Search Results (53)

Background: Predicting atrial fibrillation (AF) recurrence remains a major clinical challenge, as conventional echocardiographic parameters often fail to capture the complex electro-mechanical substrate of the arrhythmia. The prognostic significance of right ventricular (RV) function and atrial mechanical–structural coupling in paroxysmal AF (PAF) remains underexplored. Methods: We prospectively enrolled patients with PAF in sinus rhythm undergoing comprehensive echocardiography. A wide range of conventional left-sided, right-sided, and novel coupling indices was assessed. Univariable analysis was performed to screen for potential AF recurrence predictors. Based on the initial findings, receiver operating characteristic (ROC) analysis was used to determine the optimal cutoff for RV fractional area change (RV FAC). Finally, multivariable logistic regression identified independent predictors of AF recurrence over a 12-month follow-up. Results: A total of 73 patients were included, of whom 31 (42.5%) experienced AF recurrence during 12-month follow-up. Conventional left atrial (LA) indices, including LA volume index (LAVI) and reservoir strain, showed no significant association with recurrence. In univariable analysis, RV FAC, LA contraction strain, and the novel LA contraction strain/LAVI ratio were all significant predictors. ROC analysis identified an RV FAC cutoff of 42.5%, with lower values associated with significantly higher recurrence rates. In multivariable analysis, lower RV systolic performance determined by RV FAC ≤ 42.5% emerged as a primary independent predictor of recurrence (p = 0.003), while the LA contraction strain/LAVI ratio demonstrated a strong trend towards significance (p = 0.076). Conclusions: In this exploratory study of patients with PAF, atrial mechanical–structural mismatch emerged as a primary marker of the arrhythmic substrate. Additionally, an exploratory signal suggested that a subclinical reduction in RV performance may also correlate with recurrence, though this warrants further investigation in larger cohorts. Full article

Background/Objectives: Scar-related ventricular tachycardia (VT) remains a major contributor to morbidity and mortality in patients with structural heart disease (SHD), despite advances in catheter ablation (CA). Existing risk scores are limited by their focus on procedural outcomes, restricted variable sets, and insufficient integration of arrhythmic burden. This study aimed to bridge this gap in evidence and develop and internally validate two novel, clinically applicable prediction models—the VISTA-R and VISTA-M scores—for estimating the risk of 24-month arrhythmic recurrence and mortality following VT ablation. Methods: We analyzed a retrospective, single-center cohort of consecutive patients undergoing radiofrequency catheter ablation (RFCA) for scar-related VT in the setting of SHD and included a comprehensive set of clinical, arrhythmic, device-related, and procedural variables. Candidate predictors were identified through univariate logistic regression and subsequently incorporated into an exhaustive combinatorial modeling framework, generating over 1000 candidate models per endpoint. Final model selection was based on discrimination, calibration, and clinical interpretability. Internal validation was performed using leave-one-out cross-validation. Results: The VISTA-M model, incorporating left ventricular ejection fraction (LVEF), NYHA class IV at admission, number of clinical VT morphologies, and appropriate implantable-cardioverter defibrillator (ICD) shocks, demonstrated strong discriminative performance (AUC 0.866 in-sample, 0.826 cross-validated) and a pseudo R² of approximately 30%. The VISTA-R model, including history of electrical storm (ES), ICD shocks, and VT morphologies, showed moderate discrimination (AUC 0.70 in-sample, 0.63 cross-validated) with a pseudo R² of approximately 12%. Both models enabled meaningful risk stratification with progressively increasing event rates across the predefined risk classes. Conclusions: In conclusion, the VISTA scores provide parsimonious and clinically applicable tools for a comprehensive risk stratification after VT RFCA. Mortality is primarily driven by myocardial dysfunction and heart failure severity, whereas recurrence reflects arrhythmic burden and electrical instability. External validation is warranted to confirm these findings. Full article

Mitral annular disjunction (MAD) is associated with an increased risk of ventricular arrhythmias and sudden cardiac death, yet its genetic background remains poorly defined. We report the case of a 50-year-old man with MAD who survived cardiac arrest and carries three variants of unknown significance (VUS) in genes involved in cardiomyopathy pathogenesis. To explore the genetic basis of non-syndromic MAD, we performed a systematic review of the literature, identifying five case reports and one retrospective cohort study. The case reports described patients with MAD harboring four pathogenic variants and ten VUS. Two pathogenic variants were linked to cardiomyopathies, involving proteins of the nuclear envelope and cytoskeleton, while two were associated with channelopathies. The retrospective cohort study identified a recurrent variant in a gene involved in intercellular adhesion segregating within a family affected by MAD. Overall, available evidence suggests that genetic factors may hypothetically modulate susceptibility to MAD, not only in connective tissue disorders but also in isolated mitral valve disease. Variants associated with arrhythmogenic cardiomyopathies and channelopathies appear to cluster in families with non-syndromic MAD and arrhythmic phenotypes, suggesting a role in the arrhythmic substrate. However, in absence of definitive functional, segregation, or longitudinal data, the contribution of genetic variants to MAD should be interpreted with caution. Further genomic studies are needed to clarify their genetic contribution and prognostic implications. Full article

