Background/Objectives: Infective endocarditis (IE) carries substantial mortality, particularly in middle-income settings where patient profiles and microbial ecology differ from those of cohorts used to derive international prognostic scores. Syndrome-specific, locally grounded decision aids for empirical therapy are also scarce. We aimed to identify predictors of in-hospital mortality, externally evaluate the RiskE and ICE scores, and construct a Bayesian weighted-incidence syndromic combination antibiogram (WISCA) for IE. Methods: We conducted a retrospective cohort study of consecutive adults with definite or possible IE admitted between January 2019 and January 2026. Candidate predictors were screened in two phases, and a clinically specified model was estimated with maximum-likelihood and Firth penalization, with 1000-replicate bootstrap optimism correction. Calibration was assessed with bootstrap calibration plots and the Hosmer-Lemeshow test. Discrimination was compared against RiskE and ICE using DeLong's test and reclassification metrics. For empirical coverage, we built a WISCA using identified pathogens, reporting both non-Bayesian bootstrap estimates and Bayesian hierarchical partial-pooling estimates with species- and antibiotic-level random intercepts; analyses were also stratified by IE type. Results: In-hospital mortality was 22.9% in a young cohort (median 37 years) characterized by high hemodialysis prevalence (47.4%), substantial right-sided IE (46.4%), and Staphylococcus aureus predominance (32%) with no methicillin-resistant isolates. Vasopressor-requiring shock (Firth OR 9.23, 95% CI 2.40-40.61) and acute heart failure (OR 10.01, 95% CI 2.78-41.07) were the strongest predictors; the final model achieved an AUC of 0.922 (optimism-corrected 0.908), significantly outperforming RiskE (0.598) and ICE (0.632). The Bayesian WISCA identified multiple carbapenem-sparing and anti-MRSA-sparing regimens with adequate coverage (≥80%), particularly for community-acquired IE, supporting stewardship-oriented empirical selection. Coverage was consistently lower in healthcare-associated IE. Conclusions: A parsimonious three-variable model provided strong, locally valid mortality prediction in this hemodialysis-predominant, MRSA-free cohort, substantially outperforming European-derived scores. External validation in independent cohorts is required before clinical adoption. The Bayesian WISCA demonstrated that adequate empirical coverage is achievable without routine broad-spectrum agents, offering institution-specific guidance for stewardship-compatible regimen selection; multicenter validation is warranted.

Background: Right heart failure (HF) and tricuspid regurgitation (TR) are closely interrelated conditions, linked by a bidirectional and self-perpetuating pathophysiological relationship. Alterations in right-ventricular (RV) loading conditions, pulmonary vascular impedance, and ventriculo-arterial (VA) coupling play a central role in the development and progression of TR, which in turn exacerbates RV volume overload and end-organ dysfunction. Methods: This review provides a comprehensive overview of the pathophysiology of right HF and TR, focusing on the mechanisms underlying RV dysfunction, pressure-volume (PV) relationships, and pulmonary vascular load. We further examine the clinical implications of this interaction and summarize current strategies for risk stratification, with particular emphasis on disease-specific risk models. Results: TR emerges both as a consequence and a driver of RHF. Conditions such as pulmonary hypertension (PH) and left-sided heart disease promote annular dilation and leaflet tethering, leading to functional TR. Conversely, TR increases RV volume overload, worsening chamber dilation, reducing effective forward stroke volume (SV), and accelerating disease progression. This vicious cycle results in progressive RV impairment, impaired left-ventricular filling through ventricular interdependence, and systemic venous congestion affecting renal and hepatic function. Traditional risk scores fail to capture this complex pathophysiology. In this context, TRISCORE integrates clinical, biological, and echocardiographic (TTE) parameters reflecting RV dysfunction and systemic involvement, providing a more comprehensive assessment of disease severity and prognosis. Conclusions: TR should be considered not only a marker but also a key determinant of right HF progression. A multiparametric approach integrating pathophysiology and disease-specific risk stratification is essential to identifying the optimal therapeutic window and guiding clinical decision making.

