| 1. |
- Ahmed, Niaz, et al.
(author)
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Consensus statements and recommendations from the ESO-Karolinska Stroke Update Conference, Stockholm 11-13 November 2018.
- 2019
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In: European Stroke Journal. - : SAGE Publications. - 2396-9873 .- 2396-9881. ; 4:4, s. 307-317
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Journal article (peer-reviewed)abstract
- 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.
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| 2. |
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| 3. |
- Helgadottir, Anna, et al.
(author)
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Apolipoprotein(a) Genetic Sequence Variants Associated With Systemic Atherosclerosis and Coronary Atherosclerotic Burden But Not With Venous Thromboembolism
- 2012
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In: Journal of the American College of Cardiology. - : Elsevier BV. - 0735-1097 .- 1558-3597. ; 60:8, s. 722-729
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Journal article (peer-reviewed)abstract
- Objectives The purpose of this study is investigate the effects of variants in the apolipoprotein(a) gene (LPA) on vascular diseases with different atherosclerotic and thrombotic components. Background It is unclear whether the LPA variants rs10455872 and rs3798220, which correlate with lipoprotein(a) levels and coronary artery disease (CAD), confer susceptibility predominantly via atherosclerosis or thrombosis. Methods The 2 LPA variants were combined and examined as LPA scores for the association with ischemic stroke (and TOAST [Trial of Org 10172 in Acute Stroke Treatment] subtypes) (effective sample size [n(e)] = 9,396); peripheral arterial disease (n(e) = 5,215); abdominal aortic aneurysm (ne = 4,572); venous thromboembolism (ne = 4,607); intracranial aneurysm (ne = 1,328); CAD (n(e) = 12,716), carotid intima-media thickness (n = 3,714), and angiographic CAD severity (n = 5,588). Results LPA score was associated with ischemic stroke subtype large artery atherosclerosis (odds ratio [OR]: 1.27; p = 6.7 X 10(-4)), peripheral artery disease (OR: 1.47; p = 2.9 x 10(-14)), and abdominal aortic aneurysm (OR: 1.23; p = 6.0 x 10(-5)), but not with the ischemic stroke subtypes cardioembolism (OR: 1.03; p = 0.69) or small vessel disease (OR: 1.06; p = 0.52). Although the LPA variants were not associated with carotid intima-media thickness, they were associated with the number of obstructed coronary vessels (p = 4.8 x 10(-12)). Furthermore, CAD cases carrying LPA risk variants had increased susceptibility to atherosclerotic manifestations outside of the coronary tree (OR: 1.26; p = 0.0010) and had earlier onset of CAD (-1.58 years/allele; p = 8.2 x 10(-8)) than CAD cases not carrying the risk variants. There was no association of LPA score with venous thromboembolism (OR: 0.97; p = 0.63) or intracranial aneurysm (OR: 0.85; p = 0.15). Conclusions LPA sequence variants were associated with atherosclerotic burden, but not with primarily thrombotic phenotypes. (J Am Coll Cardiol 2012; 60: 722-9) (C) 2012 by the American College of Cardiology Foundation
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| 4. |
- Helgadottir, Anna, et al.
(author)
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The same sequence variant on 9p21 associates with myocardial infarction, abdominal aortic aneurysm and intracranial aneurysm
- 2008
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In: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 40:2, s. 217-224
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Journal article (peer-reviewed)abstract
- Recently, two common sequence variants on 9p21, tagged by rs10757278-G and rs10811661-T, were reported to be associated with coronary artery disease (CAD)(1-4) and type 2 diabetes (T2D)(5-7), respectively. We proceeded to further investigate the contributions of these variants to arterial diseases and T2D. Here we report that rs10757278-G is associated with, in addition to CAD, abdominal aortic aneurysm (AAA; odds ratio (OR) 1.31, P = 1.2 x 10(-12)) and intracranial aneurysm (OR = 1.29, P = 2.5 x 10(-6)), but not with T2D. This variant is the first to be described that affects the risk of AAA and intracranial aneurysm in many populations. The association of rs10811661-T to T2D replicates in our samples, but the variant does not associate with any of the five arterial diseases examined. These findings extend our insight into the role of the sequence variant tagged by rs10757278-G and show that it is not confined to atherosclerotic diseases.
