Ricerc@Sapienza

Early risk stratification for complications and death related to Coronavirus disease 2019 (COVID-19) infection is needed. Because many patients with COVID-19 who developed acute respiratory distress syndrome have diffuse alveolar inflammatory damage associated with microvessel thrombosis, we aimed to investigate a common clinical tool, the CHA(2)DS(2)-VASc, to aid in the prognostication of outcomes for COVID-19 patients.

BACKGROUND:
Obesity has been suggested to confer a survival benefit in acute heart failure. The concentrations of NT-proBNP may be reduced in patients with high body mass index (BMI).

OBJECTIVES:
To investigate the relationship among BMI, NT-proBNP, and mortality risk in decompensated chronic heart failure (DCHF).

METHODS:
This was a retrospective study. We studied 1001 patients with DCHF. Hazard ratios (HR) were calculated with Cox regression analysis.

Many patients with acute heart failure are initially managed in emergency departments (EDs) worldwide. Although some require hospitalization for further management, it is likely that a sizeable proportion could be safely discharged either directly from the ED or after a more extended period of management in an observation-type unit. Identification of low-risk patients who are safe for such an approach to management continues to be a global unmet need.

If sST2 indeed turns into the HbA1c of heart failure, its value should increase exponentially in our management of patients with heart failure. Serial sST2 levels should allow us to titrate therapy and monitor
the clinical state of the patient. In addition, since sST2 is such a strong marker of the risk of death, it would not be surprising to see a level be used to make decisions when patients are on the cusp of such
therapies as ICD, CRT, CardioMems implantation and even left ventricular assist devices.

Background: An altered IL-18 pathway in heart failure (HF) has recently been described and this cytokine was shown tobe of clinical and prognostic utility. Cardiomyocytes are a target of this cytokine which exerts inflammatory, hypertrophic,and profibrotic activities. B-type natriuretic peptide is a cardiac hormone produced in response to cardiac filling to regulatecardiovascular homeostasis.

Stem cell therapy is a regenerative medicine technique consisting in
introducing new cells into a damaged tissue in order to restore it. In this paper we
present our multidisciplinary approach about the possible use of the Human
Mesenchymal Stem Cells in treating heart failure. A multidisciplinary team
composed by biologists, mathematicians, cardiologists and bioengineers was
selected in order to investigate the feasibility of repairing the necrotic tissue
damaged by myocardial infarction by means of Mesenchymal Stem Cells and to

AIMS: Recent studies reported that cAMP-binding protein Epac1-deficient mice were protected against various forms of cardiac stress, suggesting that pharmacological inhibition of Epac1 could be beneficial for the treatment of cardiac diseases. To test this assumption, we characterized an Epac1-selective inhibitory compound and investigated its potential cardioprotective properties. METHODS AND RESULTS: We used the Epac1-BRET (bioluminescence resonance energy transfer) for searching for non-cyclic nucleotide Epac1 modulators.

Background Glycosphingolipid accumulation in Fabry cells generates a proinflammatory response that may influence disease evolution and responsiveness to enzyme replacement therapy. This study evaluated incidence, mechanism, and impact of myocarditis in Fabry disease cardiomyopathy ( FDCM ).

The effects of empagliflozin on cardiorespiratory fitness in patients with type 2 diabetes mellitus (T2DM) and heart failure with reduced ejection fraction (HFrEF) are unknown. In this pilot study we determined the effects of empagliflozin 10 mg/d for 4 weeks on peak oxygen consumption (VO2 ) in 15 patients with T2DM and HFrEF. As an exploratory analysis, we assessed whether there was an interaction of the effects of empagliflozin on peak VO2 of loop diuretics.

Rationale: Cardiotoxic β1 adrenergic receptor (β1AR)-CaMKII signaling is a major and critical feature associated with development of heart failure. Synapse-associated protein 97 (SAP97) is a multi-functional scaffold protein that binds directly to the C-terminus of β1AR and organizes a receptor signalosome.

Objective: We aim to elucidate the dynamics of β1AR-SAP97 signalosome and its potential role in chronic cardiotoxic β1AR-CaMKII signaling that contributes to development of heart failure.