-to-lymphocyte ratio (GLR) have emerged as potential indicators of systemic inflammation and metabolic stress, both of which are pivotal in ACS pathophysiology. The aim of this study was to investigate the prognostic significance of the PLR and GLR in patients with ACS. Methods: We performed a retrospective cohort study of patients hospitalized with ACS between 2017 and 2023 at Hippokration Hospital of Thessaloniki, Greece. PLR and GLR were calculated from admission blood samples. The primary endpoint was all-cause mortality. Logistic and Cox regression models were used to investigate the associations of PLR and GLR with all-cause mortality. Receiver operating characteristic (ROC) analysis, Kaplan–Meier survival curves, and restricted cubic spline (RCS) modeling were also applied. Results: In total, 853 patients (median age: 65 years, 72.3% males) were included. Higher PLR and GLR were independently associated with increased risk of long-term mortality [adjusted Odds Ratio (aOR) for PLR: 1.007, 95% CI: 1.005–1.008; and for GLR: aOR = 1.006, 95% CI: 1.003–1.008]. The optimal cut-off values were 191.92 for PLR and 66.80 for GLR. Kaplan–Meier and Cox regression analyses confirmed significantly reduced survival in patients with GLR and PLR values exceeding these thresholds. RCS analysis revealed non-linear relationships, with mortality risk rising sharply at higher levels of both markers. PLR showed superior prognostic performance (AUC: 0.673, 95% CI: 0.614–0.723) compared to GLR (AUC: 0.602, 95% CI: 0.551–0.653). Conclusions: While PLR demonstrated greater predictive accuracy, both PLR and GLR were consistently associated with mortality and may provide complementary prognostic information. Incorporating those ratios into routine clinical assessment may improve risk stratification, particularly in resource-limited settings or for patients without traditional risk factors.

Lipoprotein(a) [Lp(a)] has emerged as a significant independent risk factor for atherosclerotic cardiovascular disease (ASCVD). While plasma Lp(a) levels remain relatively stable throughout life, their clinical impact varies depending on age and concentration. This comprehensive review examines the age-dependent clinical relevance of Lp(a), from childhood through adulthood. In pediatric populations, elevated Lp(a) levels are associated with early indicators of vascular dysfunction and with conditions like familial hypercholesterolemia (FH). In adults, elevated Lp(a) is consistently linked to an increased risk of myocardial infarction (MI), stroke, and calcific aortic valve disease, particularly in those with additional cardiovascular risk factors. We also discuss emerging therapies targeting Lp(a) that may significantly alter long-term cardiovascular risk if implemented early. Understanding the lifelong implications of elevated Lp(a) highlights the need for age-specific strategies for screening, monitoring, and intervention. Future research should prioritize identifying high-risk pediatric populations, refining risk thresholds, and determining optimal timing for therapeutic initiation to improve long-term cardiovascular outcomes.