Obstructive Sleep Apnea (OSA) is a highly prevalent yet frequently underdiagnosed disorder strongly associated with cardiovascular morbidity and mortality. It is characterized by recurrent episodes of intermittent hypoxia, intrathoracic pressure swings, and sleep fragmentation that trigger sympathetic hyperactivation, oxidative stress, systemic inflammation, and progressive structural cardiac remodeling. These mechanisms translate into a wide range of electrocardiographic (ECG) abnormalities, including both nocturnal brady- and tachyarrhythmias, as well as daytime conduction and repolarization changes. This narrative review synthesizes current knowledge on ECG manifestations of OSA, encompassing atrial and ventricular ECG characteristics and the burden of supraventricular and ventricular arrhythmias. Emerging evidence suggests that several daytime ECG markers may represent accessible, low-cost indicators of subclinical cardiac remodeling and autonomic imbalance, with potential clinical implications. In addition, there is a rapidly evolving landscape of artificial intelligence applications and wearable-based ECG monitoring for OSA detection and risk stratification. Standardization of ECG-derived markers, validation across diverse populations, and integration into clinical workflows represent key priorities for future research. Recognizing ECG alterations associated with OSA may support earlier diagnosis, improved arrhythmic risk stratification, and more effective multidisciplinary management. Full article

Background: Catheter ablation is a validated treatment for ventricular arrhythmias (VA), but conventional radiofrequency (RF) energy may cause collateral injury due to non-selective thermal damage. Pulsed Field Ablation (PFA), a non-thermal modality based on irreversible electroporation, offers myocardial tissue selectivity and enhanced safety. While PFA is widely adopted for atrial arrhythmias’ ablation, its application in the ventricles remains an evolving frontier. Methods: We report a single-center experience using the Centauri PFA system integrated with a focal, contact-force sensing irrigated catheter (Tacticath™ SE, Abbott Laboratories, St. Paul, MN, USA) in four consecutive patients with drug-refractory VA. Two patients presented with frequent premature ventricular complexes (PVC) arising from the right and left ventricular outflow tract, respectively, while two had ischemic cardiomyopathy with recurrent scar-related ventricular tachycardia (VT). All procedures were guided by high-density mapping using the EnSite X system (Abbott Laboratories, St. Paul, MN, USA). Procedural safety, acute efficacy, and early follow-up outcomes were assessed. Results: All ablations achieved acute procedural success without complications. In both PVC cases, PFA led to immediate and complete suppression of ectopy, with a ≥95% reduction in arrhythmic burden at 12- and 9-months follow-up, respectively. In the VT cases, the arrhythmogenic substrate was effectively modified, rendering the clinical VT non-inducible. ICD interrogation during a 9-month follow-up showed complete absence of recurrent sustained VT. No coronary spasm, atrioventricular block, pericardial effusion, or other adverse events occurred. Conclusions: In this initial experience, focal PFA using a contact-force sensing catheter appeared feasible and effective for both focal and scar-related VA. This system provides an intuitive workflow similar to RF ablation. While our data suggest a favourable safety profile, larger studies are required to definitively confirm safety margins near critical structures. 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

The coronavirus disease 2019 (COVID-19) pandemic has revealed a close and multifaceted relationship between viral infection, systemic inflammation, and cardiovascular health. Among the cardiac complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), atrial fibrillation (AF)—especially new-onset atrial fibrillation (NOAF)—has emerged as a major determinant of disease severity and prognosis. Clinical studies and meta-analyses show that 5–10% of hospitalized COVID-19 patients develop AF, with markedly higher rates in critically ill individuals. Both pre-existing and NOAF are independently associated with increased risks of intensive care admission, mechanical ventilation, thromboembolic events, and mortality. The underlying mechanisms involve a combination of cytokine-mediated inflammation, endothelial dysfunction, microvascular injury, and dysregulation of the renin–angiotensin–aldosterone system (RAAS). Viral downregulation of angiotensin-converting enzyme 2 (ACE2) receptors contributes to myocardial fibrosis, while hypoxia, oxidative stress, and autonomic imbalance further promote electrical remodeling and arrhythmogenesis. Post-infectious studies indicate that atrial structural changes and autonomic dysfunction may persist for months, predisposing survivors to recurrent arrhythmias. Technological advances in telecardiology and digital medicine have provided new tools for early detection and long-term monitoring. Wearable electroencephalography (ECG) devices, implantable loop recorders (ILRs), and artificial intelligence (AI)-based diagnostic algorithms enable continuous rhythm surveillance and individualized management, improving outcomes in post-COVID patients. This review summarizes current evidence on the epidemiology, pathophysiology, clinical implications, and monitoring strategies of AF in COVID-19. It underscores the importance of integrating telemedicine and AI-assisted diagnostics into cardiovascular care to mitigate the long-term arrhythmic and systemic consequences of SARS-CoV-2 infection. Full article

