Heart failure (HF) represents a significant global health challenge that is still responsible for increasing morbidity and mortality despite advancements in pharmacological treatments. This review investigates the effectiveness of non-pharmacological interventions in the management of HF, examining lifestyle measures, physical activity, and the role of some electrical therapies such as catheter ablation, cardiac resynchronization therapy (CRT), and cardiac contractility modulation (CCM). Structured exercise training is a cornerstone in this field, demonstrating terrific improvements in functional status, quality of life, and mortality risk reduction, particularly in patients with HF with reduced ejection fraction (HFrEF). Catheter ablation for atrial fibrillation, premature ventricular beats, and ventricular tachycardia aids in improving left ventricular function by reducing arrhythmic burden. CRT remains a key intervention for selected HF patients, helping achieve left ventricular reverse remodeling and improving symptoms. Additionally, the emerging therapy of CCM provides a novel opportunity for patients who do not meet CRT criteria or are non-responders. Integrating non-pharmacological interventions such as digital health alongside specific medications is key for optimizing outcomes in HF management. It is imperative to tailor approaches to individual patients in this diverse patient population to maximize benefits. Further research is warranted to improve treatment strategies and enhance patient outcomes in HF management.

Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice, and it is an enormous burden worldwide because of its high morbidity, disability and mortality. It is generally acknowledged that physical activity (PA) is strongly associated with a significant reduction in the risk of cardiovascular (CV) disease and all-cause mortality. Moreover, it has been observed that moderate and regular physical activity has the potential to reduce the risk of AF, in addition to improving overall well-being. Nevertheless, some studies have associated intense physical activity with an increased risk of AF. This paper aims to review the main related literature to investigate the association between PA and AF incidence and draw pathophysiological and epidemiological conclusions.

Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a rare electrical genetic disease characterized by ventricular polymorphic tachycardia and/or bidirectional ventricular tachycardia induced by the release of catecholamines caused by intense physical or emotional stress in structurally normal hearts. Mostly, it is caused by mutations in genes that are involved in calcium homeostasis, in particular in the gene encoding for cardiac ryanodine receptor (RyR2). Our observation is the first description of familial CPVT caused by mutation of the RyR2 gene, linked to the complete AV block.

Atrial fibrillation (AF) is the most common sustained supraventricular arrhythmia, affecting 2–3% of the adult population and contributing significantly to morbidity, mortality, and healthcare burden. Catheter ablation has become a cornerstone in the treatment of symptomatic, drug-refractory AF, with pulmonary vein isolation (PVI) established as the standard approach, especially in paroxysmal AF. Over the past three decades, ablation technologies have evolved considerably—from radiofrequency and cryoballoon to the recent advent of pulsed field ablation—enhancing procedural safety, efficiency, and lesion durability. Despite these technological advancements, long-term outcomes have plateaued, suggesting that success may depend not just solely on the energy source used, but also on a more individualized, mechanism-based approach. The classification of AF based on duration alone fails to capture the complexity of its underlying pathophysiology. Tailored strategies that consider arrhythmic mechanisms, electrophysiological triggers, and patient-specific substrates—especially in persistent AF—are increasingly recognized as essential for durable results. Tools such as high-density mapping, autonomic modulation, and substrate-targeted ablation are expanding therapeutic horizons. Moreover, special populations, such as athletes, present unique arrhythmic profiles influenced by structural and autonomic remodeling, requiring nuanced management. The integration of lifestyle interventions, neuromodulation techniques, and emerging genetic and pharmacological insights further supports a comprehensive, personalized approach. In this paper, we explore whether future success in AF ablation lies more in refining technology or in advancing our understanding of arrhythmic mechanisms to guide patient-specific therapy.

Magnetic resonance imaging is a novel imaging technique for guiding electrophysiology based ablation operations for atrial flutter and typical atrial fibrillation. When compared to standard electrophysiology ablation, this innovative method allows for better outcomes. Intra-procedural imaging is important for following the catheter in real time throughout the ablation operation while also seeing cardiac architecture and determining whether the ablation is being completed appropriately utilizing oedema sequences. At the same time, intra-procedural imaging allows immediate visualization of any complications of the procedure. We describe a case of a 67 year old male underwent an isthmus-cavo-tricuspid magnetic resonance-guided thermoablation procedure for atrial flutter episodes. During the procedure we noted an atypical focal thinning of the right atrial wall at the isthmus cava-tricuspidal zone. The post-procedural Black Blood T2 STIR showed an area of hyperintensity at the hepatic dome and glissonian capsule, which was consistent with intraparenchymal hepatic oedema, in close proximity to the atrial finding. Given the opportunity to direct monitoring of adjacent tissues, we aim to highlight with our case the ability of magnetic resonance-guided cardiac ablation to immediately detect peri-procedural complications in the ablative treatment of atrial fibrillation.

Background: Intense physical exercise induces oxidative stress and inflammation in adult professional athletes, but data on adolescent elite athletes remain limited. Methods: 24 elite adolescent soccer players were recruited and evaluated three times: pre-season (T0), after one month (T1), and after the first half of the season (T2). Saliva samples were col-lected to measure oxidative stress and endothelial function. In vitro studies were per-formed on endothelial cells exposed to H₂O₂ concentrations observed in athletes. Results: Athletes showed a significant increase in oxidative stress markers (NOX2 and H₂O₂) at T1 and T2 versus T0. Endothelial dysfunction was evidenced by reduced total NO concentra-tion and elevated endothelin (ET1) levels. In vitro, endothelial cells exposed to H₂O₂ (8 µM) exhibited greater damage than untreated cells, as evidenced by increased NOX2 activation and ET1 levels. Finally, H₂O₂ (8 µM)-treated cells impaired tube formation, reducing mesh number and area. NOX2ds-tat treatment reduced cell damage and restored angiogenic capacity. Conclusions: Our findings indicate that adolescent elite athletes experience sig-nificant oxidative stress and endothelial impairment, potentially increasing cardiovascu-lar risk. These results underscore the importance of cardiovascular monitoring and the potential benefits of antioxidant strategies, even in young athletes participating in high-intensity sports.