Search Results (416)

Background and Clinical Significance: Patients with a left ventricular assist device (LVAD) are at risk of ventricular arrhythmias, which are generally hemodynamically tolerated if they occur. In such cases, patients may experience painful implantable cardioverter-defibrillator (ICD) shocks. Case Presentation: A 71-year-old patient with a history of dilated cardiomyopathy caused by a phospholamban (PLN) gain-of-function mutation, with a primary prevention ICD and an LVAD, presented with multiple ICD shocks which she experienced as painful and traumatic. She was found to have ongoing ventricular fibrillation with apparent hemodynamic stability. Conversion to sinus rhythm was achieved through intravenous administration of antiarrhythmic drugs followed by external defibrillation using stacked shocks. Due to the traumatic nature of the shocks, the shock function of the ICD was turned off. Nearly two months later, the patient presented for a second time and was again found to have ventricular fibrillation which had been present for at least six weeks. Conversion to sinus rhythm was unsuccessful and the patient was discharged to her home with an advanced care plan and her LVAD was deactivated. The patient died two months later. Conclusions: Patients with an LVAD can remain hemodynamically stable for prolonged periods of time during ventricular arrhythmias. ICD shocks are therefore mostly experienced as painful and even traumatic. Therefore, the routine use of ICD shock therapy in patients with an LVAD should be reconsidered. Adjustment of ICD programming to higher rates and longer detection may be warranted. Further investigation is warranted regarding a switch to devices with an alarm function rather than therapies for tachyarrhythmias. Full article

Kv11.1 (hERG1) channels, encoded by KCNH2, mediate the rapid delayed rectifier potassium current (I_Kr) crucial for cardiac repolarization. Disruptions, via mutations or antiarrhythmic drugs like dofetilide cause severe arrhythmogenic disorders, including Long QT Syndrome Type 2 (LQT2), Brugada Syndrome (BrS), and Torsades de Pointes (TdP). While Kv11.1’s role in channelopathies and drug-induced arrhythmias is established, understanding its complex regulation and therapeutic targeting remains a challenge. This review synthesizes the structural, functional, and regulatory aspects of Kv11.1 channels and their clinical implications. Recent studies using iPSC-derived cardiomyocytes highlight regulation by PI3K/Akt, PKC, and PKA signaling via phosphorylation (Ser283, Ser890) and interactions with proteins like 14-3-3. Beyond electrophysiology, Kv11.1 influences pathological hypertrophy and non-cardiac functions including insulin secretion. Pharmacological efforts focus on activators to shorten action potential duration and suppress TdP, and blockers with overdose risks. Mutation heterogeneity, exemplified by trafficking impairment (G785D) in LQT2 and gain-of-function (R397C) in BrS, complicates precision therapy. Clinically, systematic risk stratification using electrocardiographic parameters and genotype-specific approaches enables personalized management. Beta-blockers remain first-line therapy for LQTS2, while rigorous avoidance of QT-prolonging medications and electrolyte monitoring form the cornerstones of preventive care. Advancing Kv11.1-targeted therapies with approaches like CRISPR-Cas9 and pharmacological chaperones (e.g., lumacaftor) holds promise for personalized treatments, ultimately reducing arrhythmic events and sudden cardiac death. Full article

Background/Objectives: Atrial fibrillation (AF) is the most common sustained arrhythmia in adults, with a prevalence that increases with age. In older patients, its clinical impact is particularly relevant due to higher mortality and greater comorbidity burden. This study aimed to compare patients aged ≥80 years with younger patients in a large AF cohort. Methods: The REGUEIFA registry is an observational, prospective, multicentre study including consecutive patients with AF managed by cardiologists. Baseline clinical characteristics, comorbidities, complementary test findings, AF type, therapeutic strategies, anticoagulation patterns, and patient-reported outcomes were compared. Results: A total of 1007 patients were included, of whom 18.2% were aged ≥80 years. Older patients showed a higher prevalence of hypertension, renal dysfunction, conduction disorders, chronic obstructive pulmonary disease, and neoplastic disease, along with higher thromboembolic (CHA₂DS₂-VASc 3.7 ± 1.04 vs. 2.1 ± 1.49; p < 0.001) and haemorrhagic risk (HAS-BLED 1.3 ± 0.8 vs. 0.6 ± 0.7; p < 0.001). Permanent AF was more frequent, whereas rhythm control strategies and antiarrhythmic drug use were less common, and quality of life was poorer. Anticoagulation rates were high in both groups (≈90%), with greater use of vitamin K antagonists (VKAs) in older patients, although anticoagulation control was similar. Patients treated with direct-acting oral anticoagulants reported a lower treatment burden and greater perceived benefit than those receiving VKAs. Conclusions: Patients aged ≥80 years with AF exhibit greater comorbidity, poorer perceived health status, and higher thromboembolic and haemorrhagic risk. Their management is more often oriented towards rate control strategies and VKA use, while rhythm control approaches are more common in younger patients. Full article

