Background Chronic heart failure (CHF) is characterized by endothelial dysfunction (ED). Sodium-glucose cotransporter type 2 inhibitors (SGLT-2i) represent a unique class of anti-hyperglycemic agents for type 2 diabetes mellitus (T2DM) that selectively inhibit renal glucose reabsorption, thereby increasing urinary excretion of glucose. Several studies have demonstrated the cardioprotective effects of SGLT-2i in patients with heart failure (HF), unrelated to its glucosuric effect. Nevertheless, it is unclear whether the benefits of SGLT-2i therapy also rely on the endothelial function in patients with CHF. Aim of the study To evaluate the effect of SGLT-2i on endothelial function through flow-mediated dilatation (FMD) in patients with CHF at baseline and after 3 months. Design and Methods EFI-CHF is a multi-center, prospective study that will evaluate the effect of SGLT-2i on endothelial function in patients with chronic stable heart failure across the left ventricular ejection fraction (LVEF) spectrum. Patients with NYHA class II/III symptoms, eGFR> 25 mL/min/1.73 m2, age >18 years will be enroll. Exclusion criteria are type 1 diabetes mellitus (T1DM), previous amputation surgery, recurrent urinary tract infections. For each patient medical history, clinical and biochemistry data will be collected. Starting treatment with SGLT2 inhibitors will be included. All patients will undergo FMD in an ambulatory setting, at time of enrolment and after 3 months of begin of study. Results The primary endpoint will be the improvement of endothelial function as assessed by FMD. An univariate and multivariate analysis will be performed to search for predictors of improvement of endothelian function. Conclusions The EFI-CHF will determine whether SGLT2i therapy improves endothelian function in patients with CHF starting SGLT2i therapy.

86 years-old man was admitted to our ICCU for chest pain with an ECG diagnosis of atrial fibrillation and inferior STEMI. He had a history of hypertension and ascending aorta aneurysm (48 mm) with no other known cardiovascular risk factor. He reported few episodes of short-duration chest pain in the last days. A fast echocardiogram excluded ascending aorta dissection and pericardial effusion but showed hypokinesia of inferolateral left ventricle wall. Urgent angiography only revealed a moderate stenosis on mid left anterior descending artery associated with slow run-off. No lesions were found on the expected culprit artery. Due to persisting chest pain and patient's history of ascending aorta aneurysm, an urgent Angio CT was performed, but unexpectedly, during the exam, the patient lost consciousness with asistolia. RCP was practised with ROSC. CT scan showed mild pericardial effusion with blushing. A free wall heart rupture was suspected by radiologist. Urgent echocardiogram revealed moderate pericardial effusion with a suggestive colour doppler systolic flow originating from an apparent hole in apical inferolateral left ventricle wall. Rapid hemodynamic failure occurred so pericardiocentesis with amine support and blood transfusions were performed. Heart team excluded urgent surgery due to extremely high operative risk related to patient's age, hemodynamic impairment and poor expected repair durability consequent to acute phase of rupture. ICCU observation was made, with liable hemodynamic stability obtained with norepinephrine infusion. In accordance with patient's family other invasive measurements were not taken. Unfortunately, the patient died the day after. Only few cases of myocardial rupture in myocardial infarction-non obstructive coronary artery disease (MINOCA) are reported in literature. Recurrent chest pain makes plaque complication/embolus resolution a reliable hypothesis. New onset atrial fibrillation might have caused an embolization in coronary artery determining transmural ischaemia, as well as coronary artery plaque rupture/ulceration might have done. Unfortunately, no further exams to exploit the underneath pathological process could be performed: Coronary intravascular ultrasound, optical coherence tomography, Cardiac Magnetic resonance would be a valid help in prognosis and future treatment.

A 65-years old Caucasian woman was referred to the emergency department for chest pain, dyspnoea and high systolic blood pressure. In the previous days she complained a constant state of anxiety and worries due to family troubles. At the admission 12 – lead EKG showed sinus rhythm, ST-T segment depression >1 mm in the lateral and anterior leads (from V2 to V6). Laboratory exams showed elevated values of high sensivity troponin levels (high-sensitive troponin: 41 pg/mL – maximum laboratory cut off value: 12 pg/mL). Bedside echocardiogram showed an LVEF of 40% due to apical hyperkinesis, akynesis of the basal segments and hypokinesis of the mid segments of the left ventricle; a severe double jet MR (Fig.1); a type II diastolic dysfunction (E/A: 1,5; E/e’: 14). Several B lines (> 3) were present in all pulmonary regions assessed by lung POCUS. Cardiac angiography demonstrated non obstructive coronary artery disease. Left ventriculography showed an hyperdynamic apex and severe basal hypokinesis. Clinical and functional status rapidly improved. Daily EKGs were registered with a progressive resolution of the ST-T segment depression. She was discharged on the 7th days and the TTE in pre-discharge showed an LVEF of 60%, without wall motion abnormalities and complete recovery of mitral regurgitation. We report a case of reversible severe mitral regurgitation in a patient with basal ballooning TTS. Mital regurgitation is generally described in the contest of classical apical TTS. The potential mechanisms for severe MR are similar to those of acute myocardial infarction. Admission and daily echocardiographic evaluation is crucial in this subset of patients, with a tailored therapy following the severity of mitral valve disease. Fig. 1