Fulvio Cacciapuoti

Artificial intelligence (AI) has become increasingly integrated into chest radiograph interpretation, demonstrating excellent diagnostic performance for several thoracic abnormalities, including pneumothorax. Nevertheless, current AI systems remain predominantly image-based and do not inherently incorporate procedural or clinical information into diagnostic interpretation. We report the case of an 81-year-old man who underwent uncomplicated left-sided dual-chamber permanent pacemaker implantation. Routine post-procedural chest radiography, analyzed by an AI-assisted interpretation system, generated a positive alert for a right apical pneumothorax, highlighting the suspected abnormality with automated visual annotation. The alert was immediately considered clinically discordant by the treating team, given the left-sided venous access, normal oxygen saturation, hemodynamic stability, and absence of respiratory symptoms. Because of this clinicoradiological discordance, chest computed tomography was performed and definitively excluded pneumothorax, confirming a false-positive AI interpretation. The patient required no additional intervention and experienced an uneventful recovery. This case highlights the importance of integrating AI-generated findings with procedural details, bedside clinical assessment, and, when clinically indicated, confirmatory imaging in the presence of clinicoradiological discordance. Although AI can accurately identify many radiographic abnormalities, accurate diagnosis ultimately depends on integrating imaging findings with procedural information, clinical presentation, and pre-test probability. This case also emphasizes that AI should be regarded as a clinical decision-support tool rather than an autonomous diagnostic system and highlights the continuing importance of physician oversight in ensuring patient safety during AI-assisted post-procedural imaging interpretation. Graphical abstract Central illustration: artificial intelligence meets clinical reasoning.

Background: Large, mobile left atrial thrombi can intermittently occlude the mitral orifice and precipitate rapid hemodynamic compromise in atrial fibrillation. Timely echocardiography is pivotal to diagnosis and management. Case presentation: A 71-year-old woman with previously undocumented atrial fibrillation presented with dyspnea, rapid ventricular response, and borderline blood pressure (100/50 mmHg). Transthoracic echocardiography showed a large, mobile left atrial mass prolapsing through the mitral valve; transesophageal echocardiography confirmed a 3.3 × 2.8 cm thrombus with spontaneous echo contrast and 2 smaller septal thrombi. Mitral leaflets were thickened and calcified with commissural fusion, consistent with rheumatic disease; the transmitral gradient was mild, but biatrial enlargement suggested chronic pathology. Given thrombus size and mobility, anticoagulation and thrombolysis were deferred. The patient underwent emergency surgical thrombectomy, bioprosthetic mitral valve replacement, and left atrial appendage exclusion. Recovery was uneventful, with normal prosthetic function and no residual thrombus on follow-up imaging. Conclusion: In atrial fibrillation with suspected mechanical obstruction, bedside transthoracic echocardiography followed by transesophageal echocardiography enables rapid confirmation of a ball-valve left atrial thrombus. In this patient, rapid echocardiographic characterization and multidisciplinary assessment supported urgent surgery because of intermittent mechanical obstruction, marked thrombus mobility, associated mitral-valve disease, and the need for definitive treatment. Management should be individualized; this single case does not establish the superiority of surgery over anticoagulation for all large left atrial thrombi.

Obesity and obstructive sleep apnea (OSA) frequently coexist and synergistically contribute to cardiovascular disease through interconnected mechanical, metabolic, and autonomic mechanisms. This interplay promotes myocardial electrical instability and structural remodeling, favoring the development and persistence of cardiac arrhythmias, particularly atrial fibrillation. Among the key mediators linking obesity to arrhythmogenesis, epicardial adipose tissue has emerged as a relevant factor that may contribute to local pro-inflammatory, pro-fibrotic, and autonomic effects on the myocardium. In parallel, OSA-related intermittent hypoxia and intrathoracic pressure swings further amplify electrical instability and autonomic imbalance, reinforcing a self-sustaining arrhythmogenic substrate. Therapeutic strategies are increasingly shifting toward upstream interventions targeting these underlying mechanisms. Metabolic therapies, including the dual GIP/GLP-1 receptor agonist tirzepatide, have demonstrated substantial weight reduction and improvement in OSA severity, with potential indirect benefits on arrhythmic risk through modulation of visceral adiposity, inflammation, and metabolic dysfunction. On the electrophysiological side, cardioneuroablation has emerged as a potentially investigational option in selected patients with vagally mediated bradyarrhythmias, although its role remains to be fully defined. Overall, these observations support an integrated, phenotype-driven approach combining respiratory therapy, metabolic modulation, and targeted electrophysiological interventions. This framework may help redefine therapeutic priorities, shifting from symptom control toward modification of the underlying arrhythmogenic substrate and improvement of long-term cardiovascular outcomes.