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| 5. |
- Kostulas, Konstantinos
(author)
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Genetic analysis of ischemic stroke and predisposing carotid artery stenosis : a stroke carol
- 2007
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Doctoral thesis (other academic/artistic)abstract
- Ischemic cerebrovascular disease (ICVD), consisting of ischemic stroke and transient ischemic attacks (TIA), is a complex disease where contribution from both the environment and genes promote pathogenesis of the disease-complex. Carotid stenosis is sometimes a predisposing factor or cause for ICVD and a complex disease in itself. Studies of adoptees and twins support the idea that genes are of importance in ICVD and family studies in CS. Two different strategies have been applied to search the genome for ICVD genes, a candidate genome approach and a genome-wide search in familial disease. During the last two decades different candidate genes coding for coagulation-proteins, lipoproteins, renin-angiotensin-aldosterone system and different inflammatory genes have been investigated with different results. Successful examples of the genome-wide search are the phosphodiesterase 4D (PDE4D) gene and the 5- lipoxygenase activating protein (ALOX5AP) gene found in an Icelandic population. These genes have later been studied as a candidate gene in different populations. The South Stockholm Ischemic Stroke Study (SSISS) was started in 1996 to study genetic associations of ICVD and predisposing carotid stenosis (CS), the hypothesis being that genetic factors could be used to find more coherent pathogenetical subgroups to the ischemic cerebrovascular disease complex to facilitate a more individual treatment and prophylaxis. During the first phase of the project three suspected susceptibility genes were examined in a smaller cohort (<200) of patients, namely lipoprotein lipase (LPL), methylene-tetrahydrofolate reductase (MTHFR) and angiotensin-converting enzyme (ACE). We concluded that LPL and MTHFR polymorphisms did not contribute greatly to the overall risk of ICVD or CS. In the examination of ACE we found a significant difference for the presumed susceptibility allele in patients with CS compared to healthy controls and age-matched non-CS ICVD patients. We concluded that the ACE gene polymorphism is a risk factor for the development of CS. In the last phase of the project we expanded the material to more than 1000 patients with ICVD and phenotyped the subjects in detail including subtyping by the Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. We went on to examine PDE4D and ALOX5AP, genes discovered by linkage analysis on Iceland. We were not able confirm the association between the ALOX5AP HapA haplotype and ICVD, but a non-significant risk was observed in the large artery atherosclerosis (LAA) TOAST subtype. Our PDE4D findings although non-significant considering the number of markers and phenotypes tested, were consistent with the original Icelandic association, with a trend in the whole ICVD group, strengthened in LAA and the combined group of LAA and cardio embolic (CE) subtypes. In the last study we examined 100 polymorphisms in 47 suspected susceptibility genes and found three polymorphisms to be weakly associated with ICVD after correction for age and gender (LPL, angiotensinogen and guanine nucleotide-binding protein beta-3). These markers were differently prevalent in the subtypes examined. Factor VII, apolipoprotein E and two renin polymorphisms were significantly more frequent in patients with evidence of CS compared to non-CS patients. In conclusion we have found weak associations to some candidate genes and by subdividing ICVD patients by presence of CS the patterns of association change. We therefore conclude that larger well phenotyped ICVD cohorts are needed.
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| 6. |
- Lekander, Ingrid, et al.
(author)
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Hospital comparison of stroke care in Sweden : a register-based study
- 2017
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In: BMJ Open. - London, UK : BMJ Publishing Group Ltd. - 2044-6055. ; 7:9
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Journal article (peer-reviewed)abstract
- BACKGROUND AND PURPOSE: The objective of this study was to estimate the level of health outcomes and resource use at a hospital level during the first year after a stroke, and to identify any potential differences between hospitals after adjusting for patient characteristics (case mix).METHOD: Data from several registries were linked on individual level: seven regional patient administrative systems, Swedish Stroke Register, Statistics Sweden, National Board of Health and Welfare and Swedish Social Insurance Agency. The study population consisted of 14 125 patients presenting with a stroke during 2010. Case-mix adjusted analysis of hospital differences was made on five aspects of health outcomes and resource use, 1 year post-stroke.RESULTS: The results indicated that 26% of patients had died within a year of their stroke. Among those who survived, almost 5% had a recurrent stroke and 40% were left with a disability. On average, the patients had 22 inpatient days and 23 outpatient visits, and 13% had moved into special housing. There were significant variations between hospitals in levels of health outcomes achieved and resources used after adjusting for case mix.CONCLUSION: Differences in health outcomes and resource use between hospitals were substantial and not entirely explained by differences in patient mix, indicating tendencies of unequal stroke care in Sweden. Healthcare organisation of regions and other structural features could potentially explain parts of the differences identified.
