Search Results (1,032)

Objective and Background: With the increasing use of catheter ablation for tachyarrhythmias, continuous evaluation of in-hospital complications is essential. This study aimed at analyzing complications associated with catheter ablation for atrial fibrillation (AF), atrial flutter (AFL), and ventricular tachycardia (VT) using nationwide administrative data. Methods: We conducted a retrospective multicentric data analysis from large German ablation centers between 2018 and 2023. Patients were identified using ICD and OPS codes for AF, AFL, and VT regarding predefined in-hospital complications: mortality, stroke, pericardial tamponade, pulmonary embolism, and vascular complications requiring intervention. Results: Among 19,258 ablation procedures from 11 centers, AF was most common (n = 12,241), followed by AFL (n = 5582) and VT (n = 1435). Major complications occurred in 2.2% (n = 433) of cases. VT ablations had the highest complication rate (9.8%), followed by AF (1.6%) and AFL (1.7%). Pericardial tamponade occurred in 0.9% patients, most commonly in VT ablations (4.0%). Vascular complications requiring intervention were reported in 1.1%, while stroke (0.3%) and pulmonary embolism (0.05%) were rare. In-hospital mortality was highest in VT patients (2.4%), compared to AF (0.08%) and AFL (0.13%). Higher AFL mortality as compared to AF was associated with older age and more comorbidities. Upon exploratory analysis, no statistical association between hospital volume and complication rates could be seen. Conclusions: In this multicenter analysis, catheter ablation was associated with a low overall complication rate. VT ablations carried the highest risk, highlighting the impact of structural heart disease and comorbidities. Full article

Background: Atrial fibrillation (AF) is a prevalent arrhythmia closely associated with cardiometabolic disorders and systemic inflammation. Epicardial adipose tissue (EAT), located in direct contact with the atrial myocardium, has emerged as a biologically active tissue involved in atrial remodeling through inflammatory, fibrotic, and electrophysiological mechanisms. The objective of this review is to summarize current translational and clinical evidence on the role of EAT in AF pathophysiology and to discuss its implications for diagnostic assessment, interventional management, and cardiometabolic therapeutic strategies. Methods: A narrative, structured review of experimental, translational, and clinical studies was conducted using major biomedical databases. The literature was evaluated with a focus on mechanisms linking EAT to atrial remodeling, noninvasive imaging techniques for EAT characterization, echocardiographic and electroanatomical markers of atrial disease, outcomes of catheter ablation strategies, and pharmacological interventions targeting metabolic and inflammatory pathways. Results: The available evidence indicates that increased EAT volume and altered inflammatory activity are associated with atrial fibrosis, conduction abnormalities, and impaired atrial function, contributing to AF initiation and persistence. Multimodality imaging, including cardiac computed tomography and cardiac magnetic resonance, enables quantitative and qualitative assessment of EAT and supports clinical phenotyping. Clinical studies report an association between higher EAT burden and increased AF recurrence after pulmonary vein isolation, particularly in patients with persistent AF. Emerging cardiometabolic therapies, such as glucagon-like peptide-1 receptor agonists and dual GIP/GLP-1 agonists, have been shown to reduce EAT volume and inflammatory markers, although direct evidence linking these interventions to improved AF outcomes remains limited. Conclusions: EAT represents a relevant pathophysiological interface between metabolic disease and AF with potential clinical implications. Incorporating EAT assessment into routine evaluation may enhance risk stratification and support personalized AF management. Further prospective studies are required to define its role as a therapeutic target in clinical practice. Full article

