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Brunico - Bruneck, Italy

Gruber E.,Hospital of Bruneck | Oberhammer R.,Hospital of Bruneck | Balkenhol K.,EURAC Institute of Mountain Emergency Medicine | Strapazzon G.,EURAC Institute of Mountain Emergency Medicine | And 4 more authors.
Resuscitation | Year: 2014

Objective: In some emergency situations resuscitation and ventilation may have to be performed by basic life support trained personnel, especially in rural areas where arrival of advanced life support teams can be delayed. The use of advanced airway devices such as endotracheal intubation has been deemphasized for basically-trained personnel, but it is unclear whether supraglottic airway devices are advisable over traditional mask-ventilation. Methods: In this prospective, randomized clinical single-centre trial we compared airway management and ventilation performed by nurses using facemask, laryngeal mask Supreme (LMA-S) and laryngeal tube suction-disposable (LTS-D). Basic life support trained nurses (n= 20) received one-hour practical training with each device. ASA 1-2 patients scheduled for elective surgery were included (n= 150). After induction of anaesthesia and neuromuscular block nurses had two 90-second attempts to manage the airway and ventilate the patient with volume-controlled ventilation. Results: Ventilation failed in 34% of patients with facemask, 2% with LMA-S and 22% with LTS-D (P<0.001). In patients who could be ventilated successfully mean tidal volume was 240±210ml with facemask, 470±120ml with LMA-S and 470±140ml with LTS-D (P<0.001). Leak pressure was lower with LMA-S (23.3±10.8cm H2O, 95% CI 20.2-26.4) than with LTS-D (28.9±13.9cm·H2O, 95% CI 24.4-33.4; P=0.047). Conclusions: After one hour of introductory training, nurses were able to use LMA-S more effectively than facemask and LTS-D. High ventilation failure rates with facemask and LTS-D may indicate that additional training is required to perform airway management adequately with these devices. High-level trials are needed to confirm these results in cardiac arrest patients. © 2014 Elsevier Ireland Ltd. Source


Pechlaner R.,Innsbruck Medical University | Kiechl S.,Innsbruck Medical University | Mayr M.,Kings College London | Weger S.,Hospital of Bruneck | And 4 more authors.
Clinical Chemistry and Laboratory Medicine | Year: 2016

Background: The expression of the key iron regulatory hormone hepcidin is regulated by iron availability, inflammation, hormones, hypoxia, and anaemia. Increased serum concentrations of hepcidin have recently been linked to atherosclerosis. We studied demographic, haematologic, biochemical, and dietary correlates of serum hepcidin levels and its associations with incident cardiovascular disease and with carotid atherosclerosis. Methods: Serum hepcidin concentrations were measured by tandem mass spectrometry in samples taken in 2000 from 675 infection-free participants of the prospective population-based Bruneck study (age, mean±standard deviation, 66.0±10.2; 48.1% male). Blood parameters were measured by standard methods. Dietary intakes of iron and alcohol were surveyed with a food frequency questionnaire. Carotid atherosclerosis (365 cases) was assessed by ultrasound and subjects were observed for incident stroke, myocardial infarction, or sudden cardiac death (91 events) until 2010. Results: Median (interquartile range) hepcidin levels were 2.27 nM (0.86, 4.15). Most hepcidin correlates were in line with hepcidin as an indicator of iron stores. Independently of ferritin, hepcidin was related directly to physical activity (p=0.024) and fibrinogen (p<0.0001), and inversely to alcohol intake (p=0.006), haemoglobin (p=0.027), and γ-glutamyltransferase (p<0.0001). Hepcidin and hepcidin-to-ferritin ratio were not associated with prevalent carotid atherosclerosis (p=0.43 and p=0.79) or with incident cardiovascular disease (p=0.62 and p=0.33). Conclusions: In this random sample of the general community, fibrinogen and γ-glutamyltransferase were the most significant hepcidin correlates independent of iron stores, and hepcidin was related to neither atherosclerosis nor cardiovascular disease. © 2016 by De Gruyter 2016. Source


Mahlknecht P.,Innsbruck Medical University | Kiechl S.,Innsbruck Medical University | Bloem B.R.,Radboud University Nijmegen | Willeit J.,Innsbruck Medical University | And 5 more authors.
PLoS ONE | Year: 2013