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| 7. |
- Samuelsson, Kristin, et al.
(author)
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Idiopathic Small Fiber Neuropathy : Phenotype, Etiologies, and the Search for Fabry Disease
- 2014
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In: Journal of Clinical Neurology. - : Korean Neurological Association. - 1738-6586 .- 2005-5013. ; 10:2, s. 108-118
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Journal article (peer-reviewed)abstract
- Background and PurposeThe etiology of small fiber neuropathy (SFN) often remains unclear. Since SFN may be the only symptom of late-onset Fabry disease, it may be underdiagnosed in patients with idiopathic polyneuropathy. We aimed to uncover the etiological causes of seemingly idiopathic SFN by applying a focused investigatory procedure, to describe the clinical phenotype of true idiopathic SFN, and to elucidate the possible prevalence of late-onset Fabry disease in these patients.MethodsForty-seven adults younger than 60 years with seemingly idiopathic pure or predominantly small fiber sensory neuropathy underwent a standardized focused etiological and clinical investigation. The patients deemed to have true idiopathic SFN underwent genetic analysis of the alpha-galactosidase A gene (GLA) that encodes the enzyme alpha-galactosidase A (Fabry disease).ResultsThe following etiologies were identified in 12 patients: impaired glucose tolerance (58.3%), diabetes mellitus (16.6%), alcohol abuse (8.3%), mitochondrial disease (8.3%), and hereditary neuropathy (8.3%). Genetic alterations of unknown clinical significance in GLA were detected in 6 of the 29 patients with true idiopathic SFN, but this rate did not differ significantly from that in healthy controls (n=203). None of the patients with genetic alterations in GLA had significant biochemical abnormalities simultaneously in blood, urine, and skin tissue.ConclusionsA focused investigation may aid in uncovering further etiological factors in patients with seemingly idiopathic SFN, such as impaired glucose tolerance. However, idiopathic SFN in young to middle-aged Swedish patients does not seem to be due to late-onset Fabry disease.
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| 8. |
- Seoane, Fernando, 1976-, et al.
(author)
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Electrical Bioimpedance Spectroscopy on Acute Unilateral Stroke Patients : Initial Observations regarding Differences between Sides
- 2015
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In: BioMed Research International. - : Hindawi Publishing Corporation. - 2314-6133 .- 2314-6141. ; 2015
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Journal article (peer-reviewed)abstract
- Purpose. Electrical Bioimpedance Cerebral Monitoring is assessment in real time of health of brain tissue through study of passive dielectric properties of brain. During the last two decades theory and technology have been developed in parallel with animal experiments aiming to confirm feasibility of using bioimpedance-based technology for prompt detection of brain damage. Here, for the first time, we show that electrical bioimpedance measurements for left and right hemispheres are significantly different in acute cases of unilateral stroke within 24 hours from onset. Methods. Electrical BIS measurements have been taken in healthy volunteers and patients suffering from acute stroke within 24 hours of onset. BIS measurements have been obtained using SFB7 bioimpedance spectrometer manufactured by Impedimed ltd. and 4-electrode method. Measurement electrodes, current, and voltage have been placed according to 10–20 EEG system obtaining mutual BIS measurements from 4 different channels situated in pairs symmetrically from the midsagittal line. Obtained BIS data has been analyzed, assessing for symmetries and differences regarding healthy control data.Results. 7 out of 10 patients for Side-2-Side comparisons and 8 out 10 for central/lateral comparison presented values outside the range defined by healthy control group. When combined only 1 of 10 patients exhibited values within the healthy range. Conclusions. If these initial observations are confirmed with more patients, we can foresee emerging of noninvasive monitoring technology for brain damage with the potential to lead to paradigm shift in treatment of brain stroke and traumatic brain damage.
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