Background/Objectives: Aneurysms develop secondary to progressive weakening of arterial walls and remain a major cause of morbidity and mortality worldwide. Collagen, particularly fibrillar types I and III, is the primary tensile load-bearing component of arteries, yet its specific role in aneurysm formation, progression, and rupture is incompletely defined. This narrative review synthesizes current evidence on collagen structure, regulation, and degradation in aneurysm pathophysiology, highlighting cerebral aneurysms within the broader context of aneurysms as a whole. Methods: Searches of PubMed, MEDLINE, Embase, and Google Scholar were performed to identify all English-language studies published prior to January 2026. Search terms included “cerebral aneurysm”, “collagen”, “extracellular matrix”, “vascular remodeling”, and “aneurysm rupture”. Included studies evaluated collagen structure or content, extracellular matrix remodeling, matrix metalloproteinases, or biomechanical properties of the aneurysm wall in experimental or human models. Results: The literature search identified 348 records, of which 87 studies published between 1999 and 2025 met the inclusion criteria and were synthesized in this review. Collagen types I and III form the primary tensile scaffold of intracranial arteries, while basement membrane and regulatory collagens (e.g., types IV, V, and VI) modulate fibril organization, endothelial stability, and mechanical homeostasis. Research demonstrates that endothelial dysfunction, nitric oxide dysregulation, oxidative stress, and matrix metalloproteinase activation are key pathways driving collagen fragmentation and degradation. Genetic and epigenetic disturbances in collagen and related extracellular matrix pathways further increase aneurysm susceptibility. Conclusions: Collagen dysregulation appears to be a final common pathway through which hemodynamic, inflammatory, hormonal, and genetic insults converge to weaken intracranial arterial walls. However, existing evidence is dominated by animal and aortic models, and in vivo tools, such as Magnetic Resonance Imaging with collagen-sensitive sequences and Positron Emission Tomography Tracers, to quantify collagen integrity in cerebral aneurysms are lacking. Future efforts should prioritize human-focused studies, advanced collagen-sensitive imaging, biomarker development, and targeted strategies to preserve or restore collagen structure as potential means to improve aneurysm risk stratification, prevention, and treatment. Full article

Background/Objectives: Implantable loop recorders (ILRs) enable long-term electrocadiographic monitoring and are established diagnostic tools for syncope and atrial fibrillation (AF). However, their diagnostic yield and therapeutic impact in other clinical settings remain less well defined. We aimed to evaluate the diagnostic yield and clinical impact of ILR implantation across contemporary clinical indications. Methods: In this retrospective single-center study, 388 patients who underwent ILR implantation between 2011 and 2018 were included. Indications were categorized into seven groups: unexplained syncope, presyncope, cryptogenic stroke or transient ischemic attack (TIA), AF detection, AF recurrence after atrial flutter (AFL) ablation, risk stratification in structural or inherited heart disease, and palpitations. Results: Among 388 patients (median age 63 [51.8–71.8] years, 57.5% male; median follow-up 17.0 [IQR 6.4–32.4] months), ILRs were most frequently implanted for syncope (44.6%), AF (20.4%), and stroke/TIA (12.9%). ILR-detected arrhythmias occurred in 241 patients (62.1%), with the highest detection rates in AF (83.5%) and AFL (73.7%). Indication-fulfilling diagnoses were established in 155 patients (39.9%), most frequently in AF (73.4%) and AFL (71.1%), after a median of 4.4 months (IQR 2.4–12.5). Nearly three quarters (72.9%) of diagnoses were made within the first year. ILR findings prompted therapeutic interventions in 156 patients (40.2%), including pacemaker implantation in syncope and rhythm- or anticoagulation-based therapies in AF. AF and AFL independently predicted higher diagnostic yield, while diagnostic yield and AF history predicted ILR-triggered therapy. AF, AFL, stroke/TIA, and AF history were associated with shorter time to first arrhythmia detection. Arrhythmia-free survival differed significantly across indication groups (p < 0.0001) and was lowest in AF and AFL, which demonstrated the highest cumulative incidence of indication-fulfilling arrhythmias. Conclusions: ILRs provide substantial diagnostic and therapeutic value across a broad range of indications. Beyond established uses in syncope and AF, clinically relevant yields were observed in presyncope, risk stratification, and AFL post-ablation, supporting broader consideration of ILRs and optimized patient selection. Full article

