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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.

Atherosclerotic cardiovascular disease remains a prominent global cause of mortality, with coronary artery disease representing its most prevalent manifestation. Recently, a novel class of antidiabetic medication, namely sodium-glucose cotransporter-2 (SGLT2) inhibitors, has been reported to have remarkable cardiorenal advantages for individuals with type 2 diabetes mellitus (DM), and they may reduce cardiorenal risk even in individuals without pre-existing DM. Currently, there is no evidence regarding the safety and efficacy of these drugs in acute coronary syndrome (ACS), regardless of diabetes status. This review aims to comprehensively present the available preclinical and clinical evidence regarding the potential role of SGLT2 inhibitors in the context of ACS, as adjuncts to standard-of-care treatment for this patient population, while also discussing potential short- and long-term cardiovascular benefits. A literature search was performed through MEDLINE (via PubMed), Cochrane Central Register of Controlled Trials, and Scopus until February 26, 2024. Eligible were preclinical and clinical studies, comprising randomized controlled trials (RCTs), real-world studies, and meta-analyses. Evidence from preclinical models indicates that the use of SGLT2 inhibitors is associated with a blunted ischemia-reperfusion injury and decreased myocardial infarct size, particularly after prior treatment. Although RCTs and real-world data hint at a potential benefit in acute ischemic settings, showing improvements in left ventricular systolic and diastolic function, decongestion, and various cardiometabolic parameters such as glycemia,body weight, and blood pressure, the recently published DAPA-MI (Dapagliflozin in Myocardial Infarction without Diabetes or Heart Failure) trial did not establish a clear advantage regarding surrogate cardiovascular end points of interest. SGLT2 inhibitors appear to provide a benefit in reducing contrast-induced acute kidney injury events in patients with ACS undergoing percutaneous coronary intervention. However, data on other safety concerns, such as treatment discontinuation because of hypotension, hypovolemia, or ketoacidosis, are currently limited. Despite the well-established cardiovascular benefits observed in the general population with type 2 DM and, more recently, in other patient groups irrespective of diabetes status, existing evidence does not support the use of SGLT2 inhibitors in the context of ACS. Definitive answers to this intriguing research question, which could potentially expand the therapeutic indications of this novel drug class, require large-scale, well-designed RCTs.

SARS-CoV-2, the causative agent of the ongoing COVID-19 pandemic, has revealed a broader impact beyond the respiratory system, predominantly affecting the vascular system with various adverse manifestations. The infection induces endothelial dysfunction and immune system dysregulation, creating an inflammatory and hypercoagulable state. It affects both microvasculature and macrovasculature, leading to thromboembolic events, cardiovascular manifestations, impaired arterial stiffness, cerebrovascular complications, and nephropathy, as well as retinopathy—frequently observed in cases of severe illness. Evidence suggests that SARS-CoV-2 infection may result in persistent effects on the vascular system, identified as long-term COVID-19. This is characterized by prolonged inflammation, endotheliopathy, and an increased risk of vascular complications. Various imaging modalities, histopathological studies, and diagnostic tools such as video capillaroscopy and magnetic resonance imaging have been employed to visualize vascular alterations. This review aims to comprehensively summarize the evidence concerning short and long-term vascular alterations following COVID-19 infection, investigating their impact on patients’ prognosis, and providing an overview of preventive strategies to mitigate associated vascular complications.

