Heart failure (HF) is an increasingly prevalent disease with a major impact on morbidity and mortality worldwide. Continuous advancements in diagnostic and therapeutic strategies have significantly improved patient outcomes; however, precise biomarkers and novel therapeutic targets are still needed. In recent years, microRNAs (miRNAs) have emerged as promising biomarkers and potential therapeutic targets in HF. They consist of small, noncoding RNA molecules that regulate gene expression post-transcriptionally and are detectable in both tissues and blood, with disease-specific expression profiles that make them attractive candidates for non-invasive diagnosis, prognostic risk stratification, and even therapeutic interventions. In HF, miRNAs contribute to pathogenesis by modulating fibrosis, apoptosis, hypertrophy, and inflammation. The aim of this review is to analyze the role of circulating and tissue miRNAs in HF as biomarkers and as therapeutic targets. The future management of HF should include strategies to modulate miRNA expression in order to modify the disease trajectory and improve clinical outcomes.

Heart failure (HF) is characterized by adverse myocardial remodeling involving both the contractile cardiomyocytes and the conduction tissue. HF is often associated with atrioventricular (AV) node dysfunction, which frequently leads to conduction delays and subsequent dyssynchrony ultimately related to adverse clinical outcomes. Despite its clinical relevance, AV node pathology in HF remains poorly explored. This review aims to investigate the pathophysiology underlying AV node dysfunction and the clinical implications for patients with HF, and to provide an overview of current therapeutic approaches, including an analysis of potential future treatments.

Heart failure (HF) is a systemic syndrome in which cardiac dysfunction is closely linked to multiorgan involvement, including the gastrointestinal tract. Increasing evidence highlights the relevance of the gut–heart axis in HF pathophysiology, whereby intestinal hypoperfusion, congestion, and barrier dysfunction promote gut microbiota dysbiosis, systemic inflammation, and adverse cardiovascular outcomes. In parallel, the advent of novel HF therapies, particularly sodium–glucose cotransporter 2 inhibitors (SGLT2i) and the angiotensin receptor–neprilysin inhibitor sacubitril/valsartan, has markedly improved clinical outcomes across HF phenotypes. Beyond their established cardiovascular benefits, these therapies may exert pleiotropic effects that extend to the intestinal environment and the gut microbiota. Through integrated actions on hemodynamics, neurohormonal activation, metabolic pathways, and inflammatory processes, recent data suggest that novel HF drugs may indirectly influence the gut-microbial composition and function. Conversely, the gut microbiota may modulate drug efficacy and result in interindividual variability in therapeutic responses, suggesting a bidirectional interaction between pharmacological treatment and the gut ecosystem. This narrative review summarizes current evidence of gut microbiota alterations in HF and critically examines emerging data on interactions between the gut microbiota and novel HF therapies, focusing on SGLT2 inhibitors and sacubitril/valsartan. Understanding this crosstalk may support the development of microbiota-informed, personalized therapeutic strategies in heart failure.