Background: Moral distress and ethical climate are important issues in the workplace that appear to affect people’s quality of work life. Objectives: This study was conducted to determine the relationship of moral distress and ethical climate to job satisfaction in critical care nurses. Materials and methods: This descriptive-correlation study was conducted on 142 critical care nurses, selected from five social security hospitals in north Iran through census sampling. Data were collected using a demographic questionnaire, the Moral Distress Scale–Revised, the Olson’s Hospital Ethical Climate Survey, and the Brayfield and Rothe Job Satisfaction index. Ethical considerations: The research project was approved by the Ethics Committee of Mazandaran University of Medical Sciences and the Medical Deputy of the Social Security Organization. Findings: The mean scores obtained by the critical care nurses for moral distress, ethical climate, and job satisfaction were 87.02 ± 44.56, 3.51 ± 0.53, and 62.64 ± 9.39, respectively. Although no significant relationships were observed between moral distress and job satisfaction, the relationship between ethical climate and job satisfaction was statistically significant (p < 0.05). Conclusion: Identifying ethical stressors in the workplace and giving proper feedback to the authorities to eliminate these factors and improve the ethical climate in these workplaces can help enhance job satisfaction in nurses and lead to higher quality care.

Purpose: Anthracyclines (ANTs) are a class of active antineoplastic agents with topoisomerase-interacting activity that are considered the most active agents for the treatment of breast cancer. We investigated the efficacy of carvedilol in the inhibition of ANT-induced cardiotoxicity. Methods: In this randomized, single-blind, placebo-controlled study, 91 women with recently diagnosed breast cancer undergoing ANT therapy were randomly assigned to groups treated with either carvedilol (n = 46) or placebo (n = 45). Echocardiography was performed before and at 6 months after randomization, and absolute changes in the mean left ventricular ejection fraction, left ventricular end diastolic volume, and left ventricular end systolic volume were determined. Furthermore, the percentage change in the left atrial (LA) diameter and other variables of left ventricular (LV) diastolic function, such as transmitral Doppler parameters, including early (E wave) and late (A wave) diastolic velocities, E/A ratio and E wave deceleration time, pulmonary venous Doppler signals, including forward systolic (S wave) and diastolic (D wave) velocities into LA, late diastolic atrial reversal velocity, and early diastolic tissue Doppler mitral annular velocity (e') were measured. In addition, tissue Doppler mitral annular systolic (s') velocity, as a marker of early stage of LV systolic dysfunction, E/e' ratio, as a determinant of LV filling pressure, and troponin I level, as a marker of myocardial necrosis were measured. Results: At the end of follow-up period, left ventricular ejection fraction did not change in the carvedilol group. However, this parameter was significantly reduced in the control group (P < 0.001). Echocardiography showed that both left ventricular end systolic volume and LA diameter were significantly increased compared with the baseline measures in the control group. In pulse Doppler studies, pulmonary venous peak atrial reversal flow velocity was significantly increased in the control group. Moreover, a significant decrease in the mitral annuli early diastolic (e') and peak systolic (s') velocities and a significant increase in the E (the peak early diastolic velocity)/e' ratio in the control group were also observed. However, none of these variables were adversely changed at the end of follow-up in the carvedilol group. Furthermore, the TnI level was significantly higher in the control group than in the carvedilol group (P = 0.036) at 30 days after the initiation of chemotherapy. Conclusions: Prophylactic use of carvedilol may inhibit the development of anthracycline-induced cardiotoxicity, even at low doses.

Chemotherapy-induced cardiotoxicity is a major and leading cause of death in breast cancer survivors. It can present decades after chemotherapy and can manifest in different ways; some chemotherapeutic agents have a powerful dose-dependent relationship with cardiotoxicity. The aim of this study was to investigate the effect of rosuvastatin on preventing chemotherapy-induced cardiotoxicity in patients with breast cancer. Our study was a randomized, single-blind, placebo-controlled trial that involved 89 women with newly diagnosed breast cancer who were scheduled to receive chemotherapy. Patients were randomly assigned to receive rosuvastatin or a placebo in a 1:1 ratio for 6 months. Echocardiography, using 2-dimensional (2D) Doppler, tissue Doppler, and speckle-tracking methods, was used to determine the absolute changes in the left ventricular systolic ejection fraction (LVEF), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left atrial (LA) diameter, transmitral Doppler early diastolic velocity (E wave), tissue Doppler early diastolic (e′) and peak systolic (s′) mitral annular velocities, E/e′ ratio, and global longitudinal systolic strain. The LVEF was significantly reduced in the placebo group at the end of the study when compared with the baseline value. However, there was no significant difference in the LVEF in the intervention group (intergroup P = .012). Furthermore, compared with the intervention group at the end of the study, there was a significant increase in the 4- and 2-chamber LVESV, LA diameter, and E/e′ ratio in the placebo group (intergroup P = .019, P = .024, P < .001, and P = .021, respectively) and a significant decrease in the e′ and s′ velocities in the placebo group (intergroup P < .001 and P < .006, respectively). The present study showed that the prophylactic use of rosuvastatin may prevent the development of chemotherapy-induced cardiotoxicity.