Aims: The recurrence rates after catheter ablation (CA) and direct current (DC) cardioversion remain high, although they have been established treatments of rhythm control of atrial fibrillation (AF). This umbrella review systematically appraises published meta-analyses of both observational and randomized controlled trials (RCTs) for the association of risk and protective factors for arrhythmia recurrence after CA and DC cardioversion of AF.Methods and results: Three bibliographic databases were searched up to June 2021. Evidence of association was rated as convincing, highly suggestive, suggestive, weak, or not significant with respect to observational studies and as high, moderate, low, or very low with respect to RCTs, according to established criteria. Thirty-one meta-analyses were included. Of the 28 associations between CA and the risk of arrhythmia recurrence, none presented convincing evidence, and only the time from diagnosis to ablation over 1 year provided highly suggestive evidence. The association between hypertension and metabolic profile provided suggestive evidence. The associations of Class IC and III antiarrhythmic drugs use with the recurrence after DC cardioversion were supported by an intermediate level of evidence.Conclusion: Although AF is a major health issue, few risk- and protective factors for AF recurrence have been identified. None of these factors examined were supported by convincing evidence, whereas established factors such as female gender and left atrial volume showed only weak association. An early CA strategy combined with treatment of metabolic syndrome and hypertension prior to CA may reduce the risk of arrhythmia recurrence. The use of antiarrhythmics can increase the success rate of DC cardioversion.Systematic review registration: PROSPERO registry number: CRD42021270613.

Pulmonary arterial hypertension (PAH) is characterized by an insult in the pulmonary vasculature, with subsequent right ventricular (RV) adaptation to the increased afterload that ultimately leads to RV failure. The awareness of the importance of RV function in PAH has increased considerably because right heart failure is the predominant cause of death in PAH patients. Given its wide availability and reduced cost, echocardiography is of paramount importance in the evaluation of the right heart in PAH. Several echocardiographic parameters have been shown to have prognostic implications in PAH; however, the role of echocardiography in the risk assessment of the PAH patient is limited under the current guidelines. This review discusses the echocardiographic evaluation of the RV in PAH and during therapy, and its prognostic implications, as well as the potential significant role of repeated echocardiographic assessment in the follow-up of patients with PAH.

Cardiorenal syndrome (CRS) reflects the intricate and bidirectional interplay between cardiac and renal dysfunction, commonly resulting in diagnostic uncertainty, therapeutic dilemmas and poor outcomes. While traditional biomarkers like serum creatinine (Cr) and natriuretic peptides remain widely used, their limitations in specificity, timing and contextual interpretation often hinder optimal management. This narrative review synthesizes the current evidence on established and emerging biomarkers in CRS, with emphasis on their clinical relevance, integration into real-world practice, and potential to inform precision therapy. Markers of glomerular filtration rate beyond creatinine—such as cystatin C—offer more accurate assessment in frail or sarcopenic patients, while tubular injury markers such as NGAL, KIM-1, and urinary L-FABP (uL-FABP) provide early signals of structural renal damage. The FDA-approved NephroCheck^® test—based on TIMP-2 and IGFBP7— enables risk stratification for imminent AKI up to 24 h before functional decline. Congestion-related markers such as CA125 and bio-adrenomedullin outperform natriuretic peptides in certain CRS phenotypes, particularly in right-sided heart failure or renally impaired patients. Fibrosis and inflammation markers (galectin-3, sST2, GDF-15) add prognostic insights, especially when combined with NT-proBNP or troponin. Rather than presenting biomarkers in isolation, this review proposes a framework that links them to specific clinical contexts—such as suspected decongestion-related renal worsening or persistent congestion despite therapy—to support actionable interpretation. A tailored, scenario-based, multi-marker strategy may enhance diagnostic precision and treatment safety in CRS. Future research should prioritize prospective biomarker-guided trials and standardized pathways for clinical integration.

