Dilated cardiomyopathy (DCM) is the most common cardiomyopathy worldwide. Over the last few decades, significant progress has been made in understanding the genes responsible for DCM. A large number of variants have been detected, with heterogeneous distribution across the globe. Based on a systematic review of the available data, this review aims to investigate what we actually know about genetic, geographical and ethnic heterogeneity in DCM. What emerged is a disparity in clinical and instrumental valuations across different populations. Given the significant variability in the clinical and molecular presentation of these diseases, there is a need to develop an operational model that integrates technical and molecular diagnostics, imaging, and clinical capabilities tailored to the characteristics of different territories, while accounting for migratory flows and sex differences. By characterising specific genotypes, we could offer targeted therapies or contribute to the development of new care.

Acute myocarditis encompasses a broad clinical spectrum, ranging from mild chest pain with preserved ventricular function to fulminant heart failure, malignant ventricular arrhythmias, cardiogenic shock and sudden cardiac death. Recent advances have shifted its definition from a primarily histopathological entity toward an integrated clinical syndrome in which multimodality imaging, biomarkers and endomyocardial biopsy contribute to diagnosis and risk assessment. Cardiac magnetic resonance has become central to non-invasive tissue characterization while endomyocardial biopsy remains a relevant approach in high-risk or treatment-refractory patients, allowing identification of histological subtypes that may require specific therapy. Management is largely determined by clinical severity and aetiology, ranging from supportive care and guideline-directed heart failure therapy to immunosuppression, targeted antimicrobial treatment and temporary mechanical circulatory support in fulminant cases. Increasing evidence also highlights the relationship between myocarditis-like episodes and inherited cardiomyopathies, particularly desmosomal disease, in which recurrent “hot phases” may represent an early manifestation of a genetic substrate. Based on a structured literature search, this narrative review summarizes current concepts in the classification, diagnosis, complications and management of acute myocarditis with particular emphasis on heart failure and fulminant presentations, risk stratification and genetic susceptibility. Throughout the text, established treatments are kept separate from emerging mechanism-based strategies, which are still supported by limited evidence.

Background: Sodium–glucose cotransporter-2 inhibitors (SGLT2i) improve outcomes in heart failure (HF), but baseline characteristics associated with left ventricular (LV) changes after their initiation in routine practice are incompletely defined. Methods: In this retrospective two-centre study, 101 patients with HF (94 HFrEF, 6 HFmrEF, 1 HFpEF) initiating an SGLT2i underwent echocardiography at baseline and 6 months. For the purposes of this study, LV reverse remodelling was defined as a simultaneous reduction in LV end-diastolic (LVEDV) and end-systolic volume (LVESV); LVESV reductions ≥10% and ≥15% were used as stringent definitions. Associations were explored with Firth logistic regression adjusted for age and baseline LVEF. Death or HF hospitalisation after the 6-month visit was analysed in relation to 6-month changes (landmark analysis). Results: Median LVEF increased from 28.8% at baseline to 31.6% at 6 months, and the medians of individual paired changes in LVEDV and LVESV were −13.0% and −16.3% (all p < 0.001). The operational definition was met by 74 patients (73.3%) and an LVESV reduction ≥15% by 56 (55.4%). Higher BMI and larger baseline LVEDV were associated with LV volume reduction, and lower TAPSE with LVEF response, LVESV reduction ≥15% and NYHA improvement. No statistically significant association was observed between 6-month changes in LVEF or LV volumes and subsequent death or HF hospitalisation; confidence intervals were wide. Conclusions: In this uncontrolled cohort, SGLT2i initiation was followed by modest LV volume reduction and a small LVEF increase. These associations are exploratory and hypothesis-generating.