Background:Although gait disorders are common in the elderly, the prevalence and overall burden of these disorders in the general community is not well defined.Methods:In a cross-sectional investigation of the population-based Bruneck Study cohort, 488 community-residing elderly aged 60-97 years underwent a thorough neurological assessment including a standardized gait evaluation. Gait disorders were classified according to an accepted scheme and their associations to falls, neuropsychological measures, and quality of life were explored.Results:Overall, 32.2% (95% confidence interval [CI] 28.2%-36.4%) of participants presented with impaired gait. Prevalence increased with age (p<0.001), but 38.3% (95%CI 30.1%-47.3%) of the subjects aged 80 years or older still had a normally preserved gait. A total of 24.0% (95%CI 20.4%-28.0%) manifested neurological gait disorders, 17.4% (14.3%-21.0%) non-neurological gait problems, and 9.2% (6.9%-12.1%) a combination of both. While there was no association of neurological gait disorders with gender, non-neurological gait disorders were more frequent in women (p = 0.012). Within the group of neurological gait disorders 69.2% (95%CI 60.3%-76.9%) had a single distinct entity and 30.8% (23.1%-39.7%) had multiple neurological causes for gait impairment. Gait disorders had a significant negative impact on quantitative gait measures, but only neurological gait disorders were associated with recurrent falls (odds ratio 3.3; 95%CI 1.4-7.5; p = 0.005 for single and 7.1; 2.7-18.7; p<0.001 for multiple neurological gait disorders). Finally, we detected a significant association of gait disorders, in particular neurological gait disorders, with depressed mood, cognitive dysfunction, and compromised quality of life.Conclusions:Gait disorders are common in the general elderly population and are associated with reduced mobility. Neurological gait disorders in particular are associated with recurrent falls, lower cognitive function, depressed mood, and diminished quality of life. © 2013 Mahlknecht et al. Source


Pechlaner R.,Innsbruck Medical University | Kiechl S.,Innsbruck Medical University | Willeit P.,Innsbruck Medical University | Willeit P.,University of Cambridge | And 8 more authors.
Journal of the American Heart Association | Year: 2014

Background-Haptoglobin (Hp) is an abundant plasma protein with antioxidant properties. The Hp 2-2 genotype has previously been linked to coronary heart disease risk in individuals with elevated glycosylated hemoglobin (HbA1c). We investigated the association of Hp and HbA1c with cardiovascular disease (CVD) in the longitudinal, population-based Bruneck Study. Methods and Results-Hp genotype was determined by polymerase chain reaction according to standard procedures and HbA1c concentration by a Diabetes Control and Complications Trial-aligned assay. HbA1c was measured in 1995, 2000, and 2005. Occurrence of the combined CVD endpoint of myocardial infarction or stroke was recorded between 1995 and 2010. Outcome analyses employed the Cox proportional hazards model with HbA1c category as time-varying covariate. At baseline in 1995, 806 subjects (male sex, 49.3%; age, mean ± standard deviation, 62.70 ± 11.08 years) were included. During follow-up, 123 subjects experienced at least 1 CVD event (48 suffered myocardial infarction, 68 stroke, and 7 both). Among subjects with HbA1c≥6.5% (≥48 mmol/mol), those with the Hp 2-2 genotype did not show an elevated risk of incident CVD compared with those with other genotypes (age- and sex-adjusted hazard ratio [95% CI], 0.47 [0.19, 1.13], P=0.092) and a null association was also observed in subjects with HbA1c<6.5% (1.10 [0.75, 1.62], P=0.629) (P for interaction=0.082). Conclusions-Subjects with the Hp 2-2 genotype and elevated HbA1c compared with subjects with other Hp genotypes and elevated HbA1c did not show increased CVD risk. © 2014 The Authors. Source


Pechlaner R.,Innsbruck Medical University | Weiss G.,Innsbruck Medical University | Bansal S.,Kings College London | Mayr M.,Kings College London | And 5 more authors.
Diabetes/Metabolism Research and Reviews | Year: 2016

Background: Type 2 diabetes mellitus (T2DM) is closely associated with elevated body iron stores. The hormone hepcidin is the key regulator of iron homeostasis. Inadequately low hepcidin levels were recently reported in subjects with manifest T2DM. We investigated whether alterations of hepcidin levels precede the manifestation of T2DM and predict T2DM development independently of established risk conditions. Methods: This prospective population-based study included 675 subjects aged 50-89 years, 51.9% of whom were female. Hepcidin levels were measured by gold standard tandem mass spectrometry. Diabetes was diagnosed according to American Diabetes Association criteria, and incident diabetes was recorded between baseline in 2000 and 2010. Results: The baseline hepcidin-to-ferritin ratio in subjects that subsequently developed diabetes during follow-up was reduced on average by 29.8% as compared with subjects with normal glucose tolerance (95% confidence interval, -50.7% to -0.2%; p=0.049). After adjustment for age, sex, and serum ferritin, higher hepcidin levels were associated with reduced risk of incident diabetes (hazard ratio per 1-unit higher log2 hepcidin, 0.80; 95% confidence interval, 0.64-0.98; p=0.035; 33 events). Additional adjustment for established diabetes risk factors and determinants of hepcidin concentration did not appreciably change these results (HR, 0.81; 95% CI, 0.66-0.99). Likewise, inadequately low hepcidin levels were also detected in subjects with prevalent T2DM (n=76). Conclusions: Hepcidin levels that are inadequately low in relation to body iron stores are an independent predictor for incident T2DM and may contribute to diabetes-related tissue iron overload. © 2016 John Wiley & Sons, Ltd. Source

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