Background: Elevated cardiac troponin (cTn) levels in patients with paroxysmal supraventricular tachycardia (PSVT) often prompt coronary artery disease evaluation, though the clinical relevance of this finding remains unclear. This study aimed to identify risk factors for cTn elevation after a PSVT episode and assess its clinical significance, including the role of coronary artery disease (CAD) and long-term outcomes. Methods: We retrospectively collected data on demographics, presenting symptoms, comorbidities, chronic antiarrhythmic medication use, tachycardia duration, admission systolic blood pressure (SBP), heart rate (HR), laboratory findings, and cardioversion method in patients presenting to the Emergency Department (ED) with PSVT over a 4-year period. Patients were stratified into two groups based on the presence or absence of troponin elevation. Individuals with elevated cTn levels and at least one cardiovascular risk factor were further evaluated for CAD. One-year outcomes included SVT recurrence, rehospitalization, ablation, and mortality. Results: Among 120 patients with PSVT, 58 (48.3%) exhibited elevated cardiac troponin (cTn) levels. Independent predictors of cTn elevation included retrosternal chest pain, absence of prior SVT history, higher admission HR, and lower SBP. A heart rate cut-off of 165 bpm was identified as optimal for predicting cTn elevation (sensitivity 62.1%, specificity 72.6%). Of the 58 cTn (+) patients, 25 underwent CAD evaluation, with only 1 case (4%) confirming significant coronary disease. At one-year follow-up (n = 118), troponin elevation was not associated with increased SVT recurrence, rehospitalization, ablation, or mortality. Similarly, CAD evaluation in troponin-positive patients did not predict outcomes. Conclusions: Troponin elevation after PSVT is frequent but not prognostically significant. It is likely due to transient myocardial stress rather than CAD, supporting a conservative, individualized approach to further testing.

Introduction: Acute cardiorenal syndrome (ACRS) is a common complication of acute heart failure (AHF), leading to worse outcomes and therapeutic challenges. This study aimed to identify clinical parameters associated with ACRS and evaluate its impact on prognosis in hospitalized AHF patients. Methods: This prospective observational study included patients hospitalized for AHF at the Venizelio Cardiology Department from February to November 2023. Demographic characteristics, comorbidities, medications, laboratory and echocardiographic parameters, hospital stay, and in-hospital mortality were recorded. Patients with incomplete data or end-stage chronic kidney disease (CKD) were excluded. Survivors were followed for six months to assess renal function changes, readmissions, initiation of renal replacement therapy (RRT), and mortality. ACRS was defined as a serum creatinine increase of ≥0.3 mg/dL or ≥1.5 times baseline. Results: Among 218 hospitalized AHF patients, 112 (51.3%) developed ACRS. These patients were older, had higher CKD prevalence, worse New York Heart Association (NYHA) functional class, lower hemoglobin, and higher N-terminal Pro-B-type Natriuretic peptide (NT-proBNP) levels. Multivariate analysis identified CKD stage (OR 2.30, 95% CI 1.64–3.23, p < 0.001) and creatinine change on admission (OR 3.53, 95% CI 2.02–6.18, p < 0.001) as independent predictors of ACRS. ACRS was associated with higher in-hospital mortality, longer hospital stays, increased vasoactive medication use, worsening renal function, and higher six-month all-cause readmission and mortality rates. Conclusions: ACRS is a frequent and severe complication in AHF. CKD stage and creatinine on admission are key predictors. Early recognition for risk stratification and individualized management are crucial to improving outcomes in this high-risk population.

Chloride, long considered a passive extracellular anion, has emerged as a key determinant in the pathophysiology and management of heart failure (HF) and cardiorenal syndrome. In contrast to sodium, which primarily reflects water balance and vasopressin activity, chloride exerts broader effects on neurohormonal activation, acid–base regulation, renal tubular function, and diuretic responsiveness. Its interaction with With-no-Lysine (WNK) kinases and chloride-sensitive transporters underscores its pivotal role in electrolyte and volume homeostasis. Hypochloremia, frequently observed in HF patients treated with loop diuretics, is independently associated with adverse outcomes, diuretic resistance, and arrhythmic risk. Conversely, hyperchloremia—often iatrogenic—may contribute to renal vasoconstriction and hyperchloremic metabolic acidosis. Experimental data also implicate chloride dysregulation in myocardial electrical disturbances and an increased risk of sudden cardiac death. Despite mounting evidence of its clinical importance, serum chloride remains underappreciated in contemporary risk assessment models and treatment algorithms. This review synthesizes emerging evidence on chloride’s role in HF, explores its diagnostic and therapeutic implications, and advocates for its integration into individualized care strategies. Future studies should aim to prospectively validate these associations, evaluate chloride-guided therapeutic interventions, and assess whether incorporating chloride into prognostic models can improve risk stratification and outcomes in patients with heart failure and cardiorenal syndrome.