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Background: There is no consensus on the most efficient catheter ablation (CA) strategy for patients with atrial fibrillation (AF). The objective of this study was to compare the efficacy and safety of different CA strategies for AF ablation through network meta-analysis (NMA). Methods: A systematic search of PubMed, Web of Science, and CENTRAL was performed up to October 5th, 2020. Randomized controlled trials (RCT) comparing different CA approaches were included. Efficacy was defined as arrhythmia recurrence after CA and safety as any reported complication related to the procedure during a minimum follow-up time of 6 months. Results: In total, 67 RCTs (n = 9871) comparing 19 different CA strategies were included. The risk of recurrence was significantly decreased compared to pulmonary vein isolation (PVI) alone for PVI with renal denervation (RR: 0.60, CI: 0.38-0.94), PVI with ganglia-plexi ablation (RR: 0.62, CI: 0.41-0.94), PVI with additional ablation lines (RR: 0.8, CI: 0.68-0.95) and PVI in combination with bi-atrial modification (RR: 0.32, CI: 0.11-0.88). Strategies including PVI appeared superior to non-PVI strategies such as electrogram-based approaches. No significant differences in safety were observed. Conclusions: This NMA showed that PVI in combination with additional CA strategies, such as autonomic modulation and additional lines, seem to increase the efficacy of PVI alone. These strategies can be considered in treating patients with AF, since, additionally, no differences in safety were observed. This study provides decision-makers with comprehensive and comparative evidence about the efficacy and safety of different CA strategies. Systematic review registration: PROSPERO registry number: CRD42 02016 9494.

Cardiac arrhythmias are increasingly recognized as dynamic clinical phenotypes arising from the interplay between myocardial substrate, systemic biology, and modifiable exposures rather than as isolated disorders of cardiac electrophysiology. Advances in the field have broadened the conceptual framework of arrhythmia medicine to include structural remodeling, inflammation, autonomic dysfunction, metabolic perturbation, endothelial injury, and aging-related vulnerability as central determinants of arrhythmic risk, progression, and treatment response. In parallel, diagnostic paradigms are evolving from rhythm classification alone toward multidimensional phenotyping that integrates clinical, physiological, and imaging-based markers to identify susceptibility earlier and with greater precision. These developments are also reshaping therapeutic strategy, supporting a shift from uniform treatment algorithms toward individualized care in which rhythm control, surveillance, risk-factor modification, anticoagulation, and antiarrhythmic drug selection are aligned with the underlying biological context. This more integrated view positions arrhythmias not simply as electrical events to be suppressed, but as manifestations of broader cardiovascular and systemic disease processes that require mechanistically informed and phenotype-directed management.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and frequently co-occurs with metabolic diseases, such as diabetes and obesity. Due to the intricate and multifactorial pathophysiology of AF, this disorder often eludes effective prevention and durable control with current therapeutic strategies; thus, these strategies may not consistently mitigate the onset, persistence, and related adverse outcomes of AF. Moreover, atrial metabolic remodeling and mitochondrial stress can promote the development of atrial cardiomyopathy and AF through electrophysiological and structural changes. Hence, targeting these metabolic alterations may prevent the onset of this arrhythmia. A contemporary therapeutic paradigm prioritizes restoration of metabolic homeostasis, led by sodium–glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists and complemented by emerging mitochondria-targeted strategies with potential for incremental disease modification. Concurrently, integrative multi-omics is mapping atrial metabolic diversity in AF to support biomarker-guided, individualized interventions, while next-generation imaging is enhancing the detection of pathologic substrates and refining risk assessment. This review provides a comprehensive analysis of the mechanisms through which metabolic remodeling and mitochondrial stress cause AF, evaluates current experimental and diagnostic methods, and discusses emerging substrate-targeted therapies.

Cardiac arrhythmias are prevalent complications in pregnancy, yet their precise association with acute maternal cardiovascular morbidity and mortality remains unclear due to heterogeneous evidence. This systematic review and meta-analysis evaluated the impact of maternal arrhythmias on acute cardiovascular outcomes. We searched Medline, Scopus, and Cochrane databases for observational studies comparing pregnant women with arrhythmias to those without. Random-effects meta-analyses were used to calculate pooled risk ratios (RR) for maternal mortality and major adverse cardiovascular events (MACE). Eleven studies comprising 76,028 pregnancies with arrhythmias and over 82 million controls were included. Analysis of data, primarily derived from large administrative cohorts with low absolute event rates, indicated that arrhythmias were significantly associated with increased all-cause maternal mortality (0.78% vs. 0.01%; RR 31.94; adjusted RR 8.91) and a composite of MACE (2.90% vs. 0.03%; RR 6.48). Supraventricular tachycardia and atrial fibrillation were associated with an increased likelihood of adverse outcomes. Notably, the relative risk of mortality and heart failure in women with arrhythmias versus controls was significantly higher in the general obstetric population around delivery than in women with known structural heart disease, suggesting a “sentinel event” phenomenon. Thromboembolic events were also 15 times more likely in the arrhythmia group. Cardiac arrhythmias during pregnancy are associated with substantial maternal morbidity and mortality. New-onset arrhythmias may warrant comprehensive cardiac evaluation, as they may unmask underlying pathology and precipitate severe hemodynamic compromise, particularly in women without prior cardiac history.