Background/Objectives: Arrhythmic recurrence is a common issue affecting a significant percentage of patients undergoing transcatheter ablation (TCA) of Atrial Fibrillation (AF). The use of artificial intelligence (AI) for the identification of electrocardiographic predictors of post-ablation recurrence may offer a valuable and cost-effective approach to improve risk stratification and optimize follow-up. This study aims to investigate the relationship between post-procedural electrocardiographic (ECG) P-wave parameters, measured using AI, and AF recurrence in patients undergoing transcatheter ablation (TCA). Methods: Seventy-four patients (age 62.36 ± 10.4 years) with a diagnosis of AF were retrospectively analyzed. ECGs were processed using AI software to analyze P-wave-related variables. All patients had either an implantable loop recorder (ILR) or another form of cardiac implantable electronic device (CIED). Results: Post-procedural P-wave amplitude in lead II (PwA in lead II) showed a significant association with AF recurrence, defined as an average arrhythmic burden >6% at one-year follow-up. Conclusions: These findings underscore the potential of PwA in lead II as a biomarker for the follow-up of patients undergoing TCA and highlight the contribution of AI in the analysis of electrocardiographic parameters predictive of AF recurrence. Together, these results may contribute to the development of early risk-stratification strategies following catheter ablation. Full article

Background: Takotsubo syndrome (TTS) is an acute cardiac condition characterized by transient left ventricular dysfunction. Although generally considered reversible, early arrhythmias are a dreaded complication and their prognostic significance remains incompletely understood. Methods: In this study, 104 consecutive patients diagnosed with TTS (January 2007 to September 2024) were examined for the prognostic relevance of in-hospital arrhythmias during monitoring at the time of diagnosis. The median follow-up was 2.1 years. The primary combined endpoint included cardiac death, TTS recurrence, occurrence of arrhythmias, and rehospitalization for cardiac causes. Results: In-hospital arrhythmias occurred in 35.6% of the patients. Ventricular arrhythmias were significantly associated with an increased risk of adverse cardiac events (odds ratio 3.94, 95% confidence interval 1.22–12.69; p = 0.021). Reduced left ventricular ejection fraction and QTc prolongation, while frequently observed, were not independently associated with adverse outcomes when analyzed separately from arrhythmic events. Supraventricular arrhythmias exhibited a non-significant trend (p = 0.145). Conclusions: In a large registry of consecutive TTS patients, in-hospital ventricular arrhythmias at diagnosis were significantly associated with adverse outcomes, underscoring the importance of early rhythm monitoring. Full article

Background: Obstructive sleep apnea (OSA) is prevalent and often underdiagnosed in cardiology. Worldwide, approximately 936 million adults aged 30–69 are affected by OSA, with the highest numbers in the USA, China, Brazil, and India. In cardiovascular clinics, OSA is found in about 40–80% of patients with hypertension, heart failure, coronary artery disease, atrial fibrillation, or stroke. Meta-analyses link OSA to nearly twice the risk of cardiovascular disease, stroke, and all-cause mortality. Continuous positive airway pressure (CPAP) therapy addresses the underlying mechanisms of OSA and enhances intermediate cardiovascular indicators. Materials and Methods: We conducted a narrative review using major medical search engines (PubMed, Embase, Cochrane) to examine recent statements, meta-analyses, large cohorts, and key trials. The review focused on the cardiovascular burden of sleep apnea and its pathophysiology—including arrhythmic, hemodynamic, vascular, and coagulation aspects—as well as the effects of CPAP on intermediate cardiovascular outcomes. We aimed to provide a synthesised overview of current cardiovascular evidence related to the burden and mechanisms of OSA, and to summarise the effects of continuous positive airway pressure (CPAP) on intermediate and clinical cardiovascular outcomes. Results: Intermittent hypoxia, sleep fragmentation, and major negative fluctuations in intrathoracic pressure create a clear pathway leading to adverse cardiovascular outcomes. This occurs through mechanisms like sympathetic activation, RAAS activation, endothelial dysfunction, oxidative stress, and inflammation, linking OSA to these health issues. Studies show that greater severity of OSA correlates with higher cardiovascular risk, including increased incidence and recurrence of AF, resistant hypertension, and new cases of heart failure. CPAP effectively lowers AHI and enhances nocturnal oxygen levels, as well as intermediate cardiovascular indicators such as blood pressure, sympathetic activity, and certain aspects of ventricular function, with clinical benefits most evident in adherent patients. Conclusions: OSA is a significant, modifiable risk factor for cardiovascular disease. Routine cardiovascular care should include targeted screening for OSA, especially in cases of resistant hypertension, atrial fibrillation, and heart failure, along with timely sleep testing and adherence-focused CPAP therapy, in addition to traditional risk-reduction methods. Full article