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia, associated with significant morbidity, mortality, and healthcare burdens. Despite therapeutic advances, recurrence rates remain high, particularly in persistent AF, underscoring the need for deeper mechanistic insight. Epigenetic regulation—comprising DNA methylation, histone modifications, chromatin remodeling, RNA methylation, and non-coding RNAs—has emerged as a key contributor to the structural, electrical, and inflammatory remodeling underlying AF. These mechanisms operate at the interface of genetic susceptibility and environmental exposure, offering a dynamic framework for understanding disease progression. Systemic stressors such as aging, obesity, diabetes, hypertension, hypoxia, and alcohol have been shown to induce epigenetic reprogramming in atrial tissue, further promoting atrial cardiomyopathy and arrhythmogenesis. Additionally, circulating epigenetic markers, particularly microRNAs, are being investigated for their potential in AF diagnosis, risk stratification, and therapeutic monitoring. Therapeutic strategies targeting epigenetic pathways—ranging from histone deacetylase inhibitors and miRNA-based therapeutics to CRISPR/dCas9-mediated epigenome editing—are under investigation. Additionally, sodium-glucose cotransporter 2 inhibitors may indirectly influence epigenetic programs and miRNA expression relevant to atrial remodeling. While promising, these approaches require further validation in terms of safety, delivery specificity, and long-term efficacy. High-resolution epigenomic mapping and integrative multi-omic approaches may enhance understanding of AF heterogeneity and enable personalized treatment strategies. This review provides an integrated appraisal of epigenetic mechanisms in AF and outlines their emerging diagnostic and therapeutic relevance.

Cardiac arrhythmias are increasingly recognized as dynamic clinical phenotypes arising from the interplay between myocardial substrate, systemic biology, and modifiable exposures rather than as isolated disorders of cardiac electrophysiology. Advances in the field have broadened the conceptual framework of arrhythmia medicine to include structural remodeling, inflammation, autonomic dysfunction, metabolic perturbation, endothelial injury, and aging-related vulnerability as central determinants of arrhythmic risk, progression, and treatment response. In parallel, diagnostic paradigms are evolving from rhythm classification alone toward multidimensional phenotyping that integrates clinical, physiological, and imaging-based markers to identify susceptibility earlier and with greater precision. These developments are also reshaping therapeutic strategy, supporting a shift from uniform treatment algorithms toward individualized care in which rhythm control, surveillance, risk-factor modification, anticoagulation, and antiarrhythmic drug selection are aligned with the underlying biological context. This more integrated view positions arrhythmias not simply as electrical events to be suppressed, but as manifestations of broader cardiovascular and systemic disease processes that require mechanistically informed and phenotype-directed management.

The pathophysiological mechanism linking oxidative stress and cardiovascular disease (CVD) is not completely elucidated, especially in young individuals. This study aimed to examine redox status in an adolescent Montenegrin population in relation to cardiovascular risk score (CVRS). A cohort of 182 adolescents (76% girls) aged between 16 and 19 was examined. Total antioxidant status (TAS), superoxide dismutase (SOD), advanced oxidation protein products (AOPPs), malondialdehyde (MDA), and total oxidant status (TOS) were determined. Pro-oxy score, anti-oxy score, and oxy score were calculated as comprehensive parameters of overall redox homeostasis status. CVRS was calculated by summarizing several risk factors (i.e., sex, age, obesity, hypertension, dyslipidemia, impaired fasting glucose, and smoking). A significant positive correlation between CVRS and TOS (rho = 0.246, p = 0.001) and AOPP (rho = 0.231, p = 0.002) and MDA (rho = 0.339, p < 0.001), respectively, and a negative correlation with the TAS/TOS ratio (rho= −0.208, p = 0.005) was observed. An increase in pro-oxy scores as well as oxy scores with CVRS risk increase were observed. Anti-oxy scores did not differ between CVRS subgroups. There is a significant relationship between cardiovascular risk score and oxidative stress in the adolescent Montenegrin population. These findings support the possibility for improvement of age-specific CVD risk algorithms by adding redox homeostasis parameters in addition to conventional ones.

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.