Background/Objectives: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder for which no disease-modifying therapy that halts or substantially slows disease progression is currently available. Although antibody therapies targeting amyloid β (Aβ) have recently received FDA approval, their high cost, limited efficacy, and potential adverse effects highlight the need for alternative solutions. Therefore, the development of low-molecular-weight compounds capable of reducing toxic Aβ aggregates is of considerable interest. In this study, we investigated the effects of 2,3,4-trihydroxybenzophenone (THB) on the inhibition and disassembly of Aβ_1–42 aggregates through in vitro and in vivo experiments. Methods: In vitro assays were performed to evaluate the effects of THB on Aβ_1–42 aggregation and fibril disassembly. Cell viability assays and hippocampal slice electrophysiology were conducted to assess neurotoxicity and synaptic function. In vivo effects were examined in Aβ_1–42 aggregate-injected mice and in 5 Familial AD mutations (5XFAD) mice using behavioral, histological, and electrophysiological analyses. Results: THB inhibited Aβ_1–42 aggregation in a concentration-dependent manner and promoted the disassembly of preformed fibrils. THB attenuated Aβ_1–42-induced Neuro2a cell death and restored Aβ_1–42 aggregate-associated long-term potentiation (LTP) deficits in hippocampal slices. In Aβ_1–42 aggregate-injected and 5XFAD mice, THB reduced amyloid pathology and neuroinflammatory markers and improved synaptic function and memory performance. Conclusions: These findings suggest that THB modulates pathogenic Aβ_1–42 assemblies and provides a structural basis for the development of small-molecule modulators of Aβ_1–42 aggregation with potential preventive or disease-modifying applications in AD. Full article

Fish collagen exhibits lower denaturation temperatures and reduced mechanical stability than mammalian collagen, limiting its biomedical applicability and motivating the development of effective stabilization strategies. In this study, we address this challenge by establishing a simple and effective strategy to fabricate stable collagen gels from carp-derived collagen using phosphate buffer-induced gelation followed by genipin crosslinking. Gel properties were regulated by adjusting the gelation time prior to crosslinking. After 3 h of gelation followed by 24 h crosslinking, gels derived from carp skin, carp scale, and carp swim bladder exhibited relatively compact surfaces with irregular fibrils. Conversely, gels subjected to 24 h of gelation before crosslinking exhibited longer, thicker fibrils with less compact arrangement. Rheological and differential scanning calorimetry analyses showed that the crosslinked gels were thermally stable (40.84–47.17 °C) and structurally strong (G’: 11–50 kPa; G”: 1–8 kPa; tan δ: 0.05–0.17) gels. L929 fibroblasts cultured on these gels displayed distinct adhesion, spreading, and proliferation behaviors depending on gel microstructure. Furthermore, hyaluronic acid (HA) quantification showed that cells on the carp collagen gels stimulated HA production (25.05–26.15 ng/well). These results demonstrate that genipin-crosslinked carp collagen gels constitute tunable, cytocompatible collagen-based gels, with surface microstructure influencing fibroblast behavior, offering useful design insights for the development of stabilized fish-collagen materials for biomaterial applications. Full article

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is increasingly recognized as a risk factor for cognitive decline and dementia, independent of clinically apparent stroke. This narrative review synthesizes current evidence on pathophysiological mechanisms linking AF to cognitive decline, including cerebral hypoperfusion, silent cerebral infarction, microembolism, systemic inflammation, and shared vascular risk factors. A structured literature search was conducted in PubMed and ScienceDirect from January 2000 to October 2025, with evidence quality assessed using adapted Newcastle–Ottawa Scale criteria. Observational evidence suggests that oral anticoagulation, particularly with direct oral anticoagulants (DOACs), may be associated with reduced dementia risk compared to no treatment or vitamin K antagonists. However, most intervention studies were not designed with cognitive endpoints as primary outcomes, limiting causal inference. Current evidence supports comprehensive AF management, including guideline-directed anticoagulation, appropriate rhythm or rate control, and aggressive modification of shared risk factors. Atrial fibrillation is consistently associated with increased risk of cognitive decline and dementia through multiple interrelated mechanisms; however, randomized trials with cognitive endpoints are needed to establish causality. Full article