Ventricular arrhythmias (VAs) are common and clinically important complications in patients supported by left ventricular assist devices (LVADs), occurring in up to 50% of cases within the first year after implantation. Despite the hemodynamic support provided by LVADs, VAs are linked to increased morbidity and mortality, primarily through recurrent implantable cardioverter defibrillator (ICD) shocks and right ventricular failure. The underlying mechanisms of VAs in this population are multifactorial, involving structural myocardial remodeling, device-related factors, and pre-existing arrhythmic substrates. Catheter ablation has become a valuable treatment option when antiarrhythmic drug therapy and device reprogramming are inadequate, though procedural timing (pre-, intra-, or post-implantation) and approaches remain under discussion. Epicardial access during LVAD surgery may provide advantages for selected patients, while ablation after implantation poses technical challenges due to altered anatomy and electromagnetic interference. This review offers a comprehensive overview of the epidemiology, pathophysiology, risk stratification, and management of VAs in LVAD recipients, emphasizing technical considerations, procedural safety, and clinical outcomes of catheter ablation. A multidisciplinary approach remains essential in guiding personalized treatment and optimizing outcomes for this complex population. Undergoing studies will provide more insight into optimal management of arrhythmias, particularly regarding the optimal timing of catheter ablation. The impact of new technologies such as non-invasive mapping alongside pre-procedural imaging needs also to be further evaluated. Full article

Background: Mitral valve prolapse is a common valvular heart disorder, usually associated with a benign prognosis in the absence of significant mitral regurgitation. However, a subset of patients is at increased risk for complex ventricular arrhythmias and sudden cardiac death. Identifying these high-risk individuals remains a major clinical challenge. Case Summary: We present the case of a 71-year-old female patient with recurrent syncopal episodes, a strong family history of sudden cardiac death, and complex ventricular ectopy. Multimodality imaging revealed bileaflet mitral valve prolapse, severe mitral regurgitation, mitral annular disjunction, and the Pickelhaube sign, with no evidence of myocardial fibrosis on cardiac magnetic resonance imaging. The patient underwent minimally invasive mitral valve repair and received an implantable cardioverter-defibrillator for primary prevention of sudden cardiac death. Follow-up revealed significant reverse cardiac remodeling, marked reduction in arrhythmic burden, and restoration of mitral valve function. Family screening identified mitral annular disjunction in both of her daughters, who were asymptomatic and without arrhythmias. Discussion: Mitral annular disjunction has emerged as a potentially arrhythmogenic substrate, especially in patients with familial clustering, raising the possibility of a genetic predisposition. Risk stratification remains difficult, as no individual clinical, electrocardiographic, or imaging marker has demonstrated consistent predictive value. Surgical correction of mitral valve prolapse with associated mitral annular disjunction may lead to a reduction in arrhythmic risk and promote favorable structural remodeling. Conclusions: This case-based review emphasizes the importance of advanced imaging techniques in the identification and management of high-risk mitral valve prolapse phenotypes. Early surgical intervention and close arrhythmic surveillance may improve outcomes, although further research is necessary to define risk assessment tools and explore the genetic background of arrhythmogenic mitral valve disease. Full article

