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Atomically dispersed iron sites within N-enriched C-networks are promising low-cost catalytic materials for electrochemical applications. At odds with their often-outstanding performance in challenging electrocatalytic processes (i.e. oxygen reduction reaction, ORR) their fabrication strategy frequently relies on trial-and-error approaches. Moreover, the complex chemical nature of these hybrids is often dictated by the use of highly aggressive etching/doping thermo-chemical treatments. Therefore, the development of simplified chemical protocols based on cheap and abundant raw materials ensuring highly reproducible synthetic paths with the prevalent generation of discrete single-atom sites in a definite coordination environment remains a challenging issue to be properly addressed. In this contribution, the synthesis of hierarchically porous and N-enriched C-networks prevalently containing Cl-FeN4 sites is proposed. The outlined procedure takes advantage of citrate ions as carriers for N-sites and a sacrificial C-source for the synthesis of N/C matrices. At the same time, the chelating character of citrate polyions fosters the complexation of transition metals for their ultimate atomic dispersion in C/N matrices. The procedure is finally adapted to the use of common inorganic hard templates and porogens for the control of the material morphology. Avoiding any thermo-chemical etching/doping phase, the as-prepared catalytic material has shown remarkably high ORR performance in an alkaline environment. With a half-wave potential (E1/2) of 0.88 V, a kinetic current density up to 109.6 A g-1 (normalized to the catalyst loading at 0.8 V vs. RHE) and outstanding stability, it largely outperforms commercial Pt/C catalysts and certainly ranks among the most performing ORR Fe-single-atom-catalysts (Fe-SACs) reported so far.

Takotsubo cardiomyopathy, also known as transient left ventricular apical ballooning syndrome, is a cardiac syndrome mimicking an acute coronary syndrome and characterized by peculiar transient left ventricular wall motion in the absence of significant coronary lesions at coronary angiography. The pathogenic mechanisms linking emotional stress to Takotsubo cardiomyopathy still remain undefined. The onset of Takotsubo cardiomyopathy can be triggered by an acute, intense emotional stress. This is the first report reporting that not only negative stress but also positive stressful event may precede the syndrome.

AIM: The aim of the present study was to compare the semi-automatic measurement of carotid intima thickness (RFQIMT - Esaote, Italy), with the conventional method. METHODS: We enrolle 81 patients, mean age 46 years ±15, with no history of cardio-cerebrovascular events and we assessed the traditional cardiovascular risk factors. We examined the IMT of the common carotid artery with manual and RFQIMT method (based on the "Radio Frequency" signal), according to the ASE protocol. RESULTS: Semi-automatic measurement was on average lower than manual measurement (617 μm ±191 vs. 676 μm ± 222) with a statistically significant difference (P

Objective. The aim of our study was to evaluate the clinical utility and prognostic significance of a cluster of 27 serum cytokines for risk stratification after myocardial infarction. Materials and Methods. We enrolled 33 consecutive patients admitted to our institution for acute myocardial infarction and prospectively followed. We evaluated traditional cardiovascular risk factors and assayed, during the acute phase, 27 serum cytokines (IL-1, IL-1ra, IL-2, IL-4, IL-5, IL-6, IL -7, IL-8, IL-9, IL-10, IL-12, IL-13, IL-15, IL-17, EOTAXIN, FGF, G-CSF, GM-CSF, IFN-γ, IP-10, MCP-1, MIP-1α, MIP-1ß, PDGF, RANTES, TNF-α, VEGF) potentially associated with cardiovascular risk. Patients were divided into two groups during follow-up according to the occurrence or absence of adverse cardiovascular events (recurrence of angina, re-infarction, death, need of new revascularization, occurrence of heart failure). We developed an additive risk score by assigning one point for each cytokine that had a value greater than the median value (range 0-27). Cytokines alone and the cytokines score were related to cardiovascular events. Results. Patients with and without major adverse cardiovascular events (MACEs) at follow up had a homogenous distribution of the main cardiovascular risk factors; differences were detected only for sex and age. Patients who experienced MACE had a significantly different distribution of I troponin (p=0.036), IL-8 (p=0.006), IL-13 (p=0.06), IL-10 (p=0.02), IL-17 (p=0.015), IP-10 (p=0.02), MIP-1ß (p=0.05). At univariate analysis, IL -8 (p=0.046 OR 1.13), IL-10 (p=0.05 OR 1.14) and MIP-1ß (p=0.016, OR 1.02) were significantly associated with the occurrence of MACE. This association was not confirmed at multivariate analysis. At the analysis of variance, a higher score was significantly associated with the occurrence of adverse events at follow up (F=5.07, p=0.03). At ROC curve analysis, a score greater than 13 better predicted the occurrence of adverse events at follow-up ( AUC 0.72, p=0.03, sensibility 59.1%, specificity 81.8%). Conclusions. In our study we did not identify a single inflammatory cytokine able to predict adverse events in a long term follow up, whereas the presence of more than 13 cytokines above the median value was useful for risk stratification.