Background: Although the concomitant Maze procedure successfully restores sinus rhythm in patients with valvular atrial fibrillation, it remains unclear whether electrical restoration translates into uniform functional recovery across different valvular etiologies. To address this issue, we compared the long-term left atrial (LA) mechanical recovery between patients with mitral stenosis (MS) and mitral regurgitation (MR) after the Maze procedure. Methods: This retrospective study included 211 patients who underwent the Maze procedure concomitant with valvular surgery and maintained sinus rhythm after 1 year. Patients were stratified into three groups, namely MS (n = 51), MR (n = 98), and non-mitral (n = 62) serving as a reference. LA function was evaluated using speckle-tracking echocardiography at baseline, immediately postoperatively, and at 1 year. Primary outcomes were changes in LA reservoir (LASr), LA conduit (LAScd), and LA contractile (LASct) strains. Results: At 1-year follow-up, the non-mitral reference group exhibited the best LA function, followed by the MR group, whereas the MS group showed the most impaired values (p < 0.001). Analysis of functional recovery revealed a mechanistic divergence, i.e., although the improvement in passive stiffness (LAScd) was comparable between the MS and MR groups (p = 0.42), the recovery of active contractile strain (LASct) was significantly superior in the MR group compared to the MS group (p < 0.05). The MS group failed to regain effective atrial contraction despite successful rhythm control. Conclusions: Although the Maze procedure successfully restored sinus rhythm, functional recovery varied significantly by etiology. The superior recovery in patients with MR was driven by the restoration of active atrial contraction, whereas patients with MS exhibited persistent mechanical dysfunction attributed to irreversible myocardial structural remodeling, despite similar improvements in compliance. Therefore, electrical success does not guarantee functional success, particularly in patients with MS. Full article

Bone cement implantation syndrome (BCIS) is classically associated with acute intraoperative cardiopulmonary disturbances during cemented arthroplasty. However, accumulating clinical observations suggest that its systemic manifestations may extend beyond the immediate peri-cementation period. Hepatic involvement remains rarely reported and is poorly characterized, particularly in frail elderly patients with limited physiological reserve. We report the case of an 82-year-old woman who developed severe but reversible ischemic acute liver failure with concomitant acute kidney injury following cemented total hip arthroplasty. A brief peri-cementation episode of hypotension and mild hypoxemia was followed, within the early postoperative period, by abrupt elevation of aminotransferases (AST 4980 IU/L; ALT 3120 IU/L), coagulopathy (INR ≥ 1.5), transient neurological alteration compatible with early hepatic encephalopathy, severe acute kidney injury, and new-onset atrial fibrillation. An extensive diagnostic evaluation excluded viral, autoimmune, toxic, biliary, vascular, infectious, and structural causes of liver injury. The clinical and biochemical profile was consistent with ischemic hepatocellular injury occurring in the context of systemic hypoperfusion. Management consisted of supportive intensive care focused on hemodynamic stabilization, respiratory support, rhythm control, metabolic management, and close laboratory monitoring, resulting in complete hepatic, renal, and neurological recovery. This case describes a rare presentation of ischemic acute liver failure with multiorgan involvement following cemented total hip arthroplasty. The temporal association with transient peri-cementation hypotension and hypoxemia suggests a possible delayed systemic manifestation within the spectrum of BCIS, even in the absence of overt intraoperative collapse. Although causality cannot be established, the clinical course underscores the importance of careful postoperative evaluation in vulnerable patients who experience perioperative hemodynamic disturbances. Full article

KCa3.1 encodes the intermediate-conductance calcium-activated potassium channel KCa3.1, a regulator of membrane potential and calcium-dependent signalling in cardiovascular and immune cells. Increasing evidence indicates that KCa3.1 is a shared driver of vascular remodelling, inflammation, fibrosis, and electrical instability across multiple cardiovascular diseases. In ischaemic heart disease (IHD), KCa3.1 is upregulated in endothelial cells, vascular smooth muscle cells, macrophages, and T lymphocytes, where it promotes smooth muscle proliferation, neointimal formation, and chronic vascular inflammation. Genetic deletion or pharmacological blockade of KCa3.1 reduces atherosclerotic plaque burden and restenosis in animal models. In atrial fibrillation (AF), KCa3.1 contributes to electrical remodelling by shortening atrial action potential duration and to structural remodelling by driving fibroblast activation and collagen deposition. KCa3.1 also regulates macrophage polarisation and pro-inflammatory cytokine release in atrial tissue, linking immune activation to arrhythmogenic substrate formation. Inhibition of KCa3.1 prolongs atrial refractoriness, attenuates atrial fibrosis, and reduces AF inducibility in multiple preclinical models. Emerging data in valvular heart disease suggest that KCa3.1 is upregulated in valvular interstitial cells and regions of active calcification, where it supports myofibroblast differentiation, osteogenic signalling, and inflammatory crosstalk, implicating the channel in fibrocalcific valve degeneration. Collectively, these findings position KCa3.1 as a central molecular integrator of electrical, fibrotic, and inflammatory pathways in cardiovascular disease. The availability of selective KCa3.1 inhibitors with established human safety profiles supports the feasibility of therapeutic translation. Targeting KCa3.1 may enable disease-modifying strategies that extend beyond symptom control to suppress maladaptive cardiovascular remodelling. Full article