Pulmonary hypertension (PH) can be defined as a mean pulmonary artery pressure (mPAP) greater than 20 mm Hg at rest during right heart catheterization (RHC). The reported prevalence of PH throughout the globe has been estimated to impact approximately 1% of the total population, with a majority of those afflicted being women more than men. Numerous etiologies give rise to the pathophysiology of PH, including heart disease (i.e., left-sided heart failure), lung diseases, and other unclear causes related to chronic stages and complications surrounding long-standing pulmonary thromboembolisms, side effects of certain medications, and genetic and environmental factors. Untreated PH can lead to severe morbidities such as cardio-renal syndrome and congestive hepatopathy (cardiac cirrhosis). Management of PH focuses on decreasing pulmonary pressures by using vasodilators such as prostanoids, and phosphodiesterase type 5 (PDE-5) inhibitors, as well as newer treatments such as sotatercept, which inhibits activin signaling, thereby inhibiting excessive cell growth in the pulmonary artery vasculature and down-regulating the pro-proliferative pathways.

Glenn shunt dysfunction in single‑ventricle palliation is multifactorial. Although aorto‑pulmonary collaterals are usually considered, systemic veno‑venous collaterals and congenital portosystemic shunts (CPSS) may be underrecognized causes (1,7). Our patient, a 30‑month‑old child with mitral valve atresia, severe hypoplastic left ventricle, large ventricular septal defect (VSD), pulmonary valve atresia, and ductus arteriosus-dependent pulmonary blood flow, who was undergone some palliation stages including patent ductus arteriosus (PDA) stenting / modified Blalock-Taussig (BT) shunt and a right‑sided bidirectional cavopulmonary anastomosis (Glenn). Despite an initially acceptable course, the child developed progressive central cyanosis.

BACKGROUND Patients with left ventricular assist devices (LVADs) who require emergency non-cardiac surgery are at high risk due to long-term anticoagulation and the consequences of underlying heart failure. Approximately 3.3% of LVAD patients require emergency abdominal surgery, which is associated with a higher in-patient mortality rate. This report describes the case of a 43-year-old man with an implantable cardioverter defibrillator (ICD) and a left ventricular assist device (LVAD) who required emergency surgery for a strangulated umbilical hernia. CASE REPORT A 43-year-old man with an ICD and an LVAD who had been taking warfarin and clopidogrel presented with a 2-day history of abdominal pain and vomiting. Physical examination revealed a strangulated umbilical hernia and a non-strangulated right-sided inguinal hernia. The strangulated portion of the small intestine was resected, then an end-to-end intestinal anastomosis and closure of the umbilical and inguinal hernias were performed. In the next 2 days he developed symptoms of intraperitoneal bleeding; therefore, a decision was made to totally withhold anticoagulant and antiplatelet medication and administer 2 units of packed red blood cells concentrate and 1 unit of platelet concentrate. Despite prolonged anticoagulation interruption, the patient survived without LVAD thrombosis or ischemic complications and was transferred to the LVAD implantation center. CONCLUSIONS This report aims to accentuate the high-stakes decisions made to maintain a balance between thrombotic and hemorrhagic risk in our patient. It is advisable to consult the specialized implantation center overseeing the patient's ongoing care before performing emergency surgery.

Radiofrequency catheter ablation (RFCA) is an established treatment for paediatric arrhythmias in children weighing >15 kg, yet its role in infants with arrhythmia-induced cardiomyopathy remains less defined. This case series evaluates the efficacy and safety of RFCA in four infants (aged ≤1 year) with arrhythmia-induced cardiomyopathy through a retrospective review of clinical profiles, procedural data and outcomes. All patients had right-sided accessory pathways, with three showing atrioventricular re-entrant tachycardia and one pre-excitation-related cardiomyopathy. Each infant had failed pharmacotherapy, and presented with heart failure and cardiac enlargement. RFCA was successfully performed in all cases without complications. Within 1-6 months postprocedure, both cardiac function and size normalised in every patient. These findings support RFCA as a safe and effective treatment for medically refractory, right-sided, pathway-mediated, arrhythmia-induced cardiomyopathy in infants, highlighting its potential for complete functional recovery.

Cardiac myxomas are the most common primary cardiac tumours but are rarely found in the right ventricle. We present the case of a 53-year-old man with a large right ventricular myxoma who presented with symptoms of severe anaemia, acute kidney injury, fatigue and breathlessness. The patient underwent multiple diagnostic investigations, including transthoracic and transoesophageal echocardiograms, CT with Fluorodeoxyglucose Positron Emission Tomography (FDG PET), cardiac MRI and endomyocardial biopsy. He was treated surgically with excision of the mass and tricuspid valve repair. This case highlights the diagnostic process of assessing an intracardiac mass and the increased anatomical complexity of excision from the right ventricle.