Congestion represents a defining hallmark of heart failure (HF) leading to increased morbidity and mortality in HF patients. While it was traditionally viewed as a simple and uniform state of volume overload, contemporary understanding has emphasized its complexity, distinguishing between intravascular, interstitial, and tissue congestion. Congestion contributes to overt clinical manifestation of HF. However, subclinical congestion often goes undetected, increasing the risk of adverse outcomes. Residual congestion, in particular, remains a frequent and challenging issue, with its persistence at discharge being strongly linked to rehospitalization and poor prognosis. Clinical evaluation often fails to reliably identify the resolution of congestion, highlighting the need for supplementary diagnostic methods. Improvement in imaging modalities, including lung ultrasound, venous Doppler, and echocardiography, have significantly enhanced the detection of congestion. Moreover, biomarkers such as natriuretic peptides, bioactive adrenomedullin, soluble CD146, and carbohydrate antigen 125 offer valuable, complementary insights into fluid distribution and the severity of HF congestion. Therefore, a comprehensive, multimodal strategy that integrates clinical evaluation with imaging and biomarker data is crucial for optimizing the management of congestion in HF. Future approaches should prioritize personalized decongestive therapy, addressing both intravascular and tissue congestion, while aiming to preserve renal function and limit neurohormonal activation. Refinement of these strategies holds promise for improving long-term outcomes, reducing rehospitalizations, and enhancing overall patient prognosis.

Background/Objectives: Diabetes mellitus (DM) represents a major global public health challenge and is consistently associated with an increased risk of atrial fibrillation (AF). Despite extensive epidemiological evidence linking the two conditions, the underlying mechanisms and the influence of glucose-lowering therapies on AF susceptibility remain incompletely defined. This review aims to summarize the current knowledge on the pathophysiological pathways linking DM and AF and to assess the impact of commonly used antidiabetic therapies on arrhythmic risk. We conducted a narrative review of epidemiological studies, mechanistic research, and cardiovascular outcome trials that evaluate the association between DM and AF. We included data addressing structural, electrical, autonomic, metabolic, and inflammatory mechanisms of AF in diabetes, as well as clinical evidence regarding the impact of metformin, insulin, dipeptidyl peptidase-4 (DPP-4) inhibitors, sodium–glucose cotransporter-2 (SGLT-2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists on AF incidence or recurrence. Results: DM promotes AF development through multiple complementary mechanisms, including atrial fibrosis, electrical conduction abnormalities, autonomic dysfunction, inflammation, glycemic fluctuations, oxidative stress, and expansion of epicardial adipose tissue. These changes create a vulnerable atrial substrate that facilitates both initiation and maintenance of AF. Evidence from recent trials indicates that the arrhythmic effects of glucose-lowering therapies are heterogeneous. Metformin and SGLT-2 inhibitors appear to offer favorable or neutral effects on AF risk. GLP-1 receptor agonists provide substantial cardiovascular benefits, although their specific impact on AF remains under investigation. Insulin therapy has been linked to a higher AF risk, whereas DPP-4 inhibitors show an overall neutral effect with inconsistent findings across studies. Conclusions: AF in patients with DM results from complex interactions between metabolic disturbances, structural remodeling, and inflammatory activation. Although several antidiabetic drugs appear to have potential antiarrhythmic effects, further dedicated research is needed to clarify their role in AF prevention and management.

Introduction and Aim: Assessing decongestion in patients with acute decompensated heart failure (ADHF) is challenging, requiring multiple parameters and often remaining imprecise. The study aimed to investigate the utility of indirectly estimating plasma variation (∆ePVS) for evaluating decongestion in ADHF patients in relation to natriuretic peptides. Materials and Methods: This prospective, observational, single-center study included 111 patients (mean age 74 years, 40% female) hospitalized with ADHF and treated with intravenous diuretics along with optimized medical therapy. Patients were clinically and echocardiographically evaluated at admission, with blood tests performed at both admission and discharge. A decrease of ≥30% in NT-proBNP at discharge was considered a marker of decongestion. ∆ePVS was calculated using the Strauss formula: ∆ePVS (%) = 100 × [(Hb admission/Hb discharge) × (1 − Hct discharge)/(1 − Hct admission)] − 100. A negative ∆ePVS (<0%) at discharge was considered a marker of hemoconcentration. Patients were divided into two groups: G1 (∆ePVS < 0%, 81 patients) and G2 (∆ePVS ≥ 0%, 30 patients). Results: Both groups had similar left ventricular ejection fraction (LVEF) values of 46%, mean hemoglobin (Hb) (12 g/dL), and creatinine (1.16 ± 0.65 mg/dL). NT-proBNP decreased in 88% patients in G1 and in 26% patients in G2 (p < 0.001). During hospitalization, five patients from G2 died. At 6 months, rehospitalization occurred in 35% of G2 and 21% of G1 (p = 0.04), with mortality rates of 37% in G2 and 11% in G1 (p = 0.012). Multivariate regression identified ∆ePVS as the only significant predictor of NT-proBNP decrease (OR 0.11, 95% CI 0.04–0.33, p < 0.001). Conclusions: Indirect estimation of plasma volume and its variation are valuable, accessible, and cost-effective parameters for assessing decongestive treatment in ADHF patients, complementing natriuretic peptides.

