How to improve performance and prevent burnout in safety representatives

Background:The present work is part of a greater research project, aimed to examine Safety Representatives’ (SRs) role, twenty years after the appointment of this figure.Objectives:The study aims to investigate the role of some personal and organizational dimensions in the promotion of SRs’ well-being, in terms of reducing burnout and improving performance.Methods:The study involved 455 SRs operating in North East Italy. They completed a self-report questionnaire, regarding conflicts with co-workers, ethical conflict, training satisfaction, work engagement, performance, and burnout.Results:Structural equation models show that work engagement partially mediates (γ=-0.52, p<0.001; β=0.23, p<0.01) the relationship between conflict with co-workers and performance (γ=-0.26; p<0.01), as well as partially mediating (γ=0.14, p<0.05; β=0.23; p<0.01) the relationship between training satisfaction and performance (γ=0.21, p<0.001). Moreover, it totally mediates the relationship between conflict with co-workers and burnout (γ=-0.52, p<0.001; β=-0.40, p<0.001), as well as totally mediating the relationship between training satisfaction and burnout (γ=0.14, p<0.05; β=-0.40, p<0.001). Finally, ethical conflict is positively associated with burnout (γ=0.047, p<0.001).Conclusions:This study provides useful information about the improvement of SRs’ well-being, highlighting the importance of their involvement in this role.Key words: Safety representatives, conflict, training, work engagement, performance, burnout     

FLAG-IDA in the treatment of refractory/relapsed acute myeloid leukemia: single-center experience

We evaluated the efficacy and toxicity profiles of the combination of fludarabine, high-dose cytosine arabinoside (AraC), idarubicin, and granulocyte colony-stimulating factor (G-CSF) in refractory/relapsed acute myeloblastic leukemia (AML) patients. Between October 1998 and February 2002, 46 AML patients were treated with FLAG-IDA (fludarabine 30 mg/m(2), AraC 2 g/m(2) for 5 days, idarubicin 10 mg/m(2) for 3 days, and G-CSF 5 micro g/kg from day +6 until neutrophil recovery). Thirty patients were in relapse after conventional chemotherapy including cytarabine, etoposide, and daunorubicin or mitoxantrone according to the GIMEMA protocols. Four were in relapse after autologous peripheral stem cell transplantation and two after allogeneic bone marrow transplantation. Ten patients had refractory disease (after 10 days of standard doses of cytarabine, 3 days of mitoxantrone or daunorubicin, and 5 days of etoposide). Recovery of neutrophils and platelets required a median of 19 and 22 days from the start of therapy. Complete remission (CR) was obtained in 24 of 46 patients (52.1%) and 3 of 46 (6.6%) died during reinduction therapy: 2 due to cerebral hemorrhage and 1 due to fungemia ( Candida tropicalis). Fever >38.5 degrees C was observed in 40 of 46 patients (86.9%), 27 had fever of unknown origin (FUO) and 13 documented infections; 31 of 46 (67.3%) developed mucositis and 14 of 46 (30.4%) had grade 2 WHO transient liver toxicity. After achieving CR, 11 patients received allogeneic stem cell transplantation, 4 patients received autologous stem cell transplantation, 4 were judged unable to receive any further therapy, and 5 refused other therapy. Ten patients are at present in continuous CR after a median follow-up of 13 months (range: 4-24). In our experience, FLAG-IDA is a well-tolerated and effective regimen in relapsed/refractory AML. The toxicity is acceptable, enabling most patients to receive further treatment, including transplantation procedures.     

Left atrial thrombus and smoke resolution in patients with atrial fibrillation under chronic oral anticoagulation

Background

The study aimed to explore the resolution of left atrial and left atrial appendage (LAA) spontaneous echo-contrast or thrombus in patients with nonvalvular atrial fibrillation/flutter (AF/AFL) under chronic oral anticoagulation (OAC).

Methods

A single-center retrospective analysis of patients who underwent a transesophageal echocardiography (TOE) for an electrical cardioversion was conducted.

