37 research outputs found

    Acción : diario de Teruel y su provincia: Año II Número 80 - (23/02/33)

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    Aim: To explore and compare the impact of the physical environment on patients’ activities and care at three newly built stroke units. Background: Receiving care in a stroke unit instead of in a general ward reduces the odds of death, dependency and institutionalized care. In stroke units, the design of the physical environment should support evidence-based care. Studies on patients’ activities in relation to the design of the physical environment of stroke units are scarce. Design: This work is a comparative descriptive case study. Method: Patients (n=55) who had a confirmed diagnosis of stroke were recruited from three newly built stroke units in Sweden. The units were examined by non-participant observation using two types of data collection: behavioral mapping analyzed with descriptive statistics and field note taking analyzed with deductive content analysis. Data were collected from April 2013 to December 2015. Results: The units differed in the patients’ levels of physical activity, the proportion of the day that patients spent with health professionals, and family presence. Patients were more physically active in a unit with a combination of single and multi-bed room designs than in a unit with an entirely single room design. Stroke units that were easy to navigate and offered variations in the physical environment impacted patients’ activities and care. Conclusions: Patients’ activity levels and interactions appeared to vary with the design of the physical environments of stroke units. Stroke guidelines focused on health status assessments, avoidance of bed-rest and early rehabilitation require a supportive physical environment.status: accepte

    Patent Foramen Ovale Closure Decreases the Incidence but Not the Size of New Brain Infarction on Magnetic Resonance Imaging An Analysis of the REDUCE Trial

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    Background and Purpose: Randomized patent foramen ovale closure trials have used open-label end point ascertainment which increases the risk of bias and undermines confidence in the conclusions. The Gore REDUCE trial prospectively performed baseline and follow-up magnetic resonance imaging (MRIs) for all subjects providing an objective measure of the effectiveness of closure.Methods: We performed blinded evaluations of the presence, location, and volume of new infarct on diffusion-weighted imaging of recurrent clinical stroke or new infarct (>3 mm) on T2/fluid attenuated inversion recovery from baseline to follow-up MRI at 2 years, comparing closure to medical therapy alone. We also examined the effect of shunt size and the development of atrial fibrillation on infarct burden at follow-up.Results: At follow-up, new clinical stroke or silent MRI infarct occurred in 18/383 (4.7%) patients who underwent closure and 19/177 (10.7%) medication-only patients (relative risk, 0.44 [95% CI, 0.24-0.81], P=0.02). Clinical strokes were less common in closure patients compared with medically treated patients, 5 (1.3%) versus 12 (6.8%), P=0.001, while silent MRI infarcts were similar, 13 (3.4%) versus 7 (4.0%), P=0.81. There were no differences in number, volumes, and distribution of new infarct comparing closure patients to those treated with medication alone. There were also no differences of number, volumes, and distribution comparing silent infarcts to clinical strokes. Infarct burden was also similar for patients who developed atrial fibrillation and for those with large shunts.Conclusions: The REDUCE trial demonstrates that patent foramen ovale closure prevents recurrent brain infarction based on the objective outcome of new infarcts on MRI. Only clinical strokes were reduced by closure while silent infarctions were similar between study arms, and there were no differences in infarct volume or location comparing silent infarcts to clinical strokes.Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT00738894.</p

    A trial to evaluate the effect of the sodium–glucose co‐transporter 2 inhibitor dapagliflozin on morbidity and mortality in patients with heart failure and reduced left ventricular ejection fraction (DAPA‐HF)

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    Background: Sodium–glucose co‐transporter 2 (SGLT2) inhibitors have been shown to reduce the risk of incident heart failure hospitalization in individuals with type 2 diabetes who have, or are at high risk of, cardiovascular disease. Most patients in these trials did not have heart failure at baseline and the effect of SGLT2 inhibitors on outcomes in individuals with established heart failure (with or without diabetes) is unknown. Design and methods: The Dapagliflozin And Prevention of Adverse‐outcomes in Heart Failure trial (DAPA‐HF) is an international, multicentre, parallel group, randomized, double‐blind, study in patients with chronic heart failure, evaluating the effect of dapagliflozin 10 mg, compared with placebo, given once daily, in addition to standard care, on the primary composite outcome of a worsening heart failure event (hospitalization or equivalent event, i.e. an urgent heart failure visit) or cardiovascular death. Patients with and without diabetes are eligible and must have a left ventricular ejection fraction ≤ 40%, a moderately elevated N‐terminal pro B‐type natriuretic peptide level, and an estimated glomerular filtration rate ≥ 30 mL/min/1.73 m2. The trial is event‐driven, with a target of 844 primary outcomes. Secondary outcomes include the composite of total heart failure hospitalizations (including repeat episodes), and cardiovascular death and patient‐reported outcomes. A total of 4744 patients have been randomized. Conclusions: DAPA‐HF will determine the efficacy and safety of the SGLT2 inhibitor dapagliflozin, added to conventional therapy, in a broad spectrum of patients with heart failure and reduced ejection fraction

