The current minireview aims to assess the implications of epicardial fat secretory function in the development of coronary artery disease. The epicardial adipose tissue (EAT) is a visceral fat depot that has been described as a cardiovascular risk factor. In addition to its mechanical protection role and physiological secretory function, it seems that various secretion products of the epicardial fat are responsible for metabolic disturbances at the level of the cardiac muscle when in association with pre-existing pathological conditions, such as metabolic syndrome. There is a pathological reduction in sarcomere shortening, abnormal cytosolic Ca²⁺ fluxes, reduced expression of sarcoplasmic endoplasmic reticulum ATPase 2a and decreased insulin-mediated Akt-Ser473-phosphorylation in association with abnormal levels of epicardial fat tissue. Activin A, angiopoietin-2, and CD14-positive monocytes selectively accumulate in the diseased myocardium, resulting in reduced cardiomyocyte contractile function. At the same time, it is believed that these alterations in secretory products directly decrease the myocyte function via molecular changes, thus contributing to the development of coronary disease when certain comorbidities are associated.

Background/Objectives: Cardiac hemangiomas are rare benign vascular tumors, accounting for less than 2% of primary cardiac tumors. Despite their rarity, they can cause significant clinical effects depending on their size and location. This systematic review aims to provide an updated analysis of recent cases, focusing on epidemiology, histopathological subtypes, clinical presentation, diagnostic approaches, and treatment outcomes. Methods: A systematic search of the PubMed database identified case reports and series published between 2019 and 2025. After applying inclusion and exclusion criteria, 55 eligible cases were selected for analysis. Data were extracted on patient demographics, tumor characteristics, imaging methods, treatment strategies, and follow-up outcomes. Results: Cavernous hemangiomas were the most commonly reported subtype. Patient ages ranged from infancy to over 85 years, with a slight predominance in females. Presentations varied from asymptomatic incidental findings to symptoms such as dyspnea and chest pain. Echocardiography was the primary diagnostic tool in over 80% of cases. Surgical resection was performed in 87.3% of patients, yielding favorable outcomes and low recurrence. However, follow-up duration was inconsistent, and long-term outcomes were underreported, underscoring the lack of standardized surveillance protocols. This variability limits clinicians’ ability to assess recurrence risk and long-term prognosis, highlighting the need for evidence-based guidelines to inform structured follow-up and improve patient care. Conclusions: The increasing number of published cases likely reflects improved diagnostic imaging and greater clinical awareness. While surgery remains the preferred treatment, the variability in follow-up and diagnostic reporting highlights the need for standardized protocols. Further studies are warranted to clarify the natural history, refine classification systems, and establish evidence-based guidelines for the management of this rare cardiac tumor.

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia worldwide and is now increasingly regarded as a disease of chronic inflammation and progressive atrial fibrosis. Understanding of molecular mechanisms that mediate the linkage between systemic metabolic dysregulation, inflammation, and structural atrial changes is crucial for informing risk stratification and targeting of prevention strategies. This review provides evidence from 105 studies focusing on the contributions of transforming growth factor-β1 (TGF-β1), tumor necrosis factor-a (TNF-α), interleukin-6 (IL-6), galectin-3, and galectin-1 to cardiac fibrogenesis, atrial fibrosis, and AF pathogenesis. We also link metabolic syndrome to these biomarkers and to atrial remodeling, as well as echocardiographic correlates of fibrosis. TGF-β1 is established as the central profibrotic cytokine and promotes Smad-based fibroblast activation, collagen accumulation, and structural atrial remodeling. Its role is highly potentiated by thrombospondin-1 by turning latent TGF-β1 into its potent form. TNF-α and IL-6 also play an integral role in the inflammatory fibrotic continuum by activating NF-κB and STAT3 signaling, promoting fibroblast proliferation, electrical uncoupling, and extracellular matrix accumulation. Galectin-3 is a potent profibrotic mediator that promotes TGF-β signaling and is a risk factor for negative outcomes, whereas Gal-1 seems to regulate inflammation resolution and may exert context-dependent protective or maladaptive roles. Metabolic syndrome is strongly associated with excessive levels of these biomarkers, chronic low-grade inflammation, oxidative stress, and ventricular and atrial fibrosis. Chronic clinical findings show that metabolic syndrome (MetS) increases AF risk, exacerbates atrial dilatation, and is associated with worse postoperative outcomes. Echocardiographic data are connected to circulating biomarkers and are non-invasive for evaluating atrial remodeling. The evidence to date supports that atrial fibrosis should be considered an end point of systemic inflammation, metabolic dysfunction, and activation of profibrotic molecular pathways. Metabolic syndrome, due to its chronic low-grade inflammatory environment and prolonged levels of metabolic stress, manifests as an important upstream factor of fibrotic remodeling, which continuously promotes the release of cytokines, oxidative stress, and fibroblast activation. Circulating fibrotic biomarkers, in comparison with metabolic syndrome, serve separate yet interdependent pathways that help orchestrate atrial structural remodeling through the simultaneous process but can also provide a long-term indirect measure of ongoing profibrotic activity. The integration of these biomarkers with superior atrial imaging enables a broader understanding of the fibrotic substrate of atrial fibrillation. This combined molecular imaging approach can facilitate risk stratification, refine therapeutic decisions, and facilitate early identification of higher-risk metabolic phenotypes, thus potentially facilitating directed antifibrotic and anti-inflammatory therapy in atrial fibrillation.

