Dilated cardiomyopathy (DCM) represents one of the most common causes of non-ischemic heart failure, characterised by ventricular dilation alongside systolic dysfunction. Despite advances in therapy, DCM mortality rates remain high, and it is one of the leading causes of heart transplantation. It was recently recognised that many patients present minor structural cardiac abnormalities and express different arrhythmogenic phenotypes before overt heart-failure symptoms. This has raised several diagnostic and management challenges, including the differential diagnosis with other phenotypically similar conditions, the identification of patients at increased risk of malignant arrhythmias, and of those who will have a worse response to medical therapy. Recent developments in complementary diagnostic procedures, namely cardiac magnetic resonance and genetic testing, have shed new light on DCM understanding and management. The present review proposes a comprehensive and systematic approach to evaluating DCM, focusing on an improved diagnostic pathway and a structured stratification of arrhythmic risk that incorporates novel imaging modalities and genetic test results, which are critical for guiding clinical decision-making and improving outcomes.

Morphological changes induced by industrial noise (IN) have been experimentally observed in several organs. Histological observations of the coronary arteries showed prominent perivascular tissue and fibrosis among IN-exposed rats. The effects on the small arteries are unknown. Objective: To evaluate the histomorphometric changes induced by IN on rat heart small arteries. Methods: Twenty Wistar rats exposed to IN during a maximum period of seven months and 20 age-matched controls were studied. Hearts were transversely sectioned from ventricular apex to atria and a mid-ventricular fragment was selected for analysis. The histological images were obtained with an optical microscope using 400× magnifications. A total of 634 arterial vessels (298 IN-exposed and 336 controls) were selected. The mean lumen-to-vessel wall (L/W) and mean vessel wall-to-perivascular tissue (W/P) ratios were calculated using image J software. Results: There were no differences between exposed and control animals in their L/W ratios (p = 0.687) and time variations in this ratio were non-significant (p = 0.110). In contrast, exposed animals showed lower W/P ratios than control animals (p < 0.001), with significant time variations (p = 0.004). Conclusions: Industrial noise induced an increase in the perivascular tissue of rat small coronary arteries, with significant development of periarterial fibrosis.

Implantable cardioverter-defibrillators (ICDs) are among the most effective interventions for the prevention of sudden cardiac death. However, traditional transvenous systems are associated with venous access and intracardiac lead complications. Subcutaneous ICDs (S-ICD), which were developed to overcome these complications, are unable to provide anti-tachycardia pacing (ATP) or pause prevention pacing. The extravascular ICD (EV-ICD) is a recent technological innovation designed to mitigate these limitations by enabling cardioversion, defibrillation and pacing without entering the central venous system. Our aim was to assess the initial experience with the new EV-ICD system, as a valid alternative to transvenous ICD and S-ICD, including patient selection, implantation technique, procedure feasibility and safety, functional parameters, and immediate clinical outcomes. We conducted an observational study of all patients who underwent EV-ICD implantation between November 2024 and June 2025 at two centers. Demographic, clinical, imaging, pharmacologic and procedural data were analyzed. A total of 11 patients were included, with a mean age of 36.3 years (range 19-59); 27% were female. Main diagnoses included hypertrophic cardiomyopathy (n=3), left ventricular non-dilated cardiomyopathy (n=3), dilated cardiomyopathy (n=2), Brugada syndrome (n=1), polymorphic ventricular tachycardia (n=1) and arrhythmogenic right ventricular cardiomyopathy (n=1). There were no procedural or peri-procedural complications. The mean procedure duration ("skin-to-skin") was 68.2 minutes (range 60-78). Median fluoroscopy time was 3.9 minutes (range 2.5-6.2). Defibrillation threshold (DFT) testing was successful in all cases. During the follow-up, two patients received an inappropriate shock, one due to sinus tachycardia and the other due to oversensing of myopotentials. Our initial experience with the EV-ICD confirms the feasibility and safety of the procedure. This novel system may offer an effective alternative for selected populations, especially young patients with extended life expectancy and high cumulative device exposure. The rate of inappropriate shocks remains a concern and improvements are required to reduce these events.

Recurrent ventricular tachydisrhythmias (VT) episodes have a negative impact in the outcome of patients (P) already with an implantable cardioverter-defibrillator (ICD). Elimination of arrhythmic reentry circuits represents a difficult challenge, mainly due to the induction of intolerable VTs, with multiple ECG morphologies, requiring rapid interruption. Substrate guided ablation has been used as a promising approach strategy to treat recurrent VTs. Aim: to assess long-term results of a VT substrate-based ablation using high-density mapping in P with an ICD, severe left ventricular (LV) dysfunction and recurrent appropriate ICD therapy. Methods: 16P (12 men, non-ischemic cardiomyopathy 67%, 55 ± 13 years, LV ejection fraction 32 ± 6%) and recurrent appropriate shocks despite antiarrhythmic drug therapy and optimal heart failure medication. All P underwent a protocol of ventricular programmed stimulation (600 ms/S3) to obtain baseline VT documentation. A sinus rhythm (SR) voltage map was created using a 3D electroanatomic mapping system (CARTO) with a high-density mapping catheter (PentaRay) to delineate areas of scarred myocardium (ventricular bipolar voltage ≤0,5 mV – dense scar; 0,5-1,5 mV – border zone; ≥1,5 mV – healthy tissue) and provide high-resolution electrophysiological mapping. The substrate modification included catheter elimination of local abnormal ventricular activities (LAVA) - fractionated, splited, low-amplitude/long-lasting, late potentials, pre-systolic potentials - and linear ablation to obtain scars homogenization and scar dechanneling. Pace-mapping techniques were used when capture was possible. LV approach was retrograde in 6 cases, transeptal in 4 and endo-epicardial in 2 cases. In 2P the ablation was performed in the right ventricle. Results: VTs were induced and interrupted with bursts or external DC shocks. LAVA were identified and ablated in all P. Eleven P underwent modification of scar areas. The mean duration of the procedure was 153 mn (103-218 mn), with radiofrequency ranging from 18 to 60 mn (mean 33 min), and a mean fluoroscopy time of 16 mn. Non-inducibility was achieved in 75% of the cases. There was 1 pericardial tamponade drained successfully. During a follow-up of 48 ± 18 months, 75% had no VT recurrences, 2P underwent redo ablation, 1P died from stroke. Conclusion: Catheter ablation of VT based on substrate modification guided by high-density mapping is feasible and safe in P with LV dysfunction. This approach may be of clinical relevance, with potential benefits in reducing VT burden.