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.

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.

Background: Residual systemic congestion is common after treatment for acute decompensated heart failure (ADHF) and remains difficult to assess non-invasively. We investigated internal jugular vein distensibility (DIJV) as a dynamic marker of residual congestion and its association with established congestion parameters and clinical outcomes. Methods: In this prospective single-center study, 112 patients hospitalized with ADHF underwent clinical, laboratory, echocardiographic, and venous ultrasound assessment at admission and after decongestive treatment. DIJV was calculated as the ratio of maximal internal jugular vein diameter during Valsalva to resting diameter, with DIJV ≥ 4 indicating preserved distensibility. Results: At the final in-hospital assessment, 59 patients (52.7%) had persistent DIJV < 4. These patients had higher NT-proBNP, larger inferior vena cava diameter, greater portal vein pulsatility, higher pulmonary artery systolic pressure, and lower TAPSE/PASP compared with patients with preserved DIJV. They also had longer hospital stays and higher rates of ADHF rehospitalization and six-month mortality. Higher admission DIJV remained associated with lower odds of six-month ADHF rehospitalization after multivariable adjustment (OR 0.31 per 1-unit increase, 95% CI 0.15–0.59; p < 0.001). Conclusions: DIJV improves with decongestive treatment, but frequently remains impaired. Persistent impairment is associated with a broader residual-congestion profile and adverse clinical outcomes, supporting DIJV as a simple, dynamic adjunct to multiparametric congestion assessment.

Background and Clinical Significance: Infective endocarditis following transcatheter aortic valve implantation (TAVI) is a severe complication that may be associated with prosthetic valve dysfunction, local infectious extension, and systemic embolization. Visceral mycotic aneurysms are uncommon, particularly those involving the hepatic arterial circulation. Case Presentation: We report the case of an 80-year-old woman who developed Streptococcus gallolyticus TAVI-associated prosthetic valve endocarditis (TAVI-PVE) four months after valve implantation. Despite prolonged antimicrobial therapy and subsequent negative blood cultures, the clinical course was complicated by persistent prosthetic and periprosthetic echocardiographic abnormalities, cerebral and splenic embolic events, and new-onset abdominal pain. Contrast-enhanced computed tomography revealed two hepatic arterial aneurysmal lesions with surrounding inflammatory changes, consistent with mycotic aneurysms. After initially declining surgery, the patient underwent redo surgical aortic valve replacement; cultures of the surgically excised specimens were negative. Abdominal pain resolved and inflammatory markers normalized following surgery and continued antimicrobial therapy. Follow-up contrast-enhanced CT demonstrated marked interval enlargement of the hepatic arterial aneurysmal lesion to 28 mm × 28 mm × 26 mm despite clinical improvement and normalization of inflammatory markers. Conclusions: This case highlights that microbiological, clinical, and biological improvement does not necessarily indicate resolution of local cardiac or extracardiac structural complications and emphasizes the importance of repeated imaging, guideline-based antimicrobial therapy, timely source control, and multidisciplinary vascular management in complicated TAVI-PVE.