Metformin, the first-line drug in type 2 diabetes mellitus, elicits cardiovascular protection also in obese patients via pleiotropic effects, among which the anti-oxidant is one of the most investigated. The aim of the present study was to assess whether metformin can acutely mitigate oxidative stress in atrial tissue harvested from overweight non-diabetic patients. Right atrial appendage samples were harvested during open-heart surgery and used for the evaluation of reactive oxygen species (ROS) production by means of confocal microscopy (superoxide anion) and spectrophotometry (hydrogen peroxide). Experiments were performed after acute incubation with metformin (10 µM) in the presence vs. absence of angiotensin II (AII, 100 nM), lipopolysaccharide (LPS, 1 μg/mL), and high glucose (Gluc, 400 mg/dL). Stimulation with AII, LPS, and high Gluc increased ROS production. The magnitude of oxidative stress correlated with several echocardiographic parameters. Metformin applied in the lowest therapeutic concentration (10 µM) was able to decrease ROS generation in stimulated but also non-stimulated atrial samples. In conclusion, in a pilot group of overweight non-diabetic cardiac patients, acute incubation with metformin at a clinically relevant dose alleviated oxidative stress both in basal conditions and conditions that mimicked the activation of the renin–angiotensin–aldosterone system, acute inflammation, and uncontrolled hyperglycemia.

Background/Objectives: The primary purpose of this study is to provide a more in-depth insight into various demographic, clinical, and lifestyle factors in relation to breast cancer and to predict the extent to which certain variables described as “predictors” might lead to further investigation. By analyzing a large cohort, we are able to provide valuable and up-to-date information on breast cancer screening, support breast specialists, and further enhance international screening guidelines. Methods: We screened for breast cancer in a population of women aged 50 to 69 years by using the standardized breast cancer imaging screening method (breast mammography) and ultrasonography as a complementary imagistic tool, and we compared the results with the gold standard, breast biopsy. For this, 58,760 women with no known history of breast cancer coming from 4 major regions of Romania (North-East, North-West, South-East, and West) were first evaluated through mammography. Out of these, 3197 women with positive mammograms subsequently underwent a breast ultrasound examination. The remaining 688 patients with positive breast ultrasound were further referred for a breast biopsy. Results: The statistical analysis revealed several predictors such as the body mass index (BMI), positive family medical history of breast cancer, age at first birth, and age at menopause that influenced the progression from mammography (first stage of the screening program) towards echography (additional imaging modality). Furthermore, we established that age, age at first birth, and BMI are significant predictors of progression from echography towards biopsy (the last stage of the screening program). Furthermore, by analyzing the number of positive biopsies (688) out of the total number of patients in the study (58,760), we calculated a total breast cancer detection rate of 8 per 1000 patients. Lastly, by studying the patient demographics in the context of breast cancer (BC) screening, we observed that participants coming from an urban environment presented a higher rate of positive mammographic results as compared to ones of rural provenience. Conclusions: Our study analyzed a large cohort of patients and offers real world data which shows that multiple factors were positively associated with an increased risk of BC. Older age, older age at first birth, and an older menopausal age are all estrogen-dependent risk factors that were linked with an increased breast cancer risk in our study. Furthermore, our findings concerning the rural/urban disparities and regional differences highlight the need for region-specific interventions to address lifestyle risk factors, improve healthcare access, and enhance breast cancer screening and follow-up protocols, particularly in underserved areas like the North-East and South-East regions.

Mechanical complications after acute myocardial infarction (MI)—ventricular septal rupture (VSR), free-wall rupture (FWR), and papillary muscle rupture (PMR)—have become uncommon in the primary percutaneous coronary intervention (PCI) era, yet remain among the most lethal cardiovascular emergencies, with contemporary mortality largely driven by cardiogenic shock and delays to definitive treatment. Although major society documents agree on urgent imaging, early mechanical circulatory support when shock is present, and multidisciplinary decision-making, important transatlantic differences persist, particularly regarding timing of intervention in ventricular septal rupture. This review synthesises current surgical and transcatheter evidence and proposes a unified, physiology-centred framework integrating shock staging, anatomical feasibility, and response to mechanical support. We also introduce STABLE, a structured bedside checklist designed to support consistent daily triage across all three lesions and to align timing decisions with haemodynamic stabilisation rather than centre-specific habit.