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Mitral regurgitation (MR) is the second most frequent valve heart disease in Europe and its underlying mechanism primary-organic (due to disease of the mitral leaflets), or secondary-functional (where valve leaflets and chordae are structurally normal and MR results from alterations in left ventricle and left atrium geometry), determines the therapeutic approach. Transcatheter Edge-to-Edge Repair (TEER) with MitraClip implantation is a minimal-invasive treatment that according to 2021 ESC Guidelines should be considered (class of recomandation IIa) in selected symptomatic patients with severe MR despite optimal medical therapy, not eligible for surgery and fulfilling COAPT trial inclusion criteria, suggesting an increased chance of responding to treatment. Optimal valve morphology features for TEER are central pathology (second scallop), no leaflet calcifications, mitral valve area >4cm2, mobile length of posterior leaftel >10 mm, coaptation depth

Severe tricuspid valve (TV) regurgitation (TR) has been associated with adverse long-term outcomes in several natural history studies, but isolated TV surgery presents high mortality and morbidity rates. Transcatheter tricuspid valve interventions (TTVI) therefore represent a promising field and may currently be considered in patients with severe secondary TR that have a prohibitive surgical risk. Tricuspid transcatheter edge-to-edge repair (T-TEER) represents one of the most frequently used TTVI options. Accurate imaging of the tricuspid valve (TV) apparatus is crucial for T-TEER preprocedural planning, in order to select the right candidates, and is also fundamental for intraprocedural guidance and post-procedural follow-up. Although transesophageal echocardiography represents the main imaging modality, we describe the utility and additional value of other imaging modalities such as cardiac CT and MRI, intracardiac echocardiography, fluoroscopy, and fusion imaging to assist T-TEER. Developments in the field of 3D printing, computational models, and artificial intelligence hold great promise in improving the assessment and management of patients with valvular heart disease.

Left ventricular noncompaction (LVNC) is a rare congenital cardiomyopathy thought to be caused by arrest of normal endomyocardial morphogenesis. A 33-year-old male, smoker, dyslipidemic not on medical therapy, with family history for sudden cardiac death (SCD) presented to the ER for chest pain radiated to the left arm, unrelated to exertion. The physical examination was within normal limits. Blood tests showed increased cardiac enzymes levels (Troponin I hs 49 308.7 ng/l). The EKG showed STE in the anterior leads and diffuse ventricular repolarization anomalies, suggestive of anterior STEMI. The patient underwent coronary catheterization, with evidence of anomalous origin of the Cx from the RCA and critical stenosis on the proximal LAD, treated with PPCI and implantation of a DES with good angiographic result. The patient was transferred to the Cardiac Intensive Care Unit. TTE showed moderate LV dilatation, severe LV dysfunction (EF 30%) with apical, septal and anterior wall akinesis, and lateral wall hypertrabecularization with multiple prominent trabeculations and deep intertrabecular recesses communicating with the cavity, suggestive for LVNC. Cardiac MRI documented dilated LV with EF 34%, anterior and antero-septal wall akinesis (associated with increased T1 mapping values and areas of LGE after contrast injection, compatible with ischaemic outcomes), infero-lateral wall hypokinesia and LV free wall marked hypertrabecularization with a ratio of not compacted(T)/compacted(M) myocardium of 5 (Petersen criteria for LVNC diagnosis: T/M > 2.3 in telediastolic long-axis view). The patient was discharged in stable clinical conditions in DAPT(Cardioaspirin and Ticagrelor). At two months cardiologic follow-up the patient was asymptomatic and TTE confirmed a dilated LV with severely depressed EF (30%). In consideration of the post-ischaemic dilated cardiomyopathy with severely depressed EF and of the family history of SCD (father deceased at 54-years-old), the patient was admitted in our Cardiology Unit and he underwent subcutaneous ICD (sICD) implantation. He was discharged in stable conditions with remote home monitoring transmitter. The association between LVNC and anomalous coronary artery origin is rare. LVNC is sometimes associated with coronary artery disease, but only rare cases of acute myocardial infarction have been described in literature, with exceptionally rare cases of LVNC incidental diagnosis after STEMI. To the best of our knowledge, this is the first case of LVNC associated with anomalous coronary artery origin and STEMI reported in literature. Some authors hypothesized that a single gene responsible for both myocardial development and coronary endothelium could be involved in the pathogenesis of LVNC and at the same time predispose to coronary atherosclerosis. Further studies are necessary in order to assess the possible pathophysiological mechanisms that correlate LVNC and coronary atherosclerosis. According to European guidelines, LVNC in the absence of additional risk factors is not an indication for primary ICD implantation, and for arrhythmic risk stratification it’s recommended to follow the criteria used for non-ischaemic dilated cardiomyopathy. The anomalous origin of the Cx from the RCA has an incidence of 0.37%, and it is generally not linked to an increased risk of SCD. Involvement of RV in LVNC cannot be excluded even when RV appears normal on CMR, and if involved there is higher risk of perforation by the lead. sICD overcomes disadvantages of transvenous ICD in patients without a need for pacing therapy. In literature use of sICD is reported only in 14 patients with LVNC, mainly children and young adults.

Diabetes mellitus (DM) is a glucose metabolism disorder characterized by chronic hyperglycemia resulting from a deficit of insulin production and/or action. DM affects more than 1 in 10 adults, and it is associated with an increased risk of cardiovascular morbidity and mortality. Cardiovascular disease (CVD) accounts for two thirds of the overall deaths in diabetic patients, with coronary artery disease (CAD) and ischemic cardiomyopathy as the main contributors. Hyperglycemic damage on vascular endothelial cells leading to endothelial dysfunction represents the main initiating factor in the pathogenesis of diabetic vascular complications; however, the underlying pathophysiological mechanisms are still not entirely understood. This review addresses the current knowledge on the pathophysiological links between DM and CAD with a focus on the role of epigenetic modifications, including DNA methylation, histone modifications and noncoding RNA control. Increased knowledge of epigenetic mechanisms has contributed to the development of new pharmacological treatments (“epidrugs”) with epigenetic targets, although these approaches present several challenges. Specific epigenetic biomarkers may also be used to predict or detect the development and progression of diabetes complications. Further studies on diabetes and CAD epigenetics are needed in order to identify possible new therapeutic targets and advance personalized medicine with the prediction of individual drug responses and minimization of adverse effects.

Left ventricular non-compaction (LVNC) is a rare congenital cardiomyopathy caused by arrest of normal endomyocardial embryogenesis and characterized by the persistence of ventricular hypertrabeculation, isolated or associated to other congenital defects. A 33-year-old male, with family history of sudden cardiac death (SCD), presented to our ER with typical chest pain and was diagnosed with anterior STEMI. Coronary angiography showed an anomalous origin of the circumflex artery from the right coronary artery and a critical stenosis on the proximal left anterior descending artery, treated with primary percutaneous coronary intervention. The echocardiogram documented left ventricular severe dysfunction with lateral wall hypertrabeculation, strongly suggestive for non-compaction, confirmed by cardiac MRI. At 3 months follow up, for the persistence of the severely depressed EF (30%) and the family history for SCD, the patient underwent subcutaneous ICD (sICD) implantation for primary prevention. To the best of our knowledge, this is the first case of LVNC associated with anomalous coronary artery origin and STEMI reported in the literature. Arrhythmias are common in LVNC due to endocardial hypoperfusion and fibrosis. sICD overcomes the risks of transvenous ICD, and it is a valuable option when there is no need for pacing therapy for bradycardia, cardiac resynchronization therapy and anti-tachycardia pacing.