Are sarcopenia and myosteatosis in elderly patients with pelvic ring injury related to mortality, physical functioning and quality of life?

The purpose of this study was to evaluate the prevalence of sarcopenia and/or myosteatosis in elderly patients with pelvic ring injuries and their influence on mortality, patient-perceived physical functioning and quality of life (QoL). A multicenter retrospective cohort study was conducted including elderly patients aged ≥ 65 treated for a pelvic ring injury. Cross-sectional computed tomography (CT) muscle measurements were obtained to determine the presence of sarcopenia and/or myosteatosis. Kaplan–Meier analysis was used for survival analysis, and Cox proportional hazards regression analysis was used to determine risk factors for mortality. Patient-reported outcome measures for physical functioning (SMFA) and QoL (EQ-5D) were used. Multivariable linear regression analyses were used to determine the effect of sarcopenia and myosteatosis on patient-perceived physical functioning and QoL. Data to determine sarcopenia and myosteatosis were available for 199 patients, with a mean follow-up of 2.4 ± 2.2 years: 66 patients (33%) were diagnosed with sarcopenia and 65 (32%) with myosteatosis, while 30 of them (15%) had both. Mortality rates in patients at 1 and 3 years without sarcopenia and myosteatosis were 13% and 21%, compared to 11% and 36% in patients with sarcopenia, 17% and 31% in patients with myosteatosis and 27% and 43% in patients with both. Higher age at the time of injury and a higher Charlson Comorbidity Index (CCI) were independent risk factors for mortality. Patient-reported mental and emotional problems were significantly increased in patients with sarcopenia

Correlation between Cardiac MRI and Voltage Mapping in Evaluating Atrial Fibrosis:A Systematic Review

PURPOSE: To provide an overview of existing literature on the association between late gadolinium enhancement (LGE) cardiac MRI and low voltage areas (LVA) obtained with electroanatomic mapping (EAM) or histopathology when assessing atrial fibrosis. MATERIALS AND METHODS: A systematic literature search was conducted in the PubMed, Embase, and Cochrane Library databases to identify all studies published until June 7, 2022, comparing LGE cardiac MRI to LVA EAM and/or histopathology for evaluation of atrial fibrosis. The study protocol was registered at PROSPERO (registration no. CRD42022338243). Two reviewers independently evaluated the studies for inclusion. Risk of bias and applicability for each included study were assessed using Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2) criteria. Data regarding demographics, electrophysiology, LGE cardiac MRI, and study outcomes were extracted. RESULTS: The search yielded 1048 total results, of which 22 studies were included. Nineteen of the 22 included studies reported a significant correlation between high signal intensity at LGE cardiac MRI and LVA EAM or histopathology. However, there was great heterogeneity between included studies regarding study design, patient samples, cardiac MRI performance and postprocessing, and EAM performance. CONCLUSION: Current literature suggests a correlation between LGE cardiac MRI and LVA EAM or histopathology when evaluating atrial fibrosis but high heterogeneity between studies, demonstrating the need for uniform choices regarding cardiac MRI and EAM acquisition in future studies.Keywords: Cardiac, MR Imaging, Left Atrium Supplemental material is available for this article. © RSNA, 2022

No compensatory upregulation of placental dimethylarginine dimethylaminohydrolase activity in preeclampsia

Background/Aims: Placental dysfunction of the asymmetric dimethylarginine (ADMA) degrading enzyme dimethylarginine dimethylaminohydrolase (DDAH) has been suggested as one of the initiating events in the development of preeclampsia (PE). Our primary aim was to investigate the role of the placenta in the metabolism of ADMA during normal pregnancy and PE. Methods: We studied 27 nonpregnant healthy women (C), 15 normotensive pregnant females (P), 16 patients with PE, and 7 patients with the 'hemolysis, elevated liver enzymes and low platelets' syndrome (H). Results: There were no significant differences between P and PE with respect to fetomaternal gradient of ADMA, placental DDAH activity and placental ADMA content. During the first stage of labour, mean (+/- SD) plasma ADMA (mu mol/l) was higher in H (0.69 +/- 0.22; p <0.05) compared with C (0.44 +/- 0.07), P (0.37 +/- 0.06), and PE (0.40 +/- 0.06). ADMA was significantly associated with laboratory parameters of hepatic and renal function and with clinical parameters, including systolic and diastolic blood pressure, gestational age, birth weight, and placenta weight. Conclusions: A compensatory upregulation of placental DDAH activity is absent in patients suffering from PE and levels of ADMA in plasma and placenta are normal in patients suffering from PE. However, when the course of PE deteriorates and organ dysfunction (especially liver and kidney) becomes involved, such as during the hemolysis, elevated liver enzymes and low platelets syndrome, ADMA levels increase. Copyright (c) 2006 S. Karger AG, Base

Low plasma concentrations of arginine and asymmetric dimethylarginine in premature infants with necrotizing enterocolitis

Several studies have described reduced plasma concentrations of arginine, the substrate for nitric oxide synthase (NOS) in infants with necrotizing enterocolitis (NEC). No information on the plasma concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) in patients with NEC is currently available. We investigated whether plasma concentrations of arginine, ADMA, and their ratio differ between premature infants with and without NEC, and between survivors and non-survivors within the NEC group. In a prospective case-control study, arginine and ADMA concentrations were measured in ten premature infants with NEC (median gestational age 193 d, birth weight 968 g), and ten matched control infants (median gestational age 201 d, birth weight 1102 g), who were admitted to the Neonatal Intensive Care Unit. In the premature infants with NEC, median arginine and ADMA concentrations (micromol/l), and the arginine:ADMA ratio were lower compared to the infants without NEC: 21.4 v. 55.9, P= 0.001; 0.59 v. 0.85, P=0.009 and 36.6 v. 72.3, P=0.023 respectively. In the NEC group, median arginine (micromol/l) and the arginine:ADMA ratio were lower in non-surviving infants than in surviving infants: 14.7 v. 33.8, P=0.01 and 32.0 v. 47.5, P=0.038 respectively. In premature infants with NEC not only the NOS substrate arginine, but also the endogenous NOS inhibitor ADMA and the arginine:ADMA ratio were lower than in infants without NEC. In addition, low arginine and arginine:ADMA were associated with mortality in infants with NEC. Overall, these data suggest that a diminished nitric oxide production may be involved in the pathophysiology of NEC, but this needs further investigatio