Objectives: The aim of the work was to present a method for routine determination of antiarrhythmic drugs, propafenone (PPF), its two metabolites, 5-hydroxypropafenone (5OHPPF) and N-depropylpropafenone (NDPPF), mexiletine (MEX), amiodarone (AD) and desethylamiodarone (DEAD) in serum. Methods: A simple isocratic HPLC-UV system with a manual injector was applied. The separations were performed at ambient temperature on Supelcosil LC-CN column (150 × 4.6 mm, 5 μm). Two analytical procedures (A and B) were used: (A) for AD and (B) for PPF/MEX. The mobile phase for (A) was a mixture of: CH₃OH:CH₃CN:H₂O:0.5M KH₂PO₄ (200:100:194:6 v/v + 0.1 mL 85% H₃PO₄ per 500 mL). The slightly acidified serum sample was extracted with hexane and the analytes were detected at 240 nm. The mobile phase for (B) was a mixture of: CH₃CN:H₂O:0.5M KH₂PO₄ (185:310:5 v/v + 0.1 mL 85% H₃PO₄ per 500 mL). The alkalized serum sample was extracted with diisopropyl ether, then back extracted into 0.01M HCl and finally the analytes were detected at 210 nm. Results: The method was calibrated with adequate selectivity and specificity in the range of 20–4000 ng/mL for AD, DEAD and MEX, 10–4000 ng/mL for PPF and 10–500 ng/mL for 5OHPPF and NDPPF. For all analytes, precision and accuracy fulfilled EMA requirements, i.e., ≤15% (≤20% for LLOQ), ensuring the reliability of the measurements. Conclusions: The method can be suitable for laboratories equipped with basic HPLC apparatus as an economical alternative to the LC-MS/MS technique. Full article

Background: Obstructive sleep apnea (OSA) is a major modifiable risk factor for atrial fibrillation (AF), promoting arrhythmogenesis through intermittent hypoxia, autonomic activation, and atrial remodeling. Although continuous positive airway pressure (CPAP) effectively treats OSA, real-world evidence linking objectively measured CPAP exposure to clinically relevant AF recurrence remains limited. Aims: We aimed to evaluate the association between CPAP adherence and risk of recurrent paroxysmal AF, and to compare time to first recurrence between patients with mean nightly CPAP use ≥4 h/night versus <4 h/night. Materials and Methods: In this prospective observational cohort (2017–2024), consecutive hospitalized and outpatient adults with severe obstructive sleep apnea (OSA; apnea–hypopnea index > 30 events/h) and documented paroxysmal atrial fibrillation (AF) were enrolled. Persistent and long-standing persistent AF were excluded to ensure a homogeneous population with respect to atrial substrate. OSA was assessed using home sleep apnea testing (ResMed ApneaLink), and all patients initiated continuous positive airway pressure (CPAP) therapy (ResMed AirSense 10). Objective adherence data were obtained via the ResMed AirView telemonitoring platform. Exclusion criteria included permanent AF, prior pulmonary vein isolation, central sleep apnea, left ventricular ejection fraction < 50%, end-stage chronic kidney disease (eGFR < 15 mL/min/1.73 m² or dialysis), or inability to initiate or maintain CPAP therapy. Patients were followed for 12 months. The primary endpoint was time to first documented recurrence of paroxysmal AF (≥30 s on 12-lead electrocardiography or 24-h Holter monitoring). Progression to permanent AF, defined after unsuccessful rhythm control attempts and subsequent transition to a rate control strategy, was assessed as a secondary endpoint. Time-to-event analyses used Kaplan–Meier estimates with log-rank testing, and Cox proportional hazards regression adjusted for age, body mass index, apnea–hypopnea index, heart failure, left atrial volume index, and antiarrhythmic drug therapy. Results: The final analysis included 91 patients (mean age 62.15 ± 8.29 years; 68.13% men). Mean nightly CPAP use was ≥4 h/night in 49 patients and <4 h/night in 42 patients. During follow-up, paroxysmal AF recurrence occurred in 12/49 (24.5%) patients in the ≥4 h/night group and 16/42 (38.1%) in the <4 h/night group. Mean arrhythmia-free survival at 12 months was numerically higher in the ≥4 h/night group (11.25 vs. 10.51 months), without a statistically significant difference in Kaplan–Meier curves (log-rank p = 0.11). In multivariable Cox regression, binary adherence (≥4 h/night) was not independently associated with recurrence (HR 0.52, p = 0.13), whereas mean nightly CPAP use analyzed as a continuous variable remained independently associated with delayed recurrence (per 1-h increase: HR 0.66, 95% CI 0.48–0.91, p = 0.01). Progression to permanent AF occurred in 4/49 (10.0%) versus 9/42 (17.6%) patients, respectively (p = 0.29). Conclusions: In this real-world cohort of patients with severe OSA and paroxysmal AF, higher objectively measured CPAP exposure was independently associated with delayed AF recurrence when analyzed as a continuous variable, suggesting a graded association between objectively measured CPAP exposure and AF recurrence. Larger studies with extended follow-up and continuous rhythm monitoring are warranted to confirm long-term rhythm benefits and effects on AF progression. Full article

