Background: The “fast track” addition (within 48 h) of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) to the optimized oral lipid-lowering therapy (LLT) during hospitalization for acute coronary syndrome (ACS) has been shown to rapidly achieve the low-density lipoprotein cholesterol (LDL-C) therapeutic targets. However, so far, its efficacy in real-world settings remains understudied. Methods: We retrospectively analyzed 128 ACS patients treated at our center, comparing “PCSK9i fast track” use within 48 h to standard “stepwise” LLT. Lipid levels and incidence of major adverse cardiovascular events (MACEs) were evaluated at 30 and 180 days. Results: The “PCSK9i fast track” group achieved significantly lower LDL-C levels at 30 days (41.5 ± 27.5 vs. 85.6 ± 35.9 mg/dL, p < 0.001) and 180 days (29.6 ± 21.0 vs. 59.0 ± 32.4 mg/dL, p < 0.001). Recommended LDL-C targets (<55 mg/dL) were met by 88.3% of the “PCSK9i fast track” group at 180 days, compared with 61.9% of controls (p < 0.001). No significant differences in MACEs were observed between groups. No adverse effects from PCSK9i use were noted. Conclusions: The “PCSK9i fast track” strategy was safe and effective in achieving LDL-C targets more rapidly than conventional approaches in real-world ACS patients.

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.

Background and Clinical Significance: Scimitar Syndrome is a rare congenital cardio-pulmonary 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 this intervention is combined with mitral valve annuloplasty, the proximity to the atrioventricular node may predispose patients to late-onset conduction disturbances. 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 un-dergoing 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, beta-blockers and underwent im-plantation of a ventricular leadless pacemaker. Conclusions: This case highlights the role of atrial function imaging in guiding rhythm management and procedural choices in surgically-corrected congenital heart disease.

Obesity, sleep-disordered breathing (SDB), and epicardial adipose tissue (EAT) are increasingly recognized as interconnected contributors to cardiometabolic and cardiovascular disease, although they are often addressed as distinct clinical conditions. This narrative review aims to integrate current evidence on the reciprocal pathophysiological interactions linking these entities and their contribution to cardiovascular remodeling. A comprehensive literature search up to May 2025 was performed, focusing on clinical, imaging, and mechanistic studies examining obesity, SDB, EAT, and cardiovascular outcomes. Available data indicate that obesity promotes visceral and epicardial fat expansion, systemic inflammation, and altered cardiopulmonary mechanics, thereby facilitating the development of SDB. In turn, intermittent hypoxia and sympathetic activation associated with SDB further aggravate adipose tissue dysfunction and inflammatory activation of EAT. As a metabolically active fat depot in direct anatomical continuity with the myocardium and coronary arteries, EAT contributes to myocardial fibrosis, atrial remodeling, diastolic dysfunction, and coronary atherosclerosis through paracrine inflammatory and neurohumoral pathways. The convergence of these mechanisms delineates a high-risk cardiometabolic phenotype associated with atrial fibrillation, coronary artery disease, and heart failure with preserved ejection fraction. Recognizing obesity, SDB, and EAT as components of an integrated cardiometabolic system may support improved phenotypic stratification and inform more comprehensive approaches to residual cardiovascular risk.