Vascular calcification (VC) is a biological phenomenon characterized by an accumulation of calcium and phosphate deposits within the walls of blood vessels causing the loss of elasticity of the arterial walls. VC plays a crucial role in the incidence and progression of chronic kidney disease (CKD), leading to a significant increase in cardiovascular mortality in these patients. Different conditions such as age, sex, dyslipidemia, diabetes, and hypertension are the main risk factors in patients affected by chronic kidney disease. However, VC may occur earlier and faster in these patients if it is associated with new or non-traditional risk factors such as oxidative stress, anemia, and inflammation. In chronic kidney disease, several pathophysiological processes contribute to vascular calcifications, including osteochondrogenic differentiation of vascular cells, hyperphosphatemia and hypercalcemia, and the loss of specific vascular calcification inhibitors including pyrophosphate, fetuin-A, osteoprotegerin, and matrix GLA protein. In this review we discuss the main traditional and non-traditional risk factors that can promote VC in patients with kidney disease. In addition, we provide an overview of the main pathogenetic mechanisms responsible for VC that may be crucial to identify new prevention strategies and possible new therapeutic approaches to reduce cardiovascular risk in patients with kidney disease.

Changes in cardiac mechanics after correction of severe Aortic Stenosis (AS) are under-investigated. Myocardial Work (MW) is emerging as a useful non-invasive correlate of invasively measured myocardial performance and oxygen consumption. The aim of this study was to assess the usefulness of MW in the clinical management of patients with AS undergoing transcatheter aortic valve implantation (TAVI). Consecutive patients referred for TAVI were included in this observational study. Echocardiograms were performed before and after TAVI to measure Global Work Index (GWI), Global Constructive Work (GCW), Global Wasted Work (GWW), and Global Work Efficiency (GWE). Mean transvalvular gradient was significantly improved (p < 0.05), without significant changes in left ventricular ejection fraction, nor in global longitudinal strain (GLS). GWI (p < 0.001) and GCW (p < 0.001), but not GWW (p = 0.241) nor GWE (p = 0.854) were significantly reduced after TAVI. Patients with a low flow low gradient (LF-LG) AS had lower left ventricular ejection fraction (LVEF) (p < 0.001), worse global longitudinal strain (GLS) (p < 0.001), and lower baseline GWI (p < 0.001), GCW (p < 0.001) and GWE (p = 0.003). The improvement in GWI and GCW observed after TAVI in the general study population were abolished among LF-LG patients. In conclusion, non-invasive MW might be useful to further classify patients with AS and to predict non responders.

Cardiac arrhythmias in the pediatric population represent both diagnostic and therapeutic challenges due to their heterogeneous etiologies, age-dependent clinical presentations, and the variety of management strategies required. Although many electrophysiological mechanisms are shared with adults, several arrhythmias are unique to infancy and adolescence or are associated with congenital heart disease and inherited channelopathies. Clinical presentation varies considerably with age and may be unclear or nonspecific, especially in neonates and infants. In some cases, arrhythmias are benign and self-limiting; in others, they may represent the earliest manifestation of an underlying cardiac disorder, potentially progressing to hemodynamic instability, serious arrhythmic events, or sudden cardiac death. Recent advancements in electrophysiology, catheter ablation, and device technology have broadened the therapeutic landscape, improving outcomes even in neonatal and infant patients. This review aims to summarize current knowledge on pediatric arrhythmias, with a focus on clinical recognition, diagnostic evaluation, and personalized treatment strategies.

Cardiomyopathies are the structural and functional disorders of the myocardium. Etiopathogenesis is complex and involves an interplay of genetic, environmental, and lifestyle factors eventually leading to myocardial abnormalities. It is known that non-coding (Nc) RNAs, including micro (mi)-RNAs and long non-coding (lnc) RNAs, play a crucial role in regulating gene expression. Several studies have explored the role of miRNAs in the development of various pathologies, including heart diseases. In this review, we analyzed various patterns of ncRNAs expressed in the most common cardiomyopathies: dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic cardiomyopathy. Understanding the role of different ncRNAs implicated in cardiomyopathic processes may contribute to the identification of potential therapeutic targets and novel risk stratification models based on gene expression. The analysis of ncRNAs may also be helpful to unveil the molecular mechanisms subtended to these diseases.

Cardiovascular calcification is a multifactorial and complex process involving an array of molecular mechanisms eventually leading to calcium deposition within the arterial walls. This process increases arterial stiffness, decreases elasticity, influences shear stress events and is related to an increased risk of morbidity and mortality associated with cardiovascular disease. In numerous in vivo and in vitro models, warfarin therapy has been shown to cause vascular calcification in the arterial wall. However, the exact mechanisms of calcification formation with warfarin remain largely unknown, although several molecular pathways have been identified. Circulating miRNA have been evaluated as biomarkers for a wide range of cardiovascular diseases, but their exact role in cardiovascular calcification is limited. This review aims to describe the current state-of-the-art research on the impact of warfarin treatment on the development of vascular calcification and to highlight potential molecular targets, including microRNA, within the implicated pathways.

Background. Accurate anatomical assessment is essential for pre-procedural planning in structural heart disease. Advanced 3D imaging could offer improved visualization for more accurate reconstruction. We assessed the performance of a novel immersive 3D virtual reality (VEA) for the pre-procedural planning of transcatheter aortic valve implantation (TAVI) candidates. Methods. Measurement of cardiac-gated contrast-enhanced computed tomography (CT) scans was performed with the novel VEA and established tools: 3Mensio and Horos. Results. 50 consecutive patients were included. Annular and LVOT measurements obtained with VEA were strongly correlated with those derived from standard CT analysis. The intraclass correlation coefficient (ICC) confirmed excellent consistency for annular measurements (ICC = 0.93), while the concordance correlation coefficient indicated very good overall agreement (CCC = 0.83, 95% CI 0.73–0.90). Similarly, LVOT measurements obtained with VEA showed strong correlation with CT values, with good consistency (ICC = 0.90) and good overall agreement (CCC = 0.77, 95% CI 0.64–0.86). VEA-based planning improved prosthesis size selection accuracy, achieving higher concordance with implanted valves and a significant net reclassification gain over conventional CT. Conclusions. Given the increasing use of advanced 3D cardiac imaging technologies, understanding their diagnostic accuracy to guide pre-procedural planning of TAVI is paramount. In our study, VEA provided reliable assessment of aortic root anatomy for TAVI planning. This novel 3D software provides accurate, patient-specific reconstructions of the aortic root and surrounding structures that may optimize valve sizing, improve procedural safety and enhance procedural outcomes. This provides a rationale for future studies to assess the procedural benefit derived from a three-dimensional assessment of the aortic valve geometry.