Background: Pharmacological cardioversion (PC) with antiarrhythmic agents is a common initial rhythm control strategy in patients with new-onset atrial fibrillation (AF). However, predictive tools for estimating the likelihood of successful PC remain limited. The systemic immune-inflammation index (SII), a novel composite marker derived from neutrophil, lymphocyte, and platelet counts, may reflect atrial inflammatory burden and structural remodeling. This study aimed to investigate the prognostic value of SII in predicting pharmacological cardioversion success in patients with acute-onset symptomatic AF. Methods: This prospective observational study included patients with hemodynamically stable, new-onset symptomatic AF admitted since October 2025. All patients received intravenous amiodarone for pharmacological cardioversion. Baseline clinical, echocardiographic, and laboratory parameters were recorded. Patients were classified into cardioversion-success and non-response groups based on ECG-confirmed restoration of sinus rhythm. Logistic regression analyses were performed to identify independent predictors of rhythm control, and ROC curves were generated to determine predictive performance. Results: Among 95 patients (mean age 54.2 ± 9.8 years, 48.4% female), successful pharmacological cardioversion was achieved in 74.7%. Compared to the non-response group, the cardioversion-success group had significantly lower SII levels (p < 0.001) and left atrial volume index (LAVI, p < 0.001). Multivariate analysis identified both SII and LAVI as independent predictors of cardioversion success. Inverse correlations were observed between both SII (r = −0.419, p < 0.01) and LAVI (r = −0.567, p < 0.01) and rhythm control. The optimal SII cutoff of 645.16 predicted successful rhythm restoration with 75% sensitivity and 75% specificity (AUC: 0.803, 95% CI: 0.710–0.895). Conclusions: Higher SII levels were independently associated with lower rates of successful pharmacological cardioversion in patients with new-onset atrial fibrillation. Incorporating SII into routine assessment may enhance clinical decision-making and patient stratification for rhythm control strategies. Full article

Premature Ventricular Complexes (PVCs) are among the most frequent ventricular arrhythmias observed in daily cardiology practice. Although often benign, sustained high ectopic activity can result in left ventricular dysfunction known as PVC-induced Cardiomyopathy (PVC-CMP), a condition that is frequently reversible when the arrhythmia is effectively suppressed. The underlying mechanisms are multifaceted, involving electromechanical dyssynchrony, contractile inefficiency, abnormal calcium cycling, neurohormonal activation, and progressive structural remodeling. The likelihood of developing PVC-CMP varies among individuals and is influenced by electrophysiological and structural factors. Diagnosis relies on prolonged rhythm monitoring, comprehensive multimodality imaging, and demonstration of ventricular recovery after reducing the ectopic burden, which, in turn, confirms causality. Over the past decade, major advances in electrocardiographic mapping, cardiac imaging, and ablation therapy have transformed this field, demonstrating excellent efficacy and safety profiles. In parallel, artificial intelligence and computational mapping are emerging as powerful tools for prediction and procedural guidance. Recognition of PVC-CMP as a distinct, treatable cardiomyopathy highlights the importance of early detection and individualized therapy, offering the prospect of complete functional recovery and the prevention of heart failure progression. Full article

