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.
Background Cardiac remodelling is an adverse phenomenon linked to heart failure progression. Cardiac remodelling could represent the real therapeutic goal in the treatment of patients with heart failure with reduced ejection fraction (HFrEF), being potentially reversed through different pharmacotherapies. Currently, there are well-established drugs such as angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers and β-blockers with anti-remodelling effects; recently, angiotensin receptor neprilysin inhibitor effects on inhibiting cardiac remodelling were demonstrated. Benefits of gliflozins on left ventricular hypertrophy, dilation, and systolic and diastolic function were also described. Aim of study to evaluate possible echocardiographic differences between patients with HFrEF in treatment with ARNI or SGLT2I and patients with HFrEF in therapy with ARNI plus SGLT2i. Materials Between June 2021 and April 2022, consecutive patients with HFrEF underwent to conventional and advanced echocardography (TDI, 2DSTE). After 3 month, these patients underwent to echocardiographic follow-up. Results 76 patients (68 male, 66,51±9,68 years old) with HFrEF were enrolled in the study. After 3 month of therapy, there was an inverse relation between number of HFrEF drugs (0, 1 or 2) and echocardiographic parameters [E/E’ (r: -0,28; p: 0,036) and E/A (r: -0,37; p: 0,012)]. Conclusions About cardiac remodelling, there are not significant echocardiographic differeces but a better trend for the diastolic dysfunction in patients with HFrEF in treatment with ARNI plus SGLT2i vs HFrEF patients in therapy with ARNI or SGLT2i was showed.
Background According to 4th Universal Definition of Myocardial Infarction (MI), it is possible to differentiate clinically type 2 MI (T2MI) from type 1 MI (T1MI) and acute myocardial injury (AMI). However, in many cases this differentiation may be difficult. To date there are poor data that allow to distinguish AMI, T2MI and T1MI from the changes and the absolute or relative values of biomarkers of myocardial necrosis. We sought to compare T2MI vs T1MI and vs AMI in terms of cardiac biomarkers changes. Methods we consecutively enrolled 90 patients (30 with T1MI, 30 with T2MI and 30 with AMI). excluding patients with ST-segment elevation myocardial infarction. The ratio of the peak to the upper limit of normal (RULN) were calculated for both CK-MB and cardiac troponin T (cTnT). Moreover, the ratio of peak cTnT to peak CK-MB was also calculated. Results the ratio peak/RULN for cTnI and CK-MB were significantly higher for T1MI in comparison with T2MI (cTnI 100.8 vs 67.1, p < 0.001; CK-MB 2.1 vs 0.66, p 0.003) while there were not significant differences between T2MI and AMI (T2MI 67.1 vs AMI 47.3., p 0.159; T2MI 0.66 vs AMI 0.39, p 0.052). Interstingly, there was a higher rise of cTnT than CK-MB in type 2 compared with type 1 myocardial infarction, so that the ratio of peak cTnT to peak CK-MB was significantly higher for T1MI in comparison with T2MI (T1MI 196.2 vs AMI 20.5, p 0.008). Conclusions Both cTnT and CK-MB peaks were higher in T1MI than in T2MI. Furthermore, cTnT rises out of proportion to CK-MB in T2MI. These changes may contribute to a better differentiation between T2MI and T1MI.
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