Background: Echocardiographic imaging has become central to planning and guiding percutaneous left atrial appendage occlusion (LAAO), particularly in patient populations in whom long-term anticoagulation is unsuitable. This systematic review synthesizes current evidence on transesophageal (TEE) and intracardiac echocardiography (ICE) guidance during LAAO, with special emphasis on outcomes in high-risk cohorts, including chronic liver disease (CLD) and prior gastrointestinal (GI) bleeding. Methods: Following PRISMA 2020 guidelines, four databases (PubMed, Scopus, Web of Science, and Cochrane CENTRAL) were searched up to 5 December 2025. Eligible studies included adult patients with atrial fibrillation (AF) undergoing percutaneous LAAO with intraprocedural echocardiographic guidance. Eight studies (n = 1739 patients) met the inclusion criteria. Data were synthesized qualitatively due to heterogeneity across devices, imaging protocols, and outcomes. Results: TEE was the predominant imaging modality (62.5%), providing high spatial resolution for transseptal puncture, device positioning, and peri-device leak (PDL) assessment. ICE-guided LAAO (25.0%) was associated with high procedural success and favorable safety profiles in selected observational cohorts, while reducing anesthesia requirements and fluoroscopy time. Across all studies, procedural success ranged from 93 to 100%, with low rates of major complications. Reported follow-up durations varied substantially across studies and were predominantly short- to mid-term, limiting assessment of long-term device-related outcomes. Evidence specific to patients with chronic liver disease and prior gastrointestinal bleeding was limited, with only two included studies directly evaluating these populations, while remaining insights were extrapolated from broader LAAO cohorts. In high-risk groups, LAAO remained feasible: cirrhotic patients demonstrated high implantation success with acceptable bleeding profiles, while patients with prior GI bleeding showed low recurrence after closure. Conclusions: Both TEE and ICE provide reliable intraprocedural imaging for LAAO, with ICE offering workflow and safety advantages in patients unsuitable for general anesthesia. The available evidence suggests that LAAO is a feasible and potentially safe therapeutic option in selected patients with CLD and prior GI bleeding, although direct data remain limited. Future studies should compare imaging modalities prospectively in high-risk cohorts and evaluate emerging 3D/4D ICE technologies. Full article