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with substantial morbidity and mortality due to increased risks of stroke, heart failure, and death. Catheter ablation is now firmly established as a first-line or early rhythm control strategy in selected patients with paroxysmal AF and as a Class I indication in symptomatic patients with persistent AF refractory to antiarrhythmic drug therapy. However, outcomes remain more variable in persistent and long-standing persistent AF, reflecting greater atrial substrate complexity, procedural challenges, and ongoing uncertainty regarding optimal ablation strategies. This review provides a structured, evidence-based overview of contemporary catheter ablation approaches for AF, with particular emphasis on persistent disease. We discuss the anatomical and mechanistic rationale underlying pulmonary vein isolation and adjunctive lesion sets, summarize current clinical evidence supporting various strategies, and highlight differences in efficacy, safety, and reproducibility. In addition, we address the importance of patient selection, shared decision making, procedural expertise, and comprehensive risk factor modification as integral components of successful long-term rhythm control. By integrating guideline recommendations with mechanistic insights and clinical trial data, this review aims to clarify the current best practices and identify remaining knowledge gaps in the catheter ablation of atrial fibrillation. Full article

Melatonin, an indolic neuromodulator with putative oncostatic and proposed anti-inflammatory properties, primarily demonstrated in preclinical models, is produced at extrapineal sites—most notably in the gut. Its canonical actions are mediated by high-affinity GPCRs (MT1/MT2) and by NQO2, a cytosolic enzyme with a melatonin-binding site (historically termed “MT3”). A growing body of work highlights a bidirectional interaction between the gut microbiota and host melatonin. We integrated two lines of work: (i) three clinical cohorts—cardiac arrhythmias (n = 111; 46–75 y), epilepsy (n = 77; 20–59 y), and stage III–IV solid cancers (25–79 y)—profiled with stool 16S rRNA sequencing, SCFA measurements, and circulating melatonin/urinary 6-sulfatoxymelatonin and (ii) an age-spanning cognitive cohort with melatonin phenotyping, microbiome analyses, and exploratory immune/metabolite readouts, including a novel observation of melatonin binding on bacterial membranes. Across all three disease cohorts, we observed moderate-to-severe dysbiosis, with reduced alpha-diversity and shifted beta-structure. The core dysbiosis implicated tryptophan-active taxa (Bacteroides/Clostridiales proteolysis and indolic conversions) and depletion of SCFA-forward commensals (e.g., Faecalibacterium, Blautia, Akkermansia, and several Lactobacillus/Bifidobacterium spp.). Synthesised literature indicates that typical human gut commensals rarely secrete measurable melatonin in vitro; rather, their metabolites (SCFAs, lactate, and tryptophan derivatives) regulate host enterochromaffin serotonin/melatonin production. In arrhythmia models, dysbiosis, bile-acid remodelling, and autonomic/inflammatory tone align with melatonin-sensitive antiarrhythmic effects. Epilepsy exhibits circadian seizure patterns and tryptophan–metabolite signatures, with modest and heterogeneous responses to add-on melatonin. Cancer cohorts show broader dysbiosis consistent with melatonin’s oncostatic actions. In the cognitive cohort, the absence of dysbiosis tracked with preserved learning across ages, and exploratory immunohistochemistry suggested melatonin-binding sites on bacterial membranes in ~15–17% of samples. A unifying microbiota–tryptophan–melatonin axis plausibly integrates circadian, electrophysiologic, and immune–oncologic phenotypes. Practical levers include fiber-rich diets (to drive SCFAs), light hygiene, and time-aware therapy, with indication-specific use of melatonin. Our conclusions regarding microbiota–melatonin crosstalk rely primarily on local paracrine effects within the gut mucosa (where melatonin concentrations are 10–400× plasma levels), whereas systemic chronotherapy conclusions depend on circulating melatonin amplitude and phase. This original research article presents primary data from four prospectively enrolled clinical cohorts (total n = 577). Full article

