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.

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.

Obesity and obstructive sleep apnea (OSA) frequently coexist and synergistically contribute to cardiovascular disease through interconnected mechanical, metabolic, and autonomic mechanisms. This interplay promotes myocardial electrical instability and structural remodeling, favoring the development and persistence of cardiac arrhythmias, particularly atrial fibrillation. Among the key mediators linking obesity to arrhythmogenesis, epicardial adipose tissue has emerged as a relevant factor that may contribute to local pro-inflammatory, pro-fibrotic, and autonomic effects on the myocardium. In parallel, OSA-related intermittent hypoxia and intrathoracic pressure swings further amplify electrical instability and autonomic imbalance, reinforcing a self-sustaining arrhythmogenic substrate. Therapeutic strategies are increasingly shifting toward upstream interventions targeting these underlying mechanisms. Metabolic therapies, including the dual GIP/GLP-1 receptor agonist tirzepatide, have demonstrated substantial weight reduction and improvement in OSA severity, with potential indirect benefits on arrhythmic risk through modulation of visceral adiposity, inflammation, and metabolic dysfunction. On the electrophysiological side, cardioneuroablation has emerged as a potentially investigational option in selected patients with vagally mediated bradyarrhythmias, although its role remains to be fully defined. Overall, these observations support an integrated, phenotype-driven approach combining respiratory therapy, metabolic modulation, and targeted electrophysiological interventions. This framework may help redefine therapeutic priorities, shifting from symptom control toward modification of the underlying arrhythmogenic substrate and improvement of long-term cardiovascular outcomes.

Background and Clinical Significance: Scimitar Syndrome is a rare congenital cardiopulmonary anomaly characterized by partial anomalous pulmonary venous return, often requiring early surgical correction. It may coexist with other congenital or acquired cardiovascular anomalies, including valvular diseases such as mitral regurgitation. When surgical correction of Scimitar Syndrome is combined with mitral valve annuloplasty, the proximity to the atrioventricular node may potentially predispose patients to late-onset conduction disturbances, although causality remains speculative. Case Presentation: We describe the case of a 53-year-old male who developed paroxysmal atrial fibrillation, atrial flutter, and intermittent second-degree AV block decades after undergoing surgical correction of Scimitar Syndrome with concomitant mitral annuloplasty. Multimodal echocardiographic evaluation revealed preserved left atrial volume, normal intra-atrial conduction time, mildly reduced strain, and maintained atrial synchrony. The patient was treated with direct oral anticoagulants and beta-blockers and underwent the implantation of a ventricular leadless pacemaker. Conclusions: This case highlights the supportive role of atrial function imaging in assessing atrial health and informing rhythm management and procedural choices in surgically corrected congenital heart disease.

Heart failure with reduced ejection fraction due to ischemic cardiomyopathy remains a major challenge. Electrical conduction delays worsen symptoms by causing uncoordi-nated contractions, inefficient pumping, and increased mortality. Right ventricular pacing exacerbates dyssynchrony, while resynchronization therapy improves outcomes but has a high non-responder rate. Bundle branch pacing engages the heart’s conduction system, restoring synchronized contraction and improving function. Objective: This re-view evaluates the impact of left bundle branch block-induced dyssynchrony, advanced imaging in assessing ventricular function, and clinical outcomes of bundle branch pacing in heart failure patients. Methods: We analyzed the mechanical and hemodynamic effects of left bundle branch block, imaging techniques for dyssynchrony assessment, and the clinical benefits of bundle branch pacing compared to resynchronization therapy. Results: Conduction delays impair function, increase stress, and worsen outcomes. Advanced imaging improves patient selection. Conduction system pacing restores coordination, enhances 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. Conclusion: Bundle branch pacing advances heart failure treatment, but proper patient selection is crucial. Future research should refine implantation strategies and conduct large-scale trials to confirm long-term efficacy.

Anterior myocardial infarction is a critical condition with significant implications for cardiac function and patient prognosis. Despite advancements in reperfusion therapies, optimizing recovery during the early phases of myocardial infarction remains challenging. Anterior myocardial infarction can lead to substantial long-term effects on a patient’s health due to extensive damage to the heart muscle, particularly the left ventricle, impacting both quality of life and overall prognosis. Vericiguat, a soluble guanylate cyclase stimulator, has shown promise in heart failure, but its role in early anterior myocardial infarction has not yet been fully explored. By enhancing soluble guanylate cyclase activity, vericiguat may increase cyclic guanosine monophosphate production, leading to vasodilation, inhibition of platelet aggregation, and potential cardioprotective effects. Currently, treatment options for anterior myocardial infarction primarily focus on reperfusion strategies and managing complications. However, there is a critical need for adjunctive therapies that specifically target the pathophysiological changes occurring in the early phases of myocardial infarction. Vericiguat’s mechanism of action offers a novel approach to improving vascular function and myocardial health, potentially contributing to innovative treatment strategies that could transform the care and prognosis of patients with anterior myocardial infarction.