Upper extremity deep vein thrombosis (DVT) of the axillary/subclavian veins is rare (5–10% of DVT). After clinical suspicion and duplex ultrasound, anticoagulation, surgical decompression and sometimes thrombolysis are mandatory due to complications. We discuss the case of a young healthy orchestra conductor with primary DVT of the left upper extremity and concomitant left shoulder musculo-tendinous traumatic injury. Symptoms of both conditions and subtle signs of upper extremity DVT delayed the diagnosis until full-blown DVT occurred. After successful anticoagulation and surgical TOS (thoracic outlet syndrome) decompression, evolution was favorable, without recurrent thrombosis.

Spinal muscular atrophy (SMA) is a genetic neuromuscular disorder primarily affecting motor neurons. Emerging evidence suggests it also involves multiple organs, including potential cardiac manifestations. This study aimed to evaluate cardiac abnormalities in pediatric SMA patients compared to age-matched healthy controls, providing insight into underlying cardiomyopathy in this population. A total of 126 children were included in the study, with 63 SMA patients and 63 age-matched controls. We conducted clinical examinations, standard electrocardiography (ECG), and cardiac ultrasound (CUS) in all patients. Electrocardiographic analysis revealed a higher prevalence of sinus tachycardia in the SMA group and significantly deeper Q waves, indicating possible myocardial involvement. Echocardiographic findings demonstrated a significant reduction in left ventricular mass and left ventricular mass index in SMA patients compared to controls, despite normal systolic function. Statistical analysis confirmed that SMA diagnosis was an independent predictor of reduced myocardial mass, suggesting a distinct cardiac phenotype in SMA patients. This study provides new evidence of subclinical cardiac involvement in SMA, characterized by reduced myocardial mass, altered electrocardiographic parameters, and increased sinus tachycardia. These findings suggest a previously unrecognized form of cardiomyopathy in SMA that differs from cardiac manifestations typically seen in other neuromuscular disorders.

Background/Objectives: Atrial fibrillation (AF) and heart failure with reduced ejection fraction (HFrEF) frequently coexist and are linked by shared risk factors and pathophysiological mechanisms. Their association is consistently related to worse clinical outcomes. This narrative review summarizes current evidence regarding the epidemiology, pathophysiology, management strategies, and prognosis of patients with AF and HFrEF. Methods: This is a narrative review based on published randomized trials, registries, and observational studies evaluating the interaction between AF and HFrEF, with a focus on therapeutic strategies including rate and rhythm control, catheter ablation, stroke prevention, and guideline-directed medical therapy. Results: AF and HFrEF have a bidirectional relationship, with each condition promoting the development and progression of the other. AF contributes to hemodynamic impairment and adverse remodeling, while HFrEF promotes atrial structural and electrical changes. Management remains complex. Rate control is commonly achieved with beta-blockers and digoxin, while rhythm control is limited by the safety profile of antiarrhythmic drugs. Catheter ablation has shown improvements in left ventricular function and, in selected patients, reductions in hospitalizations and mortality, although results are not consistent across all trials. Guideline-directed medical therapy improves outcomes in HFrEF, but its interaction with AF varies across drug classes. Stroke risk is significantly increased, requiring appropriate anticoagulation. Patients with AF and HFrEF have an increased risk of mortality, hospitalization, and adverse clinical events compared with those with either condition alone, although the extent to which these outcomes are attributable to AF itself, HF severity, or the associated comorbidity burden remains uncertain. Conclusions: The coexistence of AF and HFrEF identifies a high-risk population with complex management and unfavorable outcomes. While advances in rhythm control and heart failure therapies have improved selected outcomes, optimal treatment strategies and their impact on long-term prognosis remain incompletely defined.