This review examines and hypothesizes cytoprotection as a conceptual therapeutic criterion for antiarrhythmic drugs, referring to the possibility of suppressing arrhythmias while avoiding adverse electrophysiological or systemic effects. Toward a theoretically complete cytoprotective profile—preserving benefits and eliminating toxicity—the criterion was the degree of counteraction of arrhythmias (i.e., bradycardia, tachycardia, atrioventricular (AV) block, ventricular tachycardia (VT), ST-segment changes, prolonged P, PR, QRS, and QT/QTc intervals, and repolarization). Conventional and new antiarrhythmics share class I–IV ≈ partial cytoprotection/narrow range; late INa inhibitors, IKs enhancers, RyR2 stabilizers, gap junction modulators, and atrial-selective antiarrhythmics ≈ partial cytoprotection/more extended range. Still predominantly in preclinical models, stable gastric pentadecapeptide BPC 157, in the clinic, has not demonstrated adverse effects in available human trials (non-cardiac) to date. As a prominent cytoprotection mediator (LD1 not achieved in toxicology studies), it demonstrates well-matched cytoprotective–antiarrhythmic effects, BPC 157 ≈ full cytoprotection/wide-range homeostasis. In vivo, this was across models of hypo-/hyperkalemia, hypermagnesemia, ischemia–reperfusion, myocardial infarction, drug-induced arrhythmias (including local anesthetics), and vascular occlusion. BPC 157 restores sinus rhythm, normalizes P/QRS/QT intervals, prevents AV block, suppresses VT, attenuates ST-segment changes, and stabilizes heart rate, even when insults are advanced. In vitro, HEK293 studies confirm direct membrane-stabilizing actions: BPC 157 prevents hypokalemia-induced hyperpolarization, reduces hyperkalemia- and hypermagnesemia-induced depolarization, and mitigates local anesthetic-induced Na⁺/Ca²⁺ dysregulation, reflecting bidirectional homeostatic modulation of membrane potential. Thus, to confirm the hypothesis, these BPC 157 conditional, not constitutive effects, in rodent models or in vitro systems (HEK293 cells), mandate expansion of now limited clinical data and mechanisms in human investigated as a translational cytoprotective strategy for complex arrhythmias. Full article

Background and Objectives: Pulmonary vein isolation (PVI) is an established rhythm control strategy for atrial fibrillation (AF). In many healthcare systems, increasing demand and limited procedural capacity have resulted in prolonged waiting times. The primary aim of this study was to evaluate the association between waiting time for PVI and AF progression. Secondary aims were to assess the relationship between waiting time and AF-related complications, healthcare utilization, and clinical factors associated with higher risk of progression. Materials and Methods: We performed a single-center observational cohort study of patients on the waiting list for PVI at Pauls Stradiņš Clinical University Hospital between 2016 and 2023. Results: A total of 341 patients completed structured ambulatory follow-up to assess the complication and progression rates of AF. The mean age was 64.8 ± 10.5 years, 50.9% were male, and the median waiting time was 37.2 months (IQR 15.0–61.3). AF progression occurred in 25.7% (n = 88) of patients, with longer waiting time independently associated with progression (OR, 1.017 per month; 95% CI, 1.006–1.028; p < 0.05). Electrical cardioversion during the waiting period was associated with a lower likelihood of progression (OR, 0.32; p = 0.029), and Class IC antiarrhythmic therapy was associated with reduced risk of AF progression (HR 0.78; p = 0.013). During follow-up, 45.2% of patients were hospitalized for AF paroxysms, 29.6% underwent electrical cardioversion, and 13.5% experienced complications including stroke and heart failure decompensation. Left atrial volume index and left ventricular ejection fraction were inversely correlated (ρ = −0.355, p < 0.05), but neither was associated with waiting time. Conclusions: Longer waiting times for PVI are associated with AF progression and substantial interim healthcare utilization due to complications. Strategies to prioritize higher-risk patients may help prevent disease progression and reduce complication burden. Full article