    Consensus statements and recommendations from the ESO-Karolinska Stroke Update Conference, Stockholm 11–13 November 2018

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    The purpose of the European Stroke Organisation–Karolinska Stroke Update Conference is to provide updates on recent stroke therapy research and to give an opportunity for the participants to discuss how these results may be implemented into clinical routine. The meeting started 22 years ago as Karolinska Stroke Update, but since 2014 it is a joint conference with European Stroke Organisation. Importantly, it provides a platform for discussion on the European Stroke Organisation guidelines process and on recommendations to the European Stroke Organisation guidelines committee on specific topics. By this, it adds a direct influence from stroke professionals otherwise not involved in committees and work groups on the guideline procedure. The discussions at the conference may also inspire new guidelines when motivated. The topics raised at the meeting are selected by the scientific programme committee mainly based on recent important scientific publications. This year’s European Stroke Organisation–Karolinska Stroke Update Meeting was held in Stockholm on 11–13 November 2018. There were 11 scientific sessions discussed in the meeting including two short sessions. Each session except the short sessions produced a consensus statement (Full version with background, issues, conclusions and references are published as web-material and at www.eso-karolinska.org and http://eso-stroke.org) and recommendations which were prepared by a writing committee consisting of session chair(s), scientific secretary and speakers. These statements were presented to the 250 participants of the meeting. In the open meeting, general participants commented on the consensus statement and recommendations and the final document were adjusted based on the discussion from the general participants Recommendations (grade of evidence) were graded according to the 1998 Karolinska Stroke Update meeting with regard to the strength of evidence. Grade A Evidence: Strong support from randomised controlled trials and statistical reviews (at least one randomised controlled trial plus one statistical review). Grade B Evidence: Support from randomised controlled trials and statistical reviews (one randomised controlled trial or one statistical review). Grade C Evidence: No reasonable support from randomised controlled trials, recommendations based on small randomised and/or non-randomised controlled trials evidence

    Underlying Event measurements in pp collisions at s=0.9 \sqrt {s} = 0.9 and 7 TeV with the ALICE experiment at the LHC

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    Clinical and genetic aspects on cluster headache

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    Cluster headache (CH), a primary neurovascular headache syndrome, is characterized by recurrent, unilateral, short-lasting attacks of excruciating pain in the temporal region. The pain is considered one of the most severe pain conditions known to humans. This thesis has focused on studies of the clinical picture, especially in relation to headache classification criteria, studies of the genetic background and a search for pathophysiological mechanisms through gene expression analysis. In Study I we prospectively evaluated the prognosis after one typical cluster period. We found that 13 (26.5%) had had one cluster period only during a mean observation time of 8.9 years, and conclude that some patients may suffer from one cluster period only. In the new IHS classification (2004) only one period is required for a CH diagnosis. In Study II we identified 55 affected in 21 different CH families of whom 12 had atypical symptoms. The atypical cases did not fulfil the IHS (2004) diagnostic criteria for CH, but had clinical symptoms resembling CH. We suggest that the clinical spectrum of familial CH may be broader than previously thought and that these atypical cases in CH families may represent an expanded spectrum of the disease. Mutations of the CACNA1A gene have shown to cause several, mainly episodic, neurological disorders. In Study III we studied the impact of the CACNA1A gene on CH by performing an association analysis of two polymorphic markers in 75 sporadic CH patients and 108 matched controls. We found no significant differences between the patients and controls and we conclude that a great importance of the CACNA 1 A gene in our sporadic CH patients is unlikely. Nitric oxide (NO) has been regarded as an important mediator in vascular headache pathophysiology. In Study IV we analyzed five polymorphic markers of the three different NOS genes (NOS1, NOS2a and NOS3 coding for iNOS, nNOS and eNOS respectively) in 91 CH patients and 111 matched controls. However, this study offers no support for an association between these markers and our CH patients. In Study V, an international collaboration, a genome wide scan of extended CH pedigrees was performed, without identifying a single disease locus for CH. An association analysis of two polymorphisms of the HCRTR2 gene in a Danish, Swedish and British sporadic case-control cohort could not confirm a recently reported association of CH to this gene. Complete HCRTR2 sequencing in 8 independent familial CH cases could not detect any mutaitons. Genetic predisposition to CH is likely to be complex and compounded by heterogeneity. Finally, in Study VI, by using Affymetrix microarray technology, we obtained gene expression profiles from peripheral blood from 3 CH patients during attacks, between attacks and in remission, and from 3 matched controls. An upregulation of several S 100 proteins was seen during the active phase of the disease compared to remission, which could be confirmed for the calcium-binding S100P gene with quantitative RT-PCR in 6 CH patients. These findings might indicate an inflammatory process during the active phase of CH
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