Atrial fibrillation is a prevalent cardiac arrhythmia influenced by multifactorial mechanisms, including the emerging role of epicardial adipose tissue. Left atrial epicardial adipose tissue, through its endocrine and paracrine activities, contributes to atrial remodeling by fostering inflammation, fibrosis, and electrical remodeling. Objectives: This review aims to explore the interaction between left atrial epicardial adipose tissue and atrial dysfunction, highlighting the utility of strain imaging as a diagnostic and prognostic tool in atrial fibrillation management. Additionally, it examines emerging therapeutic strategies targeting epicardial adipose tissue to improve outcomes. Methods: We analyzed recent advances in imaging techniques, with a specific focus on speckle-tracking echocardiography for non-invasive strain assessment. Strain imaging parameters, including atrial reservoir, conduit, and contractile strain, were evaluated alongside volumetric measures of epicardial adipose tissue. Emerging therapies, such as weight management and GLP-1 receptor agonists, were reviewed for their impact on left atrial epicardial adipose tissue and atrial remodeling. Results: Strain imaging demonstrates a significant association between reduced strain parameters and atrial remodeling induced by left atrial epicardial adipose tissue. Combining strain assessment with volumetric measures enhances diagnostic accuracy and stratification of patients at risk for recurrent or progressive atrial fibrillation. Emerging therapies, particularly GLP-1 receptor agonists, show promise in reducing epicardial adipose tissue volume and mitigating atrial remodeling, thereby improving catheter ablation outcomes. Conclusions: Strain imaging is a valuable tool for the early detection of atrial dysfunction and personalized treatment planning in atrial fibrillation. Integrating these imaging approaches into routine clinical practice can optimize atrial fibrillation management and improve patient outcomes.

Objectives: Our study aims to investigate the correlation between epicardial adipose tissue (EAT) volume assessed with non-contrast cardiac CT (NCCCT) and sex, age, coronary artery disease reporting and data system (CAD-RADS 2.0) categories, and coronary artery calcification (CAC) extent. The secondary aim is to establish the average values of EAT in a population considered healthy for coronary artery disease (CAD). Materials and Methods: We retrospectively analyzed patients who underwent coronary computed tomography angiography (CCTA) at our institution from January 2023 to August 2024. The CAD-RADS 2.0 scoring system was applied to assess the extent of CAD; CAC extent was quantified according to the Agatston score. EAT was segmented semi-automatically in NCCCT images, and its volume was subsequently measured. Correlation analyses between EAT volume, sex, patient age, CAC, and CAD-RADS categories were conducted. Results: A total of 489 consecutive patients met the inclusion criteria (63.96 ± 12.18 years; 214 females). The mean EAT volume ± SD in those categorized as CAD-RADS 0 (57.25 ± 15.45 years, 120 patients) was 117.43 ± 50.30 cm³: values were higher in men (121.07 ± 53.31 cm³) than in women (114.54 ± 47.98 cm³). EAT volumes positively correlated with age, male sex, CAD severity, and CAC scores. Conclusions: According to our results, males in all CAD-RADS categories have a greater amount of EAT than females. A positive correlation between the volume of EAT and factors such as age (p = 0.003), CAD-RADS categories (p: 0.004), and coronary calcium score (p = 0.0001) with a strong influence exerted by sex was demonstrated. Our results reinforce the observation that higher EAT volumes are associated with a more severe coronary artery disease.

Obesity, a multifaceted metabolic disorder, stands out as a significant risk factor in the development of heart failure with preserved ejection fraction (HFpEF). Its involvement in HFpEF pathogenesis encompasses a complex interplay with adipose tissue, particularly epicardial adipose tissue (EAT), and the effects of sleep-disordered breathing (SDB). Understanding these intricate relationships is pivotal for devising targeted therapeutic approaches to alleviate the burden of HFpEF in individuals with obesity. EAT assumes a central role in linking obesity to HFpEF. As it expands in the context of obesity, EAT contributes to systemic inflammation and insulin resistance, fostering an environment conducive to cardiac remodeling and dysfunction. Furthermore, SDB, prevalent comorbidity in the obese population, emerges as a significant mediator in HFpEF pathogenesis through various mechanisms. The convergence of obesity, EAT expansion, and SDB creates a synergistic effect, heightening the risk of HFpEF development. On the pharmaceutical front, ongoing investigations explore novel strategies targeting inflammation, oxidative stress, and metabolic pathways associated with obesity. These include the potential roles of sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists, offering innovative therapeutic avenues for managing HFpEF in individuals with obesity. In addition, lifestyle modifications such as weight management and interventions addressing SDB and EAT reduction emerge as promising approaches for preventing and managing HFpEF in the obese population. These interventions hold the potential to mitigate obesity-related cardiac risks and improve HFpEF outcomes.