Background and Clinical Significance: Early loss of pacing capture after pacemaker generator replacement is an uncommon but potentially life-threatening event, especially in pacemaker-dependent patients. In this setting, device malfunction is often initially attributed to intrinsic lead damage, prompting consideration of invasive lead revision or extraction. However, not all early failures reflect true structural lead dysfunction. Careful interpretation of device interrogation findings, particularly in relation to pacing configuration, may uncover reversible causes and support a more targeted diagnostic and management approach; Case Presentation: A 61-year-old man with complete atrioventricular block presented with recurrent syncope six days after elective pacemaker generator replacement. The electrocardiogram showed absence of effective ventricular pacing with a slow escape rhythm. Device interrogation revealed loss of ventricular capture in bipolar configuration associated with markedly elevated impedance, initially raising concern for lead malfunction. However, switching to unipolar pacing restored effective capture with normal electrical parameters, suggesting preserved lead integrity and prompting reconsideration of the underlying mechanism. Further diagnostic evaluation, including imaging and intraoperative assessment, was therefore undertaken to clarify the cause and guide management; Conclusions: Early pacing failure should not automatically be equated with lead damage. Beyond documenting a reversible lead–header interface problem, this case highlights the diagnostic value of a stepwise approach integrating pacing configuration behavior, targeted imaging, and intraoperative header-independent testing. Such an approach may facilitate rapid localization of reversible defects and help avoid unnecessary lead revision.

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.

Background and Clinical Significance: Embolization of septal occluder devices after patent foramen ovale (PFO) closure is uncommon but potentially serious, as migrated devices may lodge in the arterial system and require urgent management. Cross-sectional imaging may reveal delayed migration incidentally, and endovascular snare retrieval represents a minimally invasive first-line strategy in stable patients. Case Presentation: An 18-year-old woman presented with acute abdominal pain one month after percutaneous PFO closure performed for preventive purposes in the setting of migraine with visual aura. Contrast-enhanced computed tomography (CT), obtained for suspected intra-abdominal bleeding, demonstrated hemoperitoneum from a hemorrhagic ovarian cyst and incidentally identified the Amplatzer occluder lodged in the infrarenal abdominal aorta with preserved renal artery patency. Transthoracic echocardiography confirmed device absence at the interatrial septum. Endovascular retrieval was performed via right common femoral artery access (5 Fr upsized to 12 Fr) using a 20 mm snare system, with successful removal of the device through the introducer and no intra-procedural complications. Conclusions: Delayed migration of a PFO occluder can be detected incidentally during evaluation for unrelated symptoms. In hemodynamically stable patients, transfemoral endovascular snare capture and re-sheathing through a large-bore introducer can achieve safe and effective device retrieval while preserving aorto-iliac patency.

Reflex bradyarrhythmias and syncope related to excessive vagal tone may be refractory to conservative therapy and significantly impair quality of life. Cardioneuroablation (CNA) has emerged as a device-sparing alternative, but real-world outcome data remain limited. We retrospectively evaluated 12 consecutive patients (aged 23-55 years) with drug-refractory, vagally mediated bradyarrhythmias confirmed by tilt-table testing. All underwent biatrial CNA guided by ultra-high-density electroanatomical mapping with automated fragmented-electrogram detection and robotic magnetic navigation. A contemporaneous cohort of medically managed patients with comparable clinical profiles (n = 10) served as a control group. The primary outcome was freedom from syncope or clinically significant bradyarrhythmia without pacemaker implantation. Secondary outcomes included procedural metrics, heart-rate changes, and recurrence during follow-up. All CNA procedures were completed without acute complications and with minimal fluoroscopy exposure. Resting sinus rate increased substantially after ablation. Over a mean follow-up of approximately 12 months, most CNA-treated patients remained free of symptomatic bradyarrhythmia or syncope without requiring pacemaker implantation, whereas recurrence and pacemaker placement were less frequent compared with controls. No delayed complications were observed. In this small, retrospective real-world cohort, biatrial CNA guided by automated electrogram analysis and robotic navigation was feasible, safe, and associated with short-term autonomic modulation and symptomatic improvement over approximately 12 months of follow-up in selected patients with vagally mediated bradyarrhythmias. These findings are exploratory and warrant confirmation in larger, prospective studies with longer follow-up to assess durability and reinnervation risk.

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 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.

Embolization of intracardiac occlusion devices is an uncommon but potentially serious complication requiring interventional radiology management. We report a case of delayed migration of an Amplatzer patent foramen ovale occluder into the infrarenal abdominal aorta. An 18-year-old woman presented with acute abdominal pain one month after percutaneous PFO closure. Contrast-enhanced computed tomography performed for suspected intra-abdominal bleeding incidentally revealed the embolized device in the infrarenal aorta, with preserved renal artery patency. After multidisciplinary evaluation, endovascular retrieval was planned. Via right common femoral artery access, the device was successfully captured using a snare system and removed through a large-bore introducer sheath without complications. Final angiography confirmed normal aorto-iliac patency. This case highlights the importance of cross-sectional imaging and demonstrates that endovascular snare retrieval is a safe and effective first-line treatment for delayed device embolization.