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Acute myocardial infarction (AMI) remains the leading cause of death worldwide, with myocardial ischemia/reperfusion injury (MIRI) emerging as a significant factor influencing patient outcomes despite timely reperfusion therapy. MIRI refers to paradoxical myocardial damage that occurs upon restoration of coronary blood flow and is driven by complex inflammatory, oxidative, and metabolic mechanisms, which can exacerbate infarct size (IS), contributing to adverse outcomes. This review explores the molecular and cellular pathophysiology of MIRI, emphasizing both its clinical and forensic relevance. The principal mechanisms discussed include oxidative stress and mitochondrial dysfunction, calcium overload and ion homeostasis imbalance, inflammatory responses, with particular focus on the NLRP3 inflammasome and cytokine pathways, and multiple forms of cell death (apoptosis, necroptosis, pyroptosis, and autophagy). Additionally, the authors present original immunohistochemical findings from autopsy cases of patients who suffered ST-segment elevation myocardial infarction (STEMI) and underwent percutaneous coronary intervention (PCI), but subsequently died. These findings underscore that successful reperfusion does not completely prevent delayed complications, like arrhythmias, ventricular fibrillation (VF), and sudden cardiac death (SCD), often caused by secondary MIRI-related mechanisms. Moreover, the case series highlight the diagnostic value of inflammatory markers for pathologists in identifying MIRI as a contributing factor in such fatalities. Finally, immunotherapeutic strategies—including IL-1 and IL-6 inhibitors such as Canakinumab and Tocilizumab—are reviewed for their potential to reduce cardiovascular events and mitigate the effects of MIRI. The review advocates for continued multidisciplinary research aimed at improving our understanding of MIRI, developing effective treatments, and informing forensic investigations of reperfusion-related deaths.

Symptomatic atrial fibrillation (AF) is a common cause of emergency department (ED) referrals. In case of hemodynamic stability, the choice to either perform early cardioversion (pharmacologic or electrical) or to prescribe rate-lowering drugs and differ any attempts to restore sinus rhythm (i.e., wait-and-see approach) has been widely debated. Results of the recent Rate Control versus Electrical Cardioversion Trial 7-Acute Cardioversion versus Wait and See (RACE 7 ACWAS) have been considered a strong argument in favor of the wait-and-see approach. In this debate, we discuss several issues that would support early cardioversion, ranging from patients’ satisfaction and costs to concerns about safety. Furthermore, the wait-and-see approach may translate into a missed opportunity to encourage widespread use of a “pill-in-the-pocket” home treatment: this underused option could allow rapid solving of many AF episodes, potentially avoiding future ED referrals. Our opinion is that a delayed cardioversion may introduce unneeded complications in the straightforward management of a common clinical problem. Therefore, early cardioversion should continue to be the preferred option because of its proven efficacy, safety and convenience.

Mitochondria are central regulators of cardiac homeostasis, integrating energy production, redox balance, calcium handling, and innate immune signaling. In cardiovascular disease (CVD), mitochondrial dysfunction acts as a unifying mechanism connecting oxidative stress, metabolic inflexibility, inflammation, and structural remodeling. Disturbances in mitochondrial quality control—encompassing fusion–fission dynamics, PINK1/Parkin- and receptor-mediated mitophagy, biogenesis, and proteostasis—compromise mitochondrial integrity and amplify cardiomyocyte injury. Excess reactive oxygen species, mitochondrial DNA release, and calcium overload further activate cGAS–STING, NLRP3 inflammasomes, and mPTP-driven cell death pathways, perpetuating maladaptive remodeling. Therapeutic strategies targeting mitochondrial dysfunction have rapidly expanded, ranging from mitochondria-targeted antioxidants (such as MitoQ and SS-31), nutraceuticals, metabolic modulators (SGLT2 inhibitors, metformin), and mitophagy or biogenesis activators to innovative approaches including mtDNA editing, nanocarrier-based delivery, and mitochondrial transplantation. These interventions aim to restore organelle structure, improve bioenergetics, and reestablish balanced quality control networks. This review integrates recent mechanistic insights with emerging translational evidence, outlining how mitochondria function as bioenergetic and inflammatory hubs in CVD. By synthesizing established and next-generation therapeutic strategies, it highlights the potential of precision mitochondrial medicine to reshape the future management of cardiovascular disease.

