Heart failure with preserved ejection fraction (HFpEF) is a common clinical syndrome frequently seen in elderly patients, the incidence of which is steadily increasing due to an ageing population and the increasing incidence of diseases, such as diabetes, hypertension, obesity, chronic renal failure, and so on. It is a multifactorial disease with different phenotypic aspects that share left ventricular diastolic dysfunction, and is the cause of about 50% of hospitalizations for heart failure in the Western world. Due to the complexity of the disease, no specific therapies have been identified for a long time. Sodium-Glucose Co-Transporter 2 Inhibitors (SGLT2-Is) and Glucagon-Like Peptide Receptor Agonists (GLP-1 RAs) are antidiabetic drugs that have been shown to positively affect heart and kidney diseases. For SGLT2-Is, there are precise data on their potential benefits in heart failure with reduced ejection fraction (HFrEF) as well as in HFpEF; however, insufficient evidence is available for GLP-1 RAs. This review addresses the current knowledge on the cardiac effects and potential benefits of combined therapy with SGLT2-Is and GLP-1RAs in patients with HFpEF.

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.

Iatrogenic atrial septal defect (iASD) represents one of the main access-related cardiac complications after trancatheter edge to edge (TEER) mitral valve repair with Mitraclip system. Transesophageal echocardiography (TEE) guiding supports a controlled and safe transseptal puncture. The rate of persistent iASD is 57, 50, and 25% after 1, 6, and 12 months post procedure. An elevated left atrial pressure after clip positioning correlates with iASD persistence. Its clinical impact is controversially discussed: Post-TEER iASD has been associated with right heart volume overload, as well as increased rates of heart failure (HF) hospitalization and death in some studies. In contrast, other studies have shown an association between post-TEER iASD and improved hemodynamics. In theory, creation of an iASD can decompress an overloaded left atrium, mitigating heart failure. Some studies have demonstrated that iASD closure can reduce significantly both right and left heart failure symptoms. We did a retrospective study enrolling in the period 2012-2022 twenty-one patients with severe mitral regurgitation treated with TEER. Our aim was to evaluate the clinical outcomes (symptoms, signs of heart failure, NYHA functional class) and echocardiographic parameters (PAPs, TAPSE, Right Atrium Area) in two group of patients: Group A underwent iASD closure during the TEER and Group B after one month following the TEER. At 1-month follow-up all patients with repaired mitral regurgitation showed an improvement in the NYHA class (from IV-III to II-I) and no need for re-hospitalization with no significant differences between two groups. In the Group A there were two adverse events during the recovery (2 major bleeding); while there were no adverse events in patients undergoing iASD closure after wise. There was 1 death in the first month after the procedure in group A, while there wasn't any in group B. Statistical analysis showed no significant differences in terms of NYHA class improvement in the two groups (p=0.91). We observed a greater reduction in PAPs in patients going to encounter intraprocedural DIA closure which was found to be statistically significant (p=0.01). Regarding TAPSE, there was a difference in terms of improvement which was found to be greater in the group A. However, this finding was not found to be statistically significant. We also assessed the right atrium area: in group A, we registered a mean preprocedural value of 28 cmq and a postprocedural value of 34 cmq; in group B the values were 20 cmq and 24 cmq, respectively, with a nonstatistically significant difference in terms of atrial enlargement post device placement. In conclusion, we can assume that the improvements in symptomatology are not closely related to iASD closure. However, it must considered that patients in group A had more unfavorable echocardiographic values before the procedure than those in group B, and probably, if we had not closed the iASD immediately during the procedure, these patients would have had worse symptomatology. Therefore, targeted patient selection is essential.

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 <11mm, normal leaflet strength and mobility, flail width <15 mm, flail gap <10 mm. TEER may be considered (class IIb) only in selected cases when the COAPT criteria are not fulfilled with the aim of improving symptoms and quality of life. MR occurs during systole, that at normal heart rates represents 30-50% of the cardiac cycle. As such, marked left atrial (LA) pressure elevation is present only transiently, representing less of a drive to development of secondary pulmonary hypertension compared to chronic LA pressure elevation seen in severe mitral stenosis. Anyway, in patients with severe MR echocardiography often reveals elevated systolic pulmonary artery pressure (PAPs) and MitraClip implantation usually is associated with a slight increase of the trans-mitral gradient with possible repercussions on pulmonary pressures. To better describe the effect of MitraClip implantation on pulmonary pressures and clinical outcomes we did a retrospective study enrolling in the period 2012-2022 thirty-six patients with severe mitral regurgitation treated with TEER. Compared to the last year presentation, we add eleven patients. The target was still to evaluate the clinical outcomes (symptoms, signs of heart failure, NYHA functional class) and the pulmonary pressures assessed by an echocardiographic examination before and after the intervention. At 6-month follow-up we observed in all patients with repaired mitral regurgitation an improvement in the NYHA class (from IV to II) without re-hospitalization. In addition we notice a more pronounced trend in the reduction of the mean sistolic pulmonary arterial pressure, estimated at around 2.86 mmHg ± 14 mmHg (p 0.24, 95% C.I. -7.69 to 1.94) with an unchanged left ventricle ejection fraction. Moreover, the echocardiographic exam showed a normalization of the S and D waves pattern in the pulmonary veins at the PW Doppler evaluation. These new data reinforced the idea that the clinical improvement and the reduction of dyspnea in these patients underwent TEER is related to a reduction of pressures in the pulmonary circulation regardless of the ejection fraction. This finding could be used as a tool that the cardiologist has to evaluate in the echocardiography lab to reveal a new mitral valve disfunction. Despite the addition of the new patients, the sample is still relatively small. However, considering the improvement of the results with the enlargement of the sample, the goal is to enroll additional patients to make the study even more meaningful.

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.