Arrhythmia-induced cardiomyopathy (AIC) represents a potentially reversible form of LV dysfunction in which sustained atrial fibrillation (AF) and irregular, often rapid, ventricular activation drive maladaptive electrical, structural, and metabolic remodeling. Beyond simple rate effects, AIC reflects perturbed calcium handling, oxidative stress, and fibro-inflammatory signaling that propagate atrial–ventricular crosstalk and energetic failure. Clinically, attribution remains challenging because AF may be the cause, consequence, or marker of underlying myocardial disease; however, substantial improvement in LVEF after durable rhythm control is strongly supportive of an AIC component. A disciplined diagnostic pathway—integrating rhythm burden quantification, echocardiographic deformation indices, cardiac magnetic resonance, and natriuretic peptide trajectories—can refine pre-test probability and guide treatment intensity. Early rhythm control has emerged as a disease-modifying strategy in AF with HF, with catheter ablation often central to burden reduction and reverse remodeling; in parallel, rapid initiation of guideline-directed HF therapy and targeted cardiometabolic interventions may favor substrate regression and facilitate durable sinus rhythm. Uncertainties persist regarding standardized AIC case definition, arrhythmia burden thresholds that secure sustained recovery, optimal sequencing of rhythm- and substrate-directed therapies, and criteria for de-escalation of HF treatment after recovery. This review synthesizes contemporary mechanistic, diagnostic, and therapeutic evidence on AIC in AF and delineates priorities for future trials.

Background: Flecainide has remained largely excluded from use in structural heart disease for more than three decades, mainly because of the Cardiac Arrhythmia Suppression Trial, which showed excess mortality in post-myocardial infarction patients treated for ventricular ectopy. However, the influence of this trial has extended well beyond the population actually studied, fostering a broad safety paradigm that may not fully reflect contemporary clinical practice. Aim: This review aims to re-examine the role of flecainide in structural heart disease by examining the historical basis for its restriction and contrasting it with emerging contemporary evidence across specific structural substrates. Discussion: Flecainide remains one of the most effective antiarrhythmic drugs for rhythm control in atrial fibrillation and for the suppression of selected ventricular arrhythmias in patients without overt structural abnormalities. Emerging observational and early prospective data suggest that, in carefully selected patients with stable coronary artery disease without active ischemia, preserved left ventricular function, arrhythmogenic right ventricular cardiomyopathy, and premature ventricular complex-induced cardiomyopathy, flecainide may provide meaningful antiarrhythmic benefit without a clear signal of excess proarrhythmia or mortality. Advances in cardiac imaging, ischemia assessment, and phenotypic risk stratification further support a more individualized approach to candidate selection. Conclusions: Flecainide should not be considered uniformly contraindicated across all forms of structural heart disease. Rather than supporting indiscriminate use, the available evidence supports a mechanistically informed and phenotype-specific reassessment of its role in selected patients. Prospective studies are needed to determine whether current guideline restrictions remain justified in the modern era.

Background: Transesophageal echocardiography (TEE) is a vital diagnostic tool in clinical practice, particularly in transcatheter interventions where it aids in both pre-operative planning and intra-operative guidance. Traditional TEE probes often require general anesthesia due to patient discomfort. However, the development of miniaturized TEE probes presents a promising alternative, enabling routine examinations and interventions with minimal sedation. This study evaluates the feasibility of performing a complete 2D/4D TEE protocol with the new 4D mini-TEE probe in the echocardiography department and its application in transcatheter interventions. Methods: This is a retrospective study that included 30 consecutive patients from two high-volume European hospitals (Interbalkan Medical Center, Thessaloniki, Greece, and Rennes University, France) that underwent TEE or transcatheter interventions. The new 4D mini-TEE 9VT-D probe (GE Healthcare) was utilized. The quality of the images and the tolerance of the probe were assessed in the cath lab during interventions and in the echocardiography department during routine TEE examinations. Results: Direct comparison of the 4D mini-TEE probe with the standard 6VT-D probe confirmed the excellent image quality of this new pediatric probe. Most of the patients required minimal sedation or local oropharyngeal anesthesia, with satisfactory tolerance reported. Most of the transcatheter procedures did not require general anesthesia and intubation, resulting in shorter procedural time. Both 2D and 4D imaging modalities offered adequate intra-operative guidance for transcatheter procedures. Conclusions: The 4D mini-TEE probe delivers exceptional imaging capabilities for routine examinations and transcatheter interventions without needing sedation. Its use reduces esophageal trauma and the need for general anesthesia, enhancing patient comfort and safety.