Cardiac arrhythmias, including atrial fibrillation and ventricular arrhythmias, remain leading causes of morbidity and mortality worldwide. While structural, electrical, and metabolic remodeling have long been recognized as drivers of arrhythmogenesis, emerging evidence identifies inflammation—particularly inflammasome signaling—as a central orchestrator of this pathological triad. Among the various inflammasome complexes, the NLRP3 inflammasome has garnered particular attention due to its activation in cardiomyocytes, fibroblasts, and immune cells in diverse clinical contexts. NLRP3 activation precipitates a cascade of downstream events, including interleukin-1β and -18 maturation, oxidative stress amplification, calcium mishandling, and extracellular matrix remodeling, thereby fostering a proarrhythmic substrate. This review synthesizes mechanistic and translational data implicating inflammasome signaling in both atrial and ventricular arrhythmias, with a focus on cellular specificity and electrophysiological sequelae. We explore upstream triggers, such as metabolic stress, gut dysbiosis, and epicardial adipose inflammation, and delineate the downstream impact on cardiac conduction and structural integrity. Emerging therapeutic strategies—including NLRP3 inhibitors, IL-1 antagonists, colchicine, and SGLT2 inhibitors—are critically appraised for their anti-inflammatory and antifibrotic potential. By bridging molecular insights with clinical application, this review underscores the inflammasome as a unifying mechanistic hub in arrhythmia pathogenesis and a promising target for precision-guided therapy.

Aortic stenosis (AS), the most prevalent valvular heart disease, is increasingly recognized as an active disease process driven by a convergence of hemodynamic stress, inflammation, oxidative injury, and metabolic remodeling. While transcatheter and surgical valve replacement remain the standard interventions for severe AS, they fail to reverse the chronic myocardial remodeling that underlies adverse outcomes in many patients. Sodium–glucose cotransporter 2 (SGLT2) inhibitors have emerged as promising cardioprotective agents, with effects extending well beyond glycemic control. Recent mechanistic studies reveal that SGLT2 is expressed in the myocardium of patients with AS and is linked to pathways of fibrosis, inflammation, and energetic dysfunction. Experimental models and translational data demonstrate that SGLT2 inhibition attenuates maladaptive remodeling through modulation of TGF-β, NF-κB, NLRP3 inflammasome, and oxidative stress signaling while enhancing mitochondrial energetics and endothelial function. Importantly, clinical evidence from randomized and real-world studies suggests that SGLT2 inhibitors improve heart failure outcomes following valve replacement and may slow AS progression. This review integrates current pathophysiological insights with emerging molecular and clinical data to delineate the therapeutic rationale for SGLT2 inhibition in AS. By targeting both myocardial and valvular components of the disease, SGLT2 inhibitors may offer a novel disease-modifying strategy with potential implications across the AS continuum—from asymptomatic stages to the post-interventional setting. Ongoing and future trials are warranted to define optimal patient selection, timing, and biomarkers for response to SGLT2 inhibitor therapy in this increasingly high-risk population.

Superior mesenteric artery syndrome (SMAS) is an uncommon cause of proximal intestinal obstruction caused by compression of the third portion of the duodenum between the SMA and the abdominal aorta. We report the case of a 17-year-old boy with a 2-year history of recurrent nausea, vomiting, epigastric pain, early satiety, postprandial fullness, and progressive abdominal distension, followed by recent clinical deterioration. Despite repeated non-diagnostic investigations and empirical dietary and pharmacological treatment, symptoms persisted. Contrast-enhanced computed tomography established the diagnosis by demonstrating a markedly reduced aortomesenteric angle of approximately 10° and an aortomesenteric distance of 5.5 mm, associated with severe gastric and proximal duodenal dilatation. The patient was treated conservatively with nasogastric decompression and nutritional support. Nasogastric tube placement resulted in marked gastric decompression, with substantial improvement in abdominal distension, epigastric discomfort, early satiety, and vomiting, allowing surgical intervention to be deferred during the acute phase. Follow-up showed no further acute obstructive deterioration; however, the absence of meaningful weight gain over the subsequent six months indicated persistence of the chronic nutritional component of SMAS and the need for continued dietary rehabilitation and close monitoring. This case highlights the diagnostic difficulty of SMAS in adolescents with chronic, treatment-refractory upper gastrointestinal symptoms and emphasizes that resolution of acute obstruction should not be equated with definitive correction of the underlying disease process. Early recognition, conservative stabilization, nutritional optimization, and longitudinal reassessment are essential to prevent delayed diagnosis and guide timely escalation to surgery when conservative treatment is insufficient.