Stress cardiomyopathy, also known as apical ballooning syndrome or takotsubo cardiomyopathy, is traditionally associated with acute emotional or physical stress. However, recent evidence reveals a range of unusual triggers that can lead to this transient form of heart failure including medical and surgical procedures, neurological events (i.e., seizures and strokes), chronic psychological stress, and endocrine disorders such as hypoglycemia, pharmacological agents, infectious diseases (i.e., sepsis and COVID-19), and environmental stressors such as extreme temperatures or high altitudes. Despite the variety of these triggers, they share a common pathophysiology, primarily involving an excessive catecholamine surge that results in myocardial stunning. Recognizing these unusual causes and presentations is essential for timely diagnosis and appropriate management.

Introduction: The role of epicardial adipose tissue (EAT) in cardiovascular health has undergone a paradigm shift in recent years, evolving from a passive reservoir into a dynamic contributor to cardiovascular risk. This case critically examines the multifaceted functions of EAT, explores its implications for cardiovascular risk, and discusses the potential benefits of the GLP-1 receptor agonist Liraglutide in mitigating its effects. Case presentation: We present the case of a 62-year-old male patient who is obese, hypertensive, and has a history of chronic coronary syndrome. He was admitted to the emergency room with complaints of palpitations and shortness of breath. The 12-lead ECG revealed atrial fibrillation with a rapid ventricular response and evidence of a new-onset left bundle branch block. The transthoracic echocardiogram showed heart-rate-dependent regional dyskinesias, while both echocardiographic and computed tomographic scan findings indicated the presence of thick EAT. A coronary angiogram showed intrastent restenosis in the left anterior descending artery, which was treated with percutaneous revascularization. To address residual cardiovascular risk, the patient was initiated on Liraglutide during hospitalization. The follow-up revealed reduced low-density lipoprotein-cholesterol and high-sensitivity C-reactive protein levels, along with a decrease in EAT thickness and BMI, accompanied by improved echocardiographic parameters. Discussion: Targeted interventions aimed at reducing EAT are imperative given its active role in cardiovascular risk. GLP-1 receptor agonists, such as Liraglutide, hold promise in mitigating the effects of EAT and represent a potential avenue for therapeutic exploration in addressing residual cardiovascular risk.

Heart failure with reduced ejection fraction due to ischemic cardiomyopathy remains a significant clinical challenge. Electrical conduction delays exacerbate symptoms by causing uncoordinated contractions, reducing pumping efficiency, and increasing mortality. Right ventricular pacing further worsens dyssynchrony, while resynchronization therapy improves outcomes but has a high non-responder rate. Given these limitations, bundle branch pacing engages the heart’s conduction system, restoring synchronized contraction and enhancing cardiac function. This review examines the impact of left-bundle-branch-block-induced dyssynchrony, the role of advanced imaging in assessing ventricular function, and the clinical outcomes of bundle branch pacing in heart failure patients. Specifically, we explore the mechanical and hemodynamic effects of left bundle branch block, imaging techniques for dyssynchrony evaluation, and the comparative benefits of bundle branch pacing versus resynchronization therapy. Conduction delays impair function, increase myocardial stress, and worsen clinical outcomes. Advanced imaging plays a critical role in patient selection, identifying those most likely to benefit from conduction system pacing. By restoring electrical coordination, bundle branch pacing enhances ventricular function, reduces hospitalizations, and promotes reverse remodeling. It offers similar or superior benefits to conventional resynchronization therapy, regulates stress hormones, reduces oxidative damage, and improves calcium handling. Bundle branch pacing represents a significant advancement in heart failure management, but careful patient selection remains crucial. Future research should focus on optimizing implantation techniques and validating long-term benefits through large-scale clinical trials.