Hypertrophic cardiomyopathy (HCM) is a cardiac muscle disorder characterized by generally asymmetric abnormal hypertrophy of the left ventricle without abnormal loading conditions (such as hypertension or valvular heart disease) accounting for the left ventricular wall thickness or mass. The incidence of sudden cardiac death (SCD) in HCM patients is about 1% yearly in adults, but it is far higher in adolescence. HCM is the most frequent cause of death in athletes in the Unites States of America. HCM is an autosomal-dominant genetic cardiomyopathy, and mutations in the genes encoding sarcomeric proteins are identified in 30–60% of cases. The presence of this genetic mutation carries more than 2-fold increased risk for all outcomes, including ventricular arrhythmias. Genetic and myocardial substrate, including fibrosis and intraventricular dispersion of conduction, ventricular hypertrophy and microvascular ischemia, increased myofilament calcium sensitivity and abnormal calcium handling, all play a role as arrhythmogenic determinants. Cardiac imaging studies provide important information for risk stratification. Transthoracic echocardiography can be helpful to evaluate left ventricular (LV) wall thickness, LV outflow-tract gradient and left atrial size. Additionally, cardiac magnetic resonance can evaluate the prevalence of late gadolinium enhancement, which when higher than 15% of LV mass is a prognostic maker of SCD. Age, family history of SCD, syncope and non-sustained ventricular tachycardia at Holter ECG have also been validated as independent prognostic markers of SCD. Arrhythmic risk stratification in HCM requires careful evaluation of several clinical aspects. Symptoms combined with electrocardiogram, cardiac imaging tools and genetic counselling are the modern cornerstone for proper risk stratification.

Cardiac remodeling is an adverse phenomenon linked to heart failure (HF) progression. Cardiac remodeling could represent the real therapeutic goal in the treatment of patients with HF and reduced ejection fraction (HFrEF), being potentially reversed through different pharmacotherapies. Currently, there are well-established drugs such as ACEi/ARBs and β-blockers with anti-remodeling effects. More recently, ARNI effects on cardiac remodeling were also demonstrated; additional potential benefits of gliflozins remain non clearly demonstrated. To evaluate possible changes in cardiac remodeling in patients with HFrEF/HFmrEF in treatment with ARNI or ARNI plus SGLT2i and the potential benefit on cardiac remodeling of adding SGLT2i to ARNI. Between June 2021 and August 2023, 100 consecutive patients with HFrEF/HFmrEF underwent conventional and advanced echocardiography (TDI, 2DSTE): patients were therefore divided into three groups according to therapy with neither ARNI nor SGLT2i, just ARNI or both. After 3 months, all patients underwent echocardiographic follow-up. After a 3 months of therapy, significant improvements were observed for LVEF, LVEDD, LVEDV, LVESV, LV mass, E/e', LV GLS, TAPSE (ANOVA p< 0.01 in all cases), RV S' velocity (ANOVA p< 0.001).The trend in favor of additional treatment with SGTL2i over ARNI remained statistically significant even after multivariable analysis (p< 0.001 for LVEF, LVEDD; p< 0.01 for LV GLS, TAPSE, TRVS; p< 0.05 for LV mass). SGLT2i therapy when added to the standard treatment for HFrEF and HFmrEF is associated with an improved biventricular function and ventricular dimensions at follow-up.

Takotsubo Syndrome (TTS) is a transient left ventricular systolic dysfunction that mimics acute coronary syndrome (ACS) with unclear pathophysiology. This study aims to evaluate blood cell subtypes in TTS and ACS on admission and their impact on outcome. Admission hemograms of 466 consecutive TTS patients from the German Italian Spanish (GEIST) registry were recorded and, after propensity matching, compared with admission hemograms of 280 ACS patients. Hemogram parameters, including neutrophil lymphocyte ratio (NLR) and lymphocyte monocyte ratio (LMR), were recorded. The primary endpoint was long-term all-cause mortality; the secondary endpoint was in-hospital complications (hemodynamic or electrical instability). Higher monocyte levels and lower LMR were found in TTS compared with ACS patients (0.63 ± 0.3 vs 0.51 ± 0.24 10³/μL, p < 0.001; 2.7 (IQR 1.8-3.9) vs 3.2 (IQR 2.2-4.4), p < 0.01). One hundred thirty-three out of 466 (28.5 %) TTS patients experienced in-hospital complications. In multivariate analysis, LVEF (OR 0.92, 95 %CI 0.90-0.95, p < 0.001), physical triggers (OR 2.59, 95 %CI 1.47-4.55, p < 0.01), and NLR (OR 1.06, 95 %CI 1.03-1.09, p < 0.001) were independently associated with in-hospital complications. At multivariate analysis, including age, gender, physical trigger, admission LVEF, hemoglobin levels and NLR (model 1) or LMR (model 2), NLR (OR 1.02, 95 %CI 1.01-1.03, p < 0.01) or LMR (OR = 0.89, 95 %CI 0.81-0.99, p < 0.04) were independent predictors of long-term mortality. NLR levels above the median value and LMR levels below the median value were associated with poor survival in TTS patients (log-rank p < 0.01). TTS is featured by higher levels of monocytes and lower LMR than ACS during hospital admission. NLR and LMR are independent predictors of long-term mortality in TTS.