Atrial cardiomyopathy and remodeling play pivotal roles in the development of atrial fibrillation (AF) and heart failure (HF), involving complex changes in atrial structure and function. These changes facilitate the progression of AF and HF by creating a dynamic interplay between mechanical stress and electrical disturbances in the heart. Sodium–glucose cotransporter 2 inhibitors (SGLT2is), initially developed for the management of type 2 diabetes, have demonstrated promising cardiovascular benefits, being currently one of the cornerstone treatments in HF management. Despite recent data from randomized clinical trials indicating that SGLT2is may significantly influence atrial remodeling, their overall effectiveness in this context is still under debate. Given the emerging evidence, this review examines the molecular mechanisms through which SGLT2is exert their effects on atrial remodeling, aiming to clarify their potential benefits and limitations. By exploring these mechanisms, this review aims to provide insights into how SGLT2is can be integrated into strategies for preventing the progression of atrial remodeling and HF, as well as the development of AF.

Epicardial adipose tissue (EAT), the visceral fat layer next to the myocardium, has become an important focus in heart failure with preserved ejection fraction (HFpEF). When enlarged and inflamed, EAT increases pericardial restraint, releases fibroinflammatory mediators, and disrupts myocardial energetics, thereby reproducing the high-pressure, exercise-intolerant HFpEF phenotype regardless of body mass index. Modern echocardiography, cardiac CT, and MRI, enhanced by artificial intelligence texture analytics, now enable precise depot-specific quantification, making EAT a measurable therapeutic target. Early interventional studies suggest that caloric restriction, bariatric surgery, SGLT2 inhibitors, GLP-1 receptor agonists, statins, PCSK9 antibodies, and colchicine can reduce EAT volume or alter its inflammatory profile, with concurrent improvements in haemodynamics and biomarkers. However, definitive outcome trials are still pending. Priority directions include standardising imaging cut-offs, mapping EAT immune–metabolic niches, and testing combined metabolic–inflammatory regimens to translate EAT modulation into precision therapy for HFpEF. This review aims to synthesise current mechanistic, diagnostic, and therapeutic insights on EAT in HFpEF and outline future research priorities.

Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia globally. High-power, short-duration radiofrequency (RF) catheter ablation (CA) for AF has recently emerged, reducing ablation times and enhancing patient tolerability with comparable efficacy and safety. While the benefits of general anesthesia (GA) for standard-power, standard-duration CA are well-established, data comparing GA to mild conscious sedation (MCS) for high-power, short-duration CA are limited. Methods: We included patients undergoing high-power, short-duration CA for AF under GA (group 1) or MCS (group 2). Procedural characteristics, success rates, and mid-term outcomes were compared. Results: In total, 131 patients, 47 in the GA group and 84 in the MCS group, were included. CA was performed for paroxysmal AF in 34 patients in group 1 (72.3%) and 68 patients in group 2 (80.9%). We found lower a mean total procedure time (100 [90–120] vs. 160 [130–180] min, p < 0.0001), lower radiation exposure (932.5 [625–1716] vs. 2445 [1228–4791] μGy, p < 0.0001 and 4.5 [3–7.1] 7.3 [4.2–13.5] min, p = 0.0003) and fewer RF applications (71 [54.8–83.8] vs. 103 [88.5–120.5], p < 0.0001) in the GA group. No major complications occurred. The 6-month AF recurrence rate was comparable between the groups (21.2% vs. 33.3%, p = 0.15). Conclusion: In patients undergoing high-power, short-duration RFCA for AF, the use of GA is associated with better procedural efficiency while simultaneously associated with an early recurrence rate comparable to MCS.

Background: Heart failure with preserved ejection fraction (HFpEF) is increasingly prevalent worldwide due to ageing and comorbidities. Emerging evidence suggests that Philadelphia-negative chronic myeloproliferative neoplasms (MPNs), particularly those with JAK2 mutations, may contribute to the development of HFpEF, especially by promoting inflammation and increasing thrombotic risk. Methods: This prospective case–control study assessed 58 patients with Philadelphia-negative MPNs and 41 controls, by clinical, paraclinical, and echocardiographic evaluation, to diagnose diastolic dysfunction and HFpEF according to the ESC guideline criteria. Results: Patients with MPNs had a significantly higher prevalence of HFpEF compared to controls (p = 0.008), higher H₂FPEF scores (median 5 vs. 3, p < 0.001), and significant echocardiographic abnormalities, including a higher left ventricular mass index (LVMI) (100.1 vs. 76.6 g/m², p < 0.001), E/e’ (11.00 vs. 7.00, p < 0.001), and pulmonary artery systolic pressure (PASP) (26.0 vs. 7.42 mmHg, p < 0.001). Multivariable logistic regression models identified male sex (OR = 8.993, p = 0.001) and the presence of JAK2 mutation (OR = 5.021, p = 0.002) as independent risk factors for HFpEF in this population. Conclusions: Patients with chronic MPNs, particularly males and those with JAK2 mutations, are at an increased risk of HFpEF, highlighting the importance of routine cardiologic assessment to improve outcomes in this patient population.

Background: Atrial fibrillation (AF) is a common comorbidity in heart failure with preserved ejection fraction (HFpEF), yet the optimal rhythm control strategies and the emerging role of sodium–glucose cotransporter-2 inhibitors (SGLT2i) in maintaining sinus rhythm remain unclear. Methods: We conducted a single-centre, retrospective study of 120 consecutive HFpEF patients with paroxysmal or persistent AF, treated by electrical cardioversion, radiofrequency ablation (RFA), or cryoablation. The primary outcome was AF recurrence, with secondary outcomes including time to recurrence and the impact of SGLT2i on AF recurrence. Results: Both cryoablation (HR = 0.226, 95% CI: 0.089–0.573, p = 0.002) and RFA (HR = 0.293, 95% CI: 0.131–0.654, p = 0.003) were associated with lower AF recurrence rates and longer arrhythmia-free survival compared to electrical cardioversion. SGLT2i therapy was independently associated with fewer recurrences (HR = 0.421, 95% CI: 0.266–0.786, p = 0.007) and a 12-week extension of AF-free time. Conclusions: In HFpEF with AF, prioritising catheter ablation over cardioversion and combining rhythm control with SGLT2i improves rhythm durability.