Cardiovascular (CV) disease, chronic kidney disease, obesity, and diabetes mellitus have reached epidemic proportions over the past few decades. Accumulating evidence highlights the strong interconnection between these conditions, leading to the definition of a broader disease entity known as cardio-renal-metabolic (CRM) syndrome. This newly recognized clinical entity presents important challenges in identifying the optimal treatment strategy within a holistic, patient-centered framework. In line with this, sodium glucose cotransporter 2 inhibitors (SGLT2is), owing to their multifaceted pharmacological effects, have been suggested as possible treatment options in the management of CRM. SGLT2is exert their antihyperglycemic effects by impeding the renal reabsorption of sodium and glucose, causing glycosuria and natriuresis. Research has confirmed that their unique beneficial effects extend beyond glycemic control, reducing CV death and hospitalizations in patients with heart failure, and the incidence of kidney failure in dedicated kidney outcome studies—regardless of diabetes status. Furthermore, these agents contribute to weight loss and blood pressure reduction. Their benefits appear to stem from a combination of factors, which include reduced oxidative stress, lower levels of inflammation, regulated neurohormonal activation, improved endothelial function, and enhanced metabolic efficiency. This review aims to provide a comprehensive analysis of the pathophysiological mechanisms underlying the effects of SGLT2is in CRM syndrome, synthesize evidence from landmark clinical trials, evaluate current experimental and diagnostic approaches, and provide the emerging role of SGLT2is in the treatment of this new clinical entity.

Atrial fibrosis is a hallmark of atrial cardiomyopathy and plays a pivotal role in the pathogenesis of atrial fibrillation (AF), contributing to its onset and progression. The mechanisms underlying atrial fibrosis are multifaceted, involving stretch-induced fibroblast activation, oxidative stress, inflammation, and coagulation pathways. Variations in fibrosis types—reactive and replacement fibrosis—are influenced by patient-specific factors such as age, sex, and comorbidities, complicating therapeutic approaches. The heterogeneity of fibrosis leads to distinct electrophysiological abnormalities that promote AF via reentrant activity and enhanced automaticity mechanisms. Despite advancements in imaging, such as late gadolinium enhancement CMR and electroanatomical mapping, challenges in accurately quantifying fibrosis persist. Emerging therapeutic strategies include antifibrotic agents targeting the renin–angiotensin–aldosterone system, novel pathways like TGF-β signaling, and cardio-metabolic drugs like SGLT2 inhibitors and GLP-1 receptor agonists. Innovative interventions, including microRNA modulation and lipid nanoparticle-based therapies, show promise but require validation. Knowledge gaps remain in correlating clinical outcomes with fibrosis patterns and optimizing diagnostic tools. Future research should focus on precise phenotyping, integrating advanced imaging with molecular biomarkers, and conducting robust trials to evaluate antifibrotic therapies’ efficacy in reducing AF burden and related complications.

The global rise in diabetes prevalence has significantly contributed to the increasing burden of atherosclerotic cardiovascular disease (ASCVD), a leading cause of morbidity and mortality in this population. Diabetes accelerates atherosclerosis through mechanisms such as hyperglycemia, oxidative stress, chronic inflammation, and epigenetic dysregulation, leading to unstable plaques and an elevated risk of cardiovascular events. Despite advancements in controlling traditional risk factors like dyslipidemia and hypertension, a considerable residual cardiovascular risk persists, highlighting the need for innovative therapeutic approaches. Emerging treatments, including sodium–glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, epigenetic modulators, and RNA-based therapies, are showing promise in addressing the unique challenges of diabetes-associated ASCVD. Precision medicine strategies, such as nanoparticle-based drug delivery and cell-specific therapies, offer further potential for mitigating cardiovascular complications. Advances in multiomics and systems biology continue to deepen our understanding of the molecular mechanisms driving diabetes-associated atherosclerosis. This review synthesizes recent advances in understanding the pathophysiology and treatment of diabetes-related atherosclerosis, offering a roadmap for future research and precision medicine approaches to mitigate cardiovascular risk in this growing population.