Ceftaroline fosamil demonstrated high clinical cure and microbiological response rates in hospitalized patients with CAP of PORT risk class III or IV. Ceftaroline fosamil was well tolerated, with a safety profile similar to that of ceftriaxone and consistent with the cephalosporin class. In this study, ceftaroline fosamil was an effective and well-tolerated treatment option for CAP.

Cancer treatments can have significant cardiovascular adverse effects that can cause cardiomyopathy and heart failure with reduced survival benefit and considerable decrease in the use of antineoplastic therapy. The purpose of this study is to assess the role of TLR2 and TLR4 gene expression as an early marker for the risk of doxorubicin-induced cardiomyopathy in correlation with early diastolic dysfunction in patients treated with doxorubicin. Our study included 25 consecutive patients who received treatment with doxorubicin for hematological malignancies (leukemia, lymphomas or multiple myeloma), aged 18-65 years, with a survival probability>6 months and with left ventricular ejection fraction>50%. Exclusion criteria consisted of the following: previous anthracycline therapy, previous radiotherapy, history of heart failure or chronic renal failure, atrial fibrillation, and pregnancy. In all patients, in fasting state, a blood sample was drawn for the assessment of TLR2 and TLR4 gene expression. Gene expression was assessed by quantitative reverse transcription PCR (qRT-PCR) using blood collection, RNA isolation, cDNA reverse transcription, qRT-PCR and quantification of the relative expression. At enrollment, all patients were evaluated clinically; an ECG and an echocardiography were performed. The average amount of gene expression units was 0.113 for TLR4 (range 0.059-0.753) and 0.218 for TLR2 (range 0.046-0.269). The mean mRNA extracted quantity was 113 571 ng/μl. As for the diastolic function parameters, criteria for diastolic dysfunction were present after 6 months in 16 patients (64%). In these patients, the mean values for TLR4 were 0.1198625 and for TLR2 were 0.16454 gene expression units. As for the diastolic function parameters, criteria for diastolic dysfunction were present after 6 months in 16 patients (64%). In these patients, the mean value for TLR2 was 0.30±0.19 and for TLR4 was 0.15±0.04. The corresponding values for the patients who did not develop diastolic dysfunction were 0.16±0.07 for TLR2 (P=0.01) and 0.11±0.10 for TLR4 (P=0.2). Our study suggests that TLR4 and TLR2 expression is higher in patients under doxorubicin therapy who develop diastolic dysfunction. This may suggest a predisposition to myocardial involvement, a higher sensitivity to doxorubicin cardiac effects.

INTRODUCTION Acute kidney injury (AKI) during hospitalization is associated with increased mortality in patients with acute heart failure (AHF). In 2016, the European Society of Cardiology introduced the category of heart failure (HF) with mid-range ventricular ejection fraction (HFmrEF) as a distinct category from HF with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF). OBJECTIVES The aim of this study was to evaluate in-hospital mortality risk associated with AKI in patients with AHF, with a focus on the HFmrEF group. PATIENTS AND METHODS A total of 365 health records of patients with a primary diagnosis of acute decompensated heart failure (ADHF) were reviewed. AKI was defined according to Acute Kidney Injury Network criteria. HF was diagnosed based on Framingham criteria. Patients with ADHF were evaluated as 3 separate groups, based on ventricular ejection fraction: HFpEF (≥50%), HFmrEF (40%-49%), and HFrEF (<40%). Risk and survival analyses were conducted on de-identified data. RESULTS The AKI-associated in-hospital mortality odds ratios for HFmrEF and HFrEF groups were 4.55 (95% CI, 1.46-14.18) and 2.59 (95% CI, 1.05-6.41), respectively, with a highly significant difference between the groups (P = 0.002; Mantel-Haenszel test). The hazard ratios in the Cox proportional hazards model were 4.79 (95% CI, 1.54-14.96) and 2.94 (95% CI, 1.27-6.80) for HFmrEF and HFrEF groups, respectively. CONCLUSIONS AKI was associated with a higher risk of mortality in patients with HFmrEF when compared with those with HFrEF, suggesting a stronger prognostic impact of AKI in patients with HFmrEF.

Heart failure is a disease affecting millions of patients each year, and is responsible for burdening the world with high mortality rates. More concerns come from its numerous hospital readmissions (with an estimated number of 2.6 million per year which makes it one of the leading diseases responsible for national healthcare expenditures). Despite drastic improvement of therapies in recent years, heart failure remains a progressive disease. Thus, more attention has been given to finding potential biomarkers involved in the pathological mechanisms of this disease that would potentially lead to faster diagnosis and improved prognosis. One of the emerging biomarkers that has just recently come into the spotlight is galectin-3. It was associated in recent clinical trials with both the progression and severity of heart failure. Ventricular remodelling and myocardial fibrosis are essential for heart failure development and are linked to poor outcomes. An ever-growing body of evidence places galectin-3 as an important link between inflammation and fibrosis, which play a prominent role in cardiac remodelling.This review sums up the most relevant experimental and clinical studies about galectin-3 and its potential prognostic value in heart failure. The article also provides a better understanding of this molecule's involvement in heart failure pathology by modulating cardiac fibrosis. It also weighs whether the available data on galectin-3 are consistent enough to reduce readmissions and mortality while improving diagnosis and future therapies for heart failure, versus the possibility that it is simply"another brick in the wall?"