Neonatal arrhythmias, though relatively uncommon, can range from benign self-limiting conditions to life-threatening disorders requiring intensive management. Data on their clinical spectrum, management, and outcomes remain limited. This study aimed to evaluate the types, frequency, clinical characteristics, treatment strategies, and prognosis of neonatal arrhythmias in a tertiary pediatric cardiac center. We retrospectively reviewed neonates diagnosed with arrhythmia within the first 28 days of life at Basaksehir Cam and Sakura City Hospital between 1 January 2021 and 1 May 2025. Demographic data, electrocardiographic and echocardiographic findings, treatment modalities, recurrence, morbidity, and mortality were analyzed. Patients were categorized as having benign or non-benign arrhythmias. A total of 65 neonates (57% male, mean weight 3.2 kg) were included. Non-benign arrhythmias were more frequent (77%) compared to benign arrhythmias (23%). Supraventricular tachycardia (35%) was the most common non-benign arrhythmia, followed by long QT syndrome (10.7%) and complete atrioventricular block (9.2%). Antiarrhythmic therapy was required in 55% of patients. Pacemaker implantation was performed in seven infants with conduction disorders. Recurrence occurred in 3% of cases, exclusively among patients with supraventricular tachycardia. During a median follow-up of 12.8 months, no mortality was observed. Prenatal diagnosis and early management contribute to favorable outcomes, as reflected in the absence of mortality in this cohort. Larger, prospective studies are warranted to define optimal management strategies and treatment durations for neonatal arrhythmias. Full article

Background: Atrial dilated cardiomyopathy (ADCM) related to homozygous Natriuretic Peptide Precursor A (NPPA) pathogenic variants is an exceptionally rare inherited atrial cardiomyopathy characterized by progressive atrial enlargement, supraventricular arrhythmias, and eventual atrial standstill. Case summary: We report the case of a 9-year-old girl identified through population genetic screening as a homozygous carrier of the NPPA c.449G>A (p.Arg150Gln) variant who subsequently developed symptomatic paroxysmal atrial fibrillation (AF) at the age of 18. Although baseline cardiac investigations were normal, her current evaluation shows biatrial enlargement with preserved ventricular function. She underwent radiofrequency pulmonary vein isolation; however, recurrent symptomatic AF persists, requiring ongoing antiarrhythmic therapy and long-term oral anticoagulation (CHA₂DS₂-VA: 0; HAS-BLED: 0). Notably, patients with NPPA-related ADCM have a markedly increased thromboembolic risk due to progressive atrial mechanical failure, and anticoagulation should therefore be considered irrespective of conventional clinical risk scores. Discussion and conclusions: This case highlights the importance of genetic testing in young patients with atrial fibrillation and no underlying structural heart disease. The early identification of NPPA-related atrial dilated cardiomyopathy may aid in risk stratification and guide rhythm and anticoagulation management. Expanding genetic screening in select individuals with isolated atrial fibrillation may facilitate earlier diagnosis in this exceptionally rare condition. Full article

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. Full article

Atrioventricular (AV) node ablation represents an established therapeutic option in the management of atrial fibrillation (AF) and other atrial tachyarrhythmias, particularly in patients with symptomatic tachycardia who remain unresponsive or intolerant to pharmacological therapy. The procedure is often considered in cases of refractory arrhythmias, antiarrhythmic drugs intolerance, or tachycardiomyopathy, and plays a key role in optimizing outcomes in patients undergoing cardiac resynchronization therapy, where achieving adequate biventricular pacing is otherwise compromised by rapid ventricular responses. Traditionally, AV node ablation is performed using radiofrequency energy delivered at the region of the His bundle, guided by the earliest His potential recordings. However, the anatomical complexity of the AV node and Koch’s triangle poses important challenges, including the risk of incomplete ablation, persistence of conduction, lack of reliable junctional escape rhythms, and increased risk of proarrhythmia. Recent advances in high-resolution mapping and electroanatomical guidance have enabled a more precise anatomical approach, selectively targeting the compact AV node while reducing collateral injury. These developments offer the potential for improved procedural safety, long-term efficacy, and a more standardized strategy for patient management. This review summarizes current evidence, techniques, and clinical implications of AV node ablation, highlighting its role in the evolving landscape of arrhythmia treatment. Full article