Background: Atrial fibrillation (AF) is consistently associated with cognitive impairment and dementia through mechanisms that extend beyond classical cardioembolic stroke. However, the relative contribution of these pathways and the effectiveness of available therapeutic strategies for preserving cognition remain uncertain, as most data come from observational studies with a substantial risk of bias. Objectives: This review narratively synthesizes contemporary evidence on epidemiology, pathophysiological mechanisms, therapeutic strategies—including anticoagulation, rhythm control, and comprehensive risk-factor management—and the role of digital health technologies in the relationship between AF and cognitive decline. Methods: We performed a narrative, PRISMA-informed scoping review of observational cohorts, mechanistic studies, randomized clinical trials, systematic reviews, and meta-analyses published up to January 2026, identified through structured searches in MEDLINE/PubMed and complementary sources. Studies were selected if they examined (i) associations between AF and cognitive impairment or dementia, (ii) mechanistic pathways linking AF to brain injury, (iii) therapeutic interventions with cognitive or brain imaging outcomes, or (iv) digital health technologies applied to AF management. Heterogeneity in study design and outcome assessment precluded meta-analysis; therefore, we provide a qualitative synthesis, explicitly distinguishing observational evidence from randomized data and discussing key sources of confounding. Risk of bias was evaluated using validated tools: ROBINS-I for non-randomized studies, RoB 2.0 for RCTs, Newcastle–Ottawa Scale for observational cohorts, and AMSTAR-2 for systematic reviews. Results: Large population-based cohorts and meta-analyses indicate that AF is associated with a 1.4–2.2-fold higher risk of cognitive impairment or incident dementia, even after adjustment for shared vascular risk factors and exclusion of patients with prior stroke; nevertheless, residual confounding and selection bias cannot be excluded. Silent cerebral infarcts are detected in roughly one-quarter to two-fifths of AF patients without clinical stroke and are themselves associated with cognitive deficits, suggesting that subclinical embolism represents one important, but not exclusive, pathway. Additional mechanisms include chronic cerebral hypoperfusion, neuroinflammation, small vessel disease, and structural brain atrophy, all of which are incompletely disentangled from comorbidities. Observational data suggest that oral anticoagulation, particularly with direct oral anticoagulants (DOACs), is associated with lower rates of dementia compared with no anticoagulation or warfarin, but randomized trials such as BRAIN-AF and GIRAF have not demonstrated a clear cognitive benefit, underlining the low-to-moderate certainty of this evidence. Rhythm-control interventions, especially catheter ablation, are associated with lower dementia incidence in registry studies, yet strong selection effects and short follow-up limit causal inference. Digital health tools and ABC-pathway mobile applications improve cardiovascular outcomes and adherence, although cognitive endpoints remain largely unexplored. Conclusions: AF should be conceptualized as a neurovascular condition with important implications for brain health, rather than a purely cardiac rhythm disorder confined to stroke prevention. A comprehensive heart–brain management strategy that combines optimal anticoagulation, individualized rhythm control, aggressive vascular risk factor modification, routine cognitive screening in older or high-risk patients, and judicious use of digital health technologies may offer the best opportunity for preserving cognition, although rigorous trials with cognitive endpoints are still needed to establish causality. Full article

Atrial fibrillation (AF) is the most common prevalent sustained arrhythmia and is associated with stroke, heart failure, and impaired health-related quality of life. Due to the complexity of the initiation and the persistence of AF, the pulmonary vein isolation (PVI) using thermal or laser energy is the most commonly applied ablation strategy. However, these thermal ablation modalities have several limitations, including a substantial risk of AF recurrence and collateral damage to tissues adjacent to the heart. Pulsed field ablation (PFA) is a novel non-thermal ablation technique in which high-voltage electric fields deliver short pulses, selectively affecting cardiomyocyte cell membranes. PFA has the potential to create myocardial lesions with minimal harm to non-cardiac tissues. Clinical studies have evaluated the safety and efficacy of PFA, examining its ability to prevent AF recurrence and its impact on surrounding structures, often in comparison with conventional PVI approaches. In this review, PFA clinical studies are discussed as well as our experience with the PFA use for redo atrial fibrillation ablation cases. Full article

Background: Radiofrequency catheter ablation for atrial fibrillation (AF) restores sinus rhythm, but late recurrence is common. Left atrial (LA) size is a known predictor of AF recurrence, but the prognostic value of early post-ablation LA remodeling remains underexplored. Objective: We aimed to evaluate whether pre-ablation and early post-ablation LA volume index (LAVI) predict late atrial tachyarrhythmia recurrence after AF ablation. Methods: This is a retrospective single-center study of adults undergoing their first radiofrequency ablation for AF between January 2013 and December 2021. LA volume was measured by transthoracic echocardiography and indexed to body surface area to derive LAVI within one week before ablation and at 6 and 12 months after the procedure. The 6-month echocardiographic assessment was prespecified as the primary early post-ablation time point because it occurs beyond the 3-month blanking period and captures early structural remodeling during routine follow-up. Early recurrence was defined as atrial tachyarrhythmia occurring within 3 months after ablation, and late recurrence (LR) as any atrial tachyarrhythmic event thereafter. Multivariable Cox proportional hazards models were used to identify independent predictors of LR. Results: Among 408 patients with at least one year of follow-up, 157 (38.5%) experienced LR. Age and sex were similar between recurrence and non-recurrence groups (60.7 ± 9.8 vs. 59.9 ± 0.8 years; 56.1% vs. 64.1% male). Recurrence was associated with a higher prevalence of atrial flutter and persistent AF, higher pre-ablation and post-ablation LAVI, and lower post-ablation left ventricular ejection fraction. In multivariable analysis, atrial flutter, persistent AF, and LAVI, measured both before and after ablation, were independent predictors of LR. In receiver operating characteristic analysis, pre-ablation LAVI demonstrated modest discrimination for LR (AUC = 0.622; 95% CI 0.563–0.681; p < 0.001), with an optimal cut-off of 41.6 mL/m², while post-ablation LAVI showed similar performance (AUC = 0.597; 95% CI 0.532–0.662; p = 0.003), with a cut-off of 38.6 mL/m². Overall, discrimination was modest (AUC < 0.65), limiting LAVI as a standalone predictor. Conclusions: Elevated LAVI measured before and early after AF ablation independently predicts LR. Limited post-ablation LA reverse remodeling, reflected by persistently increased LAVI, is associated with unfavorable long-term rhythm outcomes. Serial assessment of LAVI may enhance post-ablation risk stratification. Full article