Background Several novel technologies allowing catheter ablation (CA) with a favorable safety/efficacy profile have been recently developed, but not yet extensively clinically tested in the setting of ventricular tachycardia CA. Methods In this technical report, we overview technical aspects and preclinical/clinical information concerning the application of three novel CA technologies in the ventricular milieu: a pulsed field ablation (PFA) generator (CENTAURI™, Galaxy Medical) to be used with linear, contact force-sensing radiofrequency ablation catheters; a contact force-sensing radiofrequency ablation catheter equipped with six thermocouples and three microelectrodes (QDOT Micro™, Biosense-Webster), allowing high-resolution mapping and temperature-controlled CA; and a flexible and mesh-shaped irrigation tip, contact force-sensing radiofrequency ablation catheter (Tactiflex, Abbott). We also report three challenging VT cases in which CA was performed using these technologies. Results The CENTAURI system was used with the Tacticath™ (Abbott) ablation catheter to perform ventricular PFA in a patient with advanced heart failure, electrical storm, and a deep intramural septal substrate. Microelectrode mapping using QDOT Micro™ helped to refine substrate assessment in a VT patient with congenitally corrected transposition of the great arteries, and allowed the identification of the critical components of the VT circuit, which were successfully ablated. Tactiflex™ was used in two challenging CA cases (one endocardial and one epicardial), allowing acute and mid-term control of VT episodes without adverse events. Conclusion The ideation and development of novel technologies initially intended to treat atrial arrhythmias and successfully implemented in the ventricular milieu is contributing to the progressive improvement in the clinical benefits derived from VT CA, making this procedure key for successful management of increasingly complex patients. Graphical abstract

PurposeTo provide a brief overview of some relevant technological advances in the field of three-dimensional electroanatomical mapping (3D-EAM) that have recently entered the clinical arena and their role in guiding catheter ablation (CA) of complex atrial and ventricular arrhythmias.MethodsIn this technical report, we describe the general features of three novel algorithms featured in the updated CARTO PRIME™ mapping module for CARTO®3 version 7 3D-EAM system (Biosense Webster Inc., Diamond Bar, CA, USA): local activation time (LAT) hybrid, coherent mapping and map replay modules. We also report three challenging arrhythmia cases in which CA was successfully guided by these softwares.ResultsThe LAT hybrid module was used in a case of premature ventricular complex originating from the right coronary cusp. This algorithm facilitated safe positioning of the ablation catheter away from the right coronary ostium, avoiding potential harm to this vital structure. The coherent mapping module helped to identify the critical as well as a bystander isthmus of an atrial macro-re-entrant tachycardia in a grown-up patient with congenital heart disease. The map replay module allowed rapid retrospective activation mapping of two unstable ventricular tachycardias in a case of nonischemic cocaine-associated cardiomyopathy.Conclusion3D-EAM systems offer significant advantages in the management of challenging arrhythmias, and the introduction of novel algorithms underpins improvements in patients’ outcomes. Given the increasing sophistication of these systems, however, a close collaboration among cardiac electrophysiologists, engineers and technicians is highly needed in order to get the best from the available technology.

Myocardial inflammation is an important cause of cardiovascular morbidity and sudden cardiac death in athletes. The relationship between sports practice and myocardial inflammation is complex, and recent data from studies concerning cardiac magnetic resonance imaging and endomyocardial biopsy have substantially added to our understanding of the challenges encountered in the comprehensive care of athletes with myocarditis or inflammatory cardiomyopathy (ICM). In this review, we provide an overview of the current knowledge on the epidemiology, pathophysiology, diagnosis, and treatment of myocarditis, ICM, and myopericarditis/perimyocarditis in athletes, with a special emphasis on arrhythmias, patient-tailored therapies, and sports eligibility issues.