Multifocal ectopic Purkinje-related premature contractions (MEPPC) syndrome is a recently recognized rare form of arrhythmia involving the entire His–Purkinje system and often coinciding with dilated cardiomyopathy (DCM). Certain variants in the SCN5A gene may be linked to MEPPC syndrome. We present a case of a 32-year-old Caucasian female who exhibited a high burden of premature ventricular contractions (PVCs) and non-sustained episodes of ventricular tachycardia (NSVT) with an alternating QRS pattern, and who was resistant to traditional medical therapy and radiofrequency catheter ablation (RFCA), necessitating implantation of a cardioverter-defibrillator (ICD). A positive family history (father’s death at the age of 40 years) and the rapid deterioration of left ventricular function parameters echocardiographically during recurrent arrhythmic episodes raised concern about a potentially complex disease scenario. Genetic testing revealed a heterozygous variant of the SCN5A gene, c.2440C>T, p.(Arg814Trp), confirming the diagnosis of MEPPC syndrome. Treatment with a combination of class I antiarrhythmic drugs, flecainide and mexiletine, concomitant with beta blockers, led to symptomatic improvement, a reduction of PVCs (from 66 491 (44%) to 858 (1%)), and the restoration of left ventricular function (LV EF from 44% to 53%). A lack of defined diagnostic criteria hampers timely diagnosis, leading to ineffective interventions and delayed initiation of treatment with antiarrhythmic drugs. MEPPC patients remain at significant risk for severe heart failure and sudden cardiac death. Our clinical case report underscores the importance of accurate and timely diagnosis, which allows effective treatment with a combination of antiarrhythmic drugs and mitigates the risk associated with MEPPC syndrome. Full article

Brugada syndrome (BrS) is an inherited electrical cardiac disorder that is associated with a higher risk of ventricular fibrillation (VF) and sudden cardiac death (SCD) in patients without structural heart disease. The diagnosis is based on the documentation of the typical pattern in the electrocardiogram (ECG) characterized by a J-point elevation of ≥2 mm, coved-type ST-segment elevation, and negative T wave in one or more right precordial leads, called type 1 Brugada ECG. Risk stratification is particularly difficult in asymptomatic cases. Patients who have experienced documented VF are generally recommended to receive an implantable cardioverter defibrillator to lower the likelihood of sudden death due to recurrent episodes. However, for asymptomatic individuals, the most appropriate course of action remains uncertain. Accurate risk prediction is critical to avoiding premature deaths and unnecessary treatments. Due to the challenges associated with experimental research on human cardiac tissue, alternative techniques such as computational modeling and deep learning-based artificial intelligence (AI) are becoming increasingly important. This study introduces a vision transformer (ViT) model that leverages 12-lead ECG images to predict potentially fatal arrhythmic events in BrS patients. This dataset includes a total of 278 ECGs, belonging to 210 patients which have been diagnosed with Brugada syndrome, and it is split into two classes: event and no event. The event class contains 94 ECGs of patients with documented ventricular tachycardia, ventricular fibrillation, or sudden cardiac death, while the no event class is composed of 184 ECGs used as the control group. At first, the ViT is trained on a balanced dataset, achieving satisfactory results (89% accuracy, 94% specificity, 84% sensitivity, and 89% F1-score). Then, the discarded no event ECGs are attached to additional 30 event ECGs, extracted by a 24 h recording of a singular individual, composing a new test set. Finally, the use of an optimized classification threshold improves the predictions on an unbalanced set of data (74% accuracy, 95% negative predictive value, and 90% sensitivity), suggesting that the ECG signal can reveal key information for the risk stratification of patients with Brugada syndrome. Full article

Myocarditis is an inflammatory condition of cardiac tissue presenting significant variability in clinical manifestations and outcomes. Its etiology is diverse, encompassing infectious agents (primarily viruses, but also bacteria, protozoa, and helminths) and non-infectious factors (autoimmune responses, toxins, and drugs), though often the specific cause remains unidentified. Recent research has highlighted the potential role of genetic susceptibility in the development of myocarditis (and in some cases the development of inflammatory dilated cardiomyopathy, i.e., the condition in which there is chronic inflammation (>3 months) and left ventricular dysfunction\dilatation), with several studies indicating a correlation between myocarditis and genetic backgrounds. Notably, pathogenic genetic variants linked to dilated or arrhythmic cardiomyopathy are found in 8–16% of myocarditis patients. Genetic predispositions can lead to recurrent myocarditis and a higher incidence of ventricular arrhythmias and heart failure. Moreover, the presence of DSP mutations has been associated with distinct pathological patterns and clinical outcomes in arrhythmogenic cardiomyopathy (hot phases). The interplay between genetic factors and environmental triggers, such as viral infections and physical stress, is crucial in understanding the pathogenesis of myocarditis. Identifying these genetic markers can improve the diagnosis, risk stratification, and management of patients with myocarditis, potentially guiding tailored therapeutic interventions. This review aims to synthesize current knowledge on the genetic underpinnings of myocarditis, with an emphasis on desmoplakin-related arrhythmogenic cardiomyopathy, to enhance clinical understanding and inform future research directions. Full article