Introduction: Hyperuricemia is a cardiovascular risk factor associated with oxidative stress and inflammation, conditions that are involved in the genesis of atherosclerotic disease and in the progression of ischemic heart disease to heart failure. The aim of our retrospective study is to evaluate the variations of serum uric acid level in patients with ventricular dysfunction, in order to highlight any correlations. Methods: We enrolled 118 patients. In our population we identified three groups: patients with systolic and diastolic dysfunction (ejection fraction A wave, n = 54). All patients underwent echocardiography and laboratory test (VES, PCR and serum uric acid). Results: Patients with diastolic dysfunction with or without systolic dysfunction showed higher values of serum uric acid than patients with normal ventricular function (6.54 ± 0.72 vs. 5.42 ± 0.78, p = 0.016). The linear regression in the group of patients with systolic dysfunction, showed a inverse relationship between the two variables analyzed, so with increasing serum uric acid there is a proportional reduction of the ejection fraction. Conclusions: Patients with isolated left ventricular diastolic dysfunction and patients with systolic and diastolic dysfunction had higher uric acid levels than patients with normal ventricular function and the progressive deterioration of systolic function correlates with a gradual increase in the values of serum uric acid.

High-quality chest compressions are pivotal to improve survival from cardiac arrest. Basic life support training of school students is an international priority. The aim of this trial was to assess the effectiveness of a real-time training software (Laerdal QCPR®) compared to a standard instructor-based feedback for chest compressions acquisition in secondary school students. After an interactive frontal lesson about basic life support and high quality chest compressions, 144 students were randomized to two types of chest compressions training: 1) using Laerdal QCPR® (QCPR group– 72 students) for real-time feedback during chest compressions with the guide of an instructor who considered software data for students’ correction 2) based on standard instructor-based feedback (SF group– 72 students). Both groups had a minimum of a 2-minute chest compressions training session. Students were required to reach a minimum technical skill level before the evaluation. We evaluated all students at 7 days from the training with a 2-minute chest compressions session. The primary outcome was the compression score, which is an overall measure of chest compressions quality calculated by the software expressed as percentage. 125 students were present at the evaluation session (60 from QCPR group and 65 from SF group). Students in QCPR group had a significantly higher compression score (median 90%, IQR 81.9–96.0) compared to SF group (median 67%, IQR 27.7–87.5), p = 0.0003. Students in QCPR group performed significantly higher percentage of fully released chest compressions (71% [IQR 24.5–99.0] vs 24% [IQR 2.5–88.2]; p = 0.005) and better chest compression rate (117.5/min [IQR 106–123.5] vs 125/min [115–135.2]; p = 0.001). In secondary school students, a training for chest compressions based on a real-time feedback software (Laerdal QCPR®) guided by an instructor is superior to instructor-based feedback training in terms of chest compression technical skill acquisition. Trial Registration: Australian New Zealand Clinical Trials Registry ACTRN12616000383460

The use of noninvasive ventilation (NIV) has increased significantly in patients with acute respiratory failure (ARF) in order to prevent tracheal intubation and its complications. Unfortunately, NIV failure represents a frequent event, with rates that in some cases reach 40%. Mask intolerance, agitation, and delirium may lead to NIV failure, thus requiring endotracheal intubation. NIV failure rates are higher in patients without chronic obstructive pulmonary disease (COPD), and, when used in acute hypoxemic failure, its failure is associated with an increased mortality rate. The practice of sedation during NIV could be a valuable option for patients at risk of intubation. Sedation may decrease patient's discomfort and agitation which is often related to mask intolerance, without significant effects on respiratory drive, respiratory frequency, or hemodynamics. Sedation may also reduce transpulmonary pressure and the associated risk of exposing the patient to high tidal volume hence preventing ventilator-induced lung injury (VILI).

AIMS: The aim of our study was to evaluate the relationship between insulin resistance and the detection of precocious echocardiographic signs of heart failure in patients with cardiovascular risk factors. METHODS: We enrolled 34 consecutive patients with cardiovascular risk factors. All patients underwent coronary angiography, echocardiography, and laboratory tests. Exclusion criteria were diabetes (fasting glucose greater than 126 mg/dl or treatment with insulin or oral hypoglycemic agents), coronary artery disease, creatinine above 1.5 mg/dl, left-ventricular hypertrophy, valvular heart disease, ejection fraction below 50%, atrial fibrillation, or other severe arrhythmia. The presence of insulin resistance was assessed by using the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). Ventricular function was investigated by echocardiography. RESULTS: Distinguishing patients with insulin resistance, based on the median value of HOMA-IR (4.06), we observed that in the group with higher levels of HOMA-IR, there were echocardiographic signs of subclinical ventricular dysfunction statistically more frequent (E/A in group with HOMA 4.06: 0.87 + 0.29, P = 0.0136; E/E': 6.42 + 4 vs. 15.52 + 3.26, P = 0.001; Tei index: 0.393 + 0.088 vs. 0.489 + 0.079, P = 0.0029; S wave: 0112 + 0.015 vs. 0.114 + 0.027, P = 0.0001; ejection fraction 59.11 + 4.75 vs. 58.88 + 6.81, P = 0.9078). Grade II diastolic dysfunction was observed in 5 patients, grade I in 12 patients, and 17 patients had normal diastolic function. On multivariate analysis, HOMA-IR (P = 0.0092), hypertension (P = 0.0287), waist circumference (P = 0.0009), high-density lipoprotein (P = 0.0004), and fasting blood glucose (P = 0.0003) were variables independently associated with diastolic dysfunction. On analysis of covariance, we found that the variables that influence diastolic dysfunction are HOMA-IR, waist circumference, BMI, and age, and that the only variable that influences Tei index is HOMA-IR. CONCLUSION: Insulin resistance is frequently associated with subclinical left-ventricular dysfunction. Patients with cardiovascular risk factors and increased HOMA-IR levels, although without diabetes mellitus, overt coronary artery disease, or hypertensive cardiomyopathy, may represent a target population for screening programs, recommended changes in lifestyle, and possibly the use of pharmacological interventions to prevent the onset of heart failure.