Background and Objectives: Diabetes mellitus (DM) has been consistently linked to severe coronavirus disease 2019 (COVID-19) and adverse outcomes; however, the extent to which DM independently predicts mortality and cardiovascular complications in real-world hospitalized cohorts remains debated, particularly in Eastern Europe. This study aimed to evaluate the impact of DM on cardiovascular complications and in-hospital outcomes among adults hospitalized with SARS-CoV-2 infection. Materials and Methods: We conducted a single-center retrospective observational cohort study including consecutive adult patients hospitalized with laboratory-confirmed SARS-CoV-2 infection between March 2020 and December 2024 at the “Victor Babeș” Clinical Hospital of Infectious Diseases and Pneumophthisiology, Timișoara, Romania. DM status (type 1, type 2, or newly diagnosed diabetes) was defined using structured dataset fields. The primary outcome was in-hospital all-cause mortality. Secondary outcomes included ICU admission, length of stay, pulmonary embolism (PE) on CT pulmonary angiography (CTPA), and a composite of in-hospital cardiovascular/thromboembolic complications. Multivariable logistic regression models adjusted for clinically relevant covariates (age, sex, BMI, vaccination status, hypertension, ischemic heart disease, atrial fibrillation, prior ischemic stroke, and admission creatinine). Results: A total of 395 patients were included; 98 (24.8%) had DM. Diabetic patients exhibited a high cardiometabolic burden (arterial hypertension: 83.7% vs. 77.4%, p = 0.242) and higher admission renal markers (urea: 55.6 [41.0–79.1] vs. 48.6 [39.2–68.0] mg/dL, p = 0.047; creatinine: 1.04 [0.76–1.52] vs. 0.88 [0.59–1.33] mg/dL, p = 0.008). In-hospital mortality was numerically higher in DM (9.2% vs. 6.7%, p = 0.560), as was ICU admission (7.1% vs. 4.7%, p = 0.503), without statistical significance. PE on CTPA occurred in 13.3% of DM vs. 11.4% of non-DM patients (p = 0.763). In univariable analysis, DM was not significantly associated with mortality (OR 1.40, 95% CI 0.62–3.19; p = 0.422) or ICU admission (OR 1.55, 95% CI 0.61–3.97; p = 0.356). After multivariable adjustment, DM remained not independently associated with mortality (adjusted OR 1.09, 95% CI 0.42–2.83; p = 0.854) or ICU admission (adjusted OR 1.19, 95% CI 0.42–3.36; p = 0.747). Conclusions: In this real-world Eastern European cohort of hospitalized adults with SARS-CoV-2 infection, diabetes mellitus was common and associated with significantly worse renal function at admission, but it was not statistically associated with in-hospital mortality or ICU admission after multivariable adjustment; however, the limited number of events and low events-per-variable raise concerns about model stability and potential false-negative findings. These findings support a risk-marker model in which adverse COVID-19 outcomes in diabetic patients are driven primarily by clustered vulnerability and organ dysfunction rather than diabetes status alone. Full article