Background: Heart failure (HF) and atrial fibrillation (AF) often coexist, and this has a major impact on prognosis. Only a limited amount of data is available on the effect of integrated strategies to improve prognosis in patients with HF and AF. We aimed to evaluate the association between HF subtype, HF optimal medical therapy (OMT), adherence to the Atrial Fibrillation Better Care (ABC) pathway, and all-cause death. Methods: Hospitalized patients and outpatients were enrolled in the Heart failuRe ObsErvational Study, which is a prospective, multicenter cohort study, between April 2022 and January 2024. Our analysis included patients with both HF and AF, who were divided into three groups: ABC + OMT, noABC + OMT, and noABC + noOMT. Results: A total of 627 patients, of whom 51.7% had HF with reduced ejection fraction, were included in this study. Direct oral anticoagulants were prescribed to 70.8% of patients, and 71.6% of these received the recommended doses. The patients were divided into the following groups: 49.8% were assigned to the ABC + OMT group, 25.2% to the noABC + OMT group, and 25% to the noABC + noOMT group. All-cause death occurred in 19.5% of patients. OMT compliance was associated with lower risk of all-cause death (HR0.61, 95% CI 0.42–0.9, p = 0.01), whereas management compliant with the ABC pathway was not (HR0.74, 95% CI 0.51–1.09, p = 0.12). In the ABC + OMT group, the risk of all-cause death was lower than in the noABC + noOMT group (HR0.60, 95% CI 0.39–0.92, p = 0.02). Conclusions: Integrated treatment strategies were implemented in half of the population with HF and AF, and this was associated with better long-term prognosis compared with patients who did not receive a complex treatment strategy.

Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a common condition, also in the population of patients with psychiatric disorders. Aim: This narrative research investigated the complex association of depression and anxiety disorders with MASLD and identified the common underlying mechanisms of the conditions. Material and methods: A systematic review of the literature on depression, anxiety disorders, and MASLD was conducted. Relevant articles were identified using PubMed and Google Scholar, with a primary focus on recent publications. This article expands on the findings of the selected studies. The inclusion criteria prioritized peer-reviewed studies published in the last eight years and those with clinically relevant outcomes. Results and discussion: Patients with depression and anxiety disorders often lead sedentary lifestyles, are physically inactive, and have unhealthy eating habits, which may contribute to obesity, diabetes, hypertension, and hypercholesterolemia. These conditions are components of metabolic syndrome, which is directly linked to MASLD. Abnormal gut microbiota is also significantly associated with the condition. Chronic stress, sleep disturbances, and neuroendocrine dysregulation may further exacerbate metabolic imbalance. Special attention should be given to the appropriate selection of psychiatric medications in this patient group in consideration of the metabolic profile of each drug. Conclusions: In clinical practice, careful management is essential for psychiatric patients with a well-established diagnosis of MASLD. Their management should consider the potential risks of weight gain and increased appetite. Multidisciplinary collaboration between psychiatrists, hepatologists, and dietitians may improve treatment outcomes. Further research is needed to explore the pathophysiological mechanisms underlying the observed associations and the potential consequences of MASLD in depression and anxiety disorders. Keywords: anxiety disorders depression fatty liver disease metabolic dysfunction-associated steatotic liver disease

Introduction: Heart failure (HF) with mildly reduced ejection fraction (HFmrEF) is a heterogeneous phenotype, and whether the prognostic weight of ischemic versus non-ischemic etiology differs across left ventricular ejection fraction (LVEF) categories remains uncertain. We examined whether the association between etiology and long-term all-cause mortality is modified by HF phenotype. Material and methods: Within the prospective multicenter HEROES registry, 1,410 patients with HF were classified as having ischemic or non-ischemic etiology and categorized by LVEF. All-cause mortality was obtained through national administrative linkage with complete follow-up. Entropy balancing (13 covariates) and weighted Cox models were applied within each phenotype, with formal testing for etiology-by-phenotype interaction. Robustness was evaluated using restricted mean survival time (RMST), the E-value, and sensitivity analyses. Results: Over a median follow-up of 14.8 months, 219 (15.5%) deaths occurred. Crude mortality was identical between etiologies (15.5% vs. 15.5%; p = 0.93). After balancing, no difference was observed in HFrEF (adjusted hazard ratio [aHR] 1.03, 95% CI: 0.68–1.58) or HFpEF (aHR = 0.84, 95% CI: 0.37–1.90), whereas non-ischemic etiology was associated with higher mortality in HFmrEF (aHR = 3.99, 95% CI: 1.51–10.51; p = 0.005). The etiology-by-phenotype interaction was significant (p = 0.032). In HFmrEF, the RMST difference at 23 months was −2.38 months (95% CI: −3.69 to −1.00), with an E-value of 4.55 (lower confidence limit 1.99); findings were consistent across sensitivity analyses. Conclusions: The prognostic impact of HF etiology appears phenotype-dependent, concentrated within HFmrEF, where non-ischemic etiology substantially worse survival. Given the limited number of events, this phenotype-specific signal is hypothesis-generating and warrants confirmation.