Results

Among 277 TOE performed, 73 cases (26%) of LAA echo-contrast or thrombus were detected, 53 patients with LAA/LA echo-contrast (19%) and 20 (7%) with a thrombus. All patients were under chronic anticoagulation with a VKA (65%) or with a NOAC (35%). The Echo-contrast Group maintained the same OAC strategy in 49 patients (93%). The Thrombus Group kept the same OAC strategy with a NOAC in 6 cases (30%) and changed the strategy in 14 patients (70%), titrating NOAC dose in 1 (5%) and the VKA dose in 4 (20%) and switching from NOAC to VKA in 5 (25%), from VKA to NOAC in 3 (15%), and from NOAC to NOAC in 1 (5%). Smoke resolution was observed in 4/40 cases (10%) of the smoke group and thrombus resolution in 8/15 (53%) of the thrombus group. Patients with thrombus resolution had a lower CHA2DS2-Vasc score (3.5?±?2 vs 4?±?1, p?=?0.05), were more often under NOAC (37.5 vs 28%, p?=?0.07), and had a longer anticoagulation time (7.5 vs 4 months, p?=?0.08).

Conclusion (s)

Changing OAC strategy is associated with thrombus resolution in more than 50% of chronically anticoagulated patients.

     

Patients with hibernating myocardium show altered left ventricular volumes and shape, which revert after revascularization: evidence that dyssynergy might directly induce cardiac remodeling.

OBJECTIVES: The purpose of this study was to investigate whether post-ischemic left ventricular (LV) remodeling might be induced by regional contractile dysfunction per se (i.e., in the absence of transmural necrosis) and whether this phenomenon is potentially reversible after contractile recovery. BACKGROUND: Formation of extensive scar tissue is thought to be chiefly responsible for post-infarction LV remodeling; however, myocardial necrosis also causes loss of contractility. We investigated LV geometry and shape in a setting in which contractile dysfunction occurs in the presence of preserved myocyte viability, and thus it is potentially reversible. METHODS: In 42 patients with chronically dysfunctional myocardium, we evaluated (by two-dimensional echocardiography) LV global and regional function, volumes, and sphericity index (SI), at baseline and 8 +/- 3 months after coronary revascularization. Myocardial viability before revascularization was evaluated by dobutamine echocardiography. RESULTS: At baseline, regional and global function were depressed and LV dilation was present. Revascularization was followed by recovery of ejection fraction (from 33 +/- 6% to 45 +/- 10%, p < 0.0001) and wall motion score index (from 2.29 +/- 0.31 to 1.74 +/- 0.42, p < 0.0001). After revascularization, significant improvement of end-systolic volume index (from 78 +/- 23 ml/m2 to 56 +/- 23 ml/m2, p < 0.0001), end-diastolic volume index (from 118 +/- 26 ml/m2 to 99 +/- 26 ml/m2, p < 0.0001), and SI (from 0.69 +/- 0.14 to 0.52 +/- 0.11, p < 0.0001) was also observed. Improvement in LV volumes and SI were significantly correlated to the number of segments recovering function after revascularization. CONCLUSIONS: Hibernating myocardium is associated with major alterations in LV volumes and shape, which significantly revert after revascularization. Thus, chronic dyssynergy per se is sufficient to induce ischemic LV remodeling in patients.     

Use of tyrosine kinase inhibitors in a patient with Brugada syndrome and chronic myeloid leukemia

The treatment and prognosis of chronic myeloid leukemia have dramatically changed since the introduction of tyrosine kinase inhibitors, but although several clinical trials have examined their safety with respect to heart function, no data are yet available about the use of these drugs in patients with Brugada syndrome. We report a case of Brugada syndrome diagnosed during tyrosine kinase inhibitor therapy in a 69-year-old Caucasian male with meningioma and chronic myeloid leukemia. This case report highlights the importance of an integrated approach among hematologists and cardiologists to ensure appropriate treatment with tyrosine kinase inhibitors in patients affected by chronic myeloid leukemia who also suffer from Brugada syndrome.     

Aspects of gene polymorphisms in cardiovascular disease: the renin-angiotensin system

The renin-angiotensin system (RAS) plays a central role in cardiovascular homeostasis. Angiotensin is the key peptide of the RAS, and exerts its influence on the heart and blood vessels both through its haemodynamic effects (via its influence on after-load and pre-load and determining coronary vasoconstriction) and through its direct cellular effects (via its actions on cell proliferation). Numerous studies in the past 10 years have demonstrated that the pharmacological inhibition of angiotensin converting enzyme (ACE), one of the two critical enzymes of the RAS, improves the outcome in patients with several cardiovascular disorders (hypertension, heart failure, ischaemic heart disease). These studies suggest a role of the RAS as a major determinant of cardiovascular risk. Recent data suggest that genetics may in turn contribute to modulating the effects of angiotensin on coronary vascular biology and ischaemia. This paper reviews the physiologic characteristics of the RAS and recent research developments related to angiotensin cell biology and pathobiology in heart disease. In particular, this review will cover the genetic aspects of RAS and their implications in cardiovascular disease.