Premature ventricular contractions in the absence of structural heart disease are among the most common arrhythmias in clinical practice, with well-defined sites of origin in the right and left ventricle. In this review, starting from the electrocardiographic localization of premature ventricular contractions, we investigated the mechanisms, prevalence in the general population, diagnostic work-up, prognosis and treatment of premature ventricular contractions, according to current scientific evidence.

The application of cardiac magnetic resonance (CMR) imaging in clinical practice has grown due to technological advancements and expanded clinical indications, highlighting its superior capabilities when compared to echocardiography for the assessment of myocardial tissue. Similarly, the utilization of implantable cardiac electronic devices (CIEDs) has significantly increased in cardiac arrhythmia management, and the requirements of CMR examinations in patients with CIEDs has become more common. However, this type of exam often presents challenges due to safety concerns and image artifacts. Until a few years ago, the presence of CIED was considered an absolute contraindication to CMR. To address these challenges, various technical improvements in CIED technology, like the reduction of the ferromagnetic components, and in CMR examinations, such as the introduction of new sequences, have been developed. Moreover, a rigorous protocol involving multidisciplinary collaboration is recommended for safe CMR examinations in patients with CIEDs, emphasizing risk assessment, careful monitoring during CMR, and post-scan device evaluation. Alternative methods to CMR, such as computed tomography coronary angiography with tissue characterization techniques like dual-energy and photon-counting, offer alternative potential solutions, although their diagnostic accuracy and availability do limit their use. Despite technological advancements, close collaboration and specialized staff training remain crucial for obtaining safe diagnostic CMR images in patients with CIEDs, thus justifying the presence of specialized centers that are equipped to handle these type of exams.

Valve leaflets and chordae structurally normal characterize functional mitral regurgitation (FMR), which in heart failure (HF) setting results from an imbalance between closing and tethering forces secondary to alterations in the left ventricle (LV) and left atrium geometry. In this context, FMR impacts the quality of life and increases mortality. Despite multiple medical and surgical attempts to treat FMR, to date, there is no univocal treatment for many patients. The pathophysiology of FMR is highly complex and involves several underlying mechanisms. Left ventricle dyssynchrony may contribute to FMR onset and worsening and represents an important target for FMR management. In this article, we discuss the mechanisms of FMR and review the potential therapeutic role of CRT, providing a comprehensive review of the available data coming from clinical studies and trials.

Background/Objectives: Excessive trabeculation of the left ventricle, previously known as left ventricular non-compaction (LVNC), is a rare phenotypic trait whose mechanisms and pathogenesis still remain conflictual. Its presentations may range from heart failure to embolism and, most importantly, ventricular arrhythmias (VAs). This study aims to find novel predictive factors for the occurrence of potentially fatal VAs in patients with left ventricular hypertrabeculation. Methods: All consecutive patients meeting the echocardiographic (Chin, Jenny or Stöllberger) and/or MRI criteria (Petersen) for hypertrabeculation were prospectively enrolled from October 2009 to December 2023. The primary outcome was a composite of sudden cardiac death, sustained ventricular tachycardias (sVTs), ventricular fibrillation (VF) or appropriate implantable cardioverter defibrillator (ICD) interventions. The secondary outcome was a composite of cardiovascular death and cardiovascular hospitalizations. Results: Overall, 64 patients (41 males, mean age 46 ± 19 years old) were enrolled and followed for a median time of 2.2 years. Six patients (9.4%) experienced a composite outcome at eight years, three with previous sVTs and three with previous non-sustained VTs (nsVTs). The strongest predictor of the primary endpoint was the anamnesis of nsVTs and sVTs before LVNC diagnosis. In addition, nsVTs and sVTs were significantly associated with the secondary outcome. Conclusions: Hypertrabeculation of the left ventricle is a complex and poorly understood condition whose status of cardiomyopathy is currently challenged. In our population, patients with a trabecular pattern experienced a high incidence of VAs, cardiovascular death and hospitalizations. VAs before LVNC diagnosis were predictive of the outcome independently from systolic function.