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  • 1.
    Medin, Jennie
    et al.
    Linköping University, Department of Department of Health and Society, National Centre for Work and Rehabilitation. Linköping University, Faculty of Health Sciences.
    Nordlund, Anders
    Linköping University, Department of Department of Health and Society, National Centre for Work and Rehabilitation. Linköping University, Faculty of Health Sciences.
    Ekberg, Kerstin
    Linköping University, Department of Department of Health and Society, National Centre for Work and Rehabilitation. Linköping University, Faculty of Health Sciences.
    Increasing stroke incidence in Sweden between 1989 and 2000 among persons aged 30 to 65 years: evidence from the Swedish Hospital Discharge Register2004In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 35, no 5, p. 1047-1051Article in journal (Refereed)
    Abstract [en]

    Background and Purpose— Stroke mortality is decreasing in Sweden, as is the case in other Western European countries. However, both decreases and increases have been reported in Sweden for persons younger than age 65 years. The aim of this study was to compare the incidence of stroke in Sweden between the periods 1989 and 1991 and 1998 and 2000 in persons aged 30 to 65 years.

    Methods— All first-ever stroke patients aged 30 to 65 years in the Swedish Hospital Discharge Register between 1989 and 2000 were included.

    Results— The age-standardized, 3-year average incidence increased by 19%, from 98.9 to 118.0 per 100 000 among men, and by 33%, from 48.4 to 64.4 among women, between 1989 and 1991 and 1998 and 2000. The largest increase was seen among those younger than 60 years. On a county level, the change in age-standardized stroke incidence varied from small decreases (−3%) to large increases (82%).

    Conclusion— Stroke incidence increased in Sweden for both men and women between 1989 and 2000. The increase was larger among women. This calls for action when it comes to studying risk factors and planning for prevention and health promotion and indicates the need for gender-specific studies.

  • 2.
    Murray, V
    et al.
    Danderyd Hosp, Div Med, Stockholm, Sweden Reg Hosp, Dept Geriatr Med, Orebro, Sweden Linkoping Univ Hosp, Dept Neurol, S-58185 Linkoping, Sweden Acad Hosp, Dept Med, Uppsala, Sweden Reg Hosp, Dept Neurol, Orebro, Sweden Karolinska Hosp, Dept Clin Neurosci, S-10401 Stockholm, Sweden Danderyd Hosp, Dept Rehabil Med, Stockholm, Sweden Linkoping Univ Hosp, Dept Psychiat, S-58185 Linkoping, Sweden.
    Von Arbin, M
    Danderyd Hosp, Div Med, Stockholm, Sweden Reg Hosp, Dept Geriatr Med, Orebro, Sweden Linkoping Univ Hosp, Dept Neurol, S-58185 Linkoping, Sweden Acad Hosp, Dept Med, Uppsala, Sweden Reg Hosp, Dept Neurol, Orebro, Sweden Karolinska Hosp, Dept Clin Neurosci, S-10401 Stockholm, Sweden Danderyd Hosp, Dept Rehabil Med, Stockholm, Sweden Linkoping Univ Hosp, Dept Psychiat, S-58185 Linkoping, Sweden.
    Varelius, R
    Danderyd Hosp, Div Med, Stockholm, Sweden Reg Hosp, Dept Geriatr Med, Orebro, Sweden Linkoping Univ Hosp, Dept Neurol, S-58185 Linkoping, Sweden Acad Hosp, Dept Med, Uppsala, Sweden Reg Hosp, Dept Neurol, Orebro, Sweden Karolinska Hosp, Dept Clin Neurosci, S-10401 Stockholm, Sweden Danderyd Hosp, Dept Rehabil Med, Stockholm, Sweden Linkoping Univ Hosp, Dept Psychiat, S-58185 Linkoping, Sweden.
    Olsson, Jan-Edvin
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Neurology . Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Neurology.
    Terent, A
    Danderyd Hosp, Div Med, Stockholm, Sweden Reg Hosp, Dept Geriatr Med, Orebro, Sweden Linkoping Univ Hosp, Dept Neurol, S-58185 Linkoping, Sweden Acad Hosp, Dept Med, Uppsala, Sweden Reg Hosp, Dept Neurol, Orebro, Sweden Karolinska Hosp, Dept Clin Neurosci, S-10401 Stockholm, Sweden Danderyd Hosp, Dept Rehabil Med, Stockholm, Sweden Linkoping Univ Hosp, Dept Psychiat, S-58185 Linkoping, Sweden.
    Samuelsson, M
    Berggren, AL
    Landtblom, Anne-Marie
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Neurology.
    Asberg, M
    Bartfai, A
    Danderyd Hosp, Div Med, Stockholm, Sweden Reg Hosp, Dept Geriatr Med, Orebro, Sweden Linkoping Univ Hosp, Dept Neurol, S-58185 Linkoping, Sweden Acad Hosp, Dept Med, Uppsala, Sweden Reg Hosp, Dept Neurol, Orebro, Sweden Karolinska Hosp, Dept Clin Neurosci, S-10401 Stockholm, Sweden Danderyd Hosp, Dept Rehabil Med, Stockholm, Sweden Linkoping Univ Hosp, Dept Psychiat, S-58185 Linkoping, Sweden.
    Bengtsson, F
    Martensson, B
    Sertraline in poststroke depression - A controlled study2002In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 33, no 1, p. P292-Conference paper (Other academic)
  • 3. Wester, Per
    et al.
    Rådberg, Johan
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Neurology.
    Lundgren, Bo
    Peltonen, Markku
    Factors associated with delayed admission to hospital and in-hospital delays in acute stroke and TIA. A prospective, multicenter study.1999In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 30, p. 40-48Article in journal (Refereed)
  • 4.
    Wiklund, P.-G.
    et al.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Sweden, Department of Medicine, University Hospital, SE-901 85 Umeå, Sweden.
    Nilsson, Lennart
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Ardnor, S.N.
    Department of Medical Clinical Genetics, Umeå University, Sweden.
    Eriksson, P.
    Atherosclerosis Research Unit, King Gustav V Research Institute, Karolinska Hospital, Stockholm, Sweden.
    Johansson, L.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Sweden.
    Stegmayr, B.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Sweden.
    Hamsten, A.
    Atherosclerosis Research Unit, King Gustav V Research Institute, Karolinska Hospital, Stockholm, Sweden.
    Holmberg, D.
    Department of Medical Clinical Genetics, Umeå University, Sweden.
    Asplund, K.
    Department of Public Health and Clinical Medicine, Umeå University Hospital, Sweden.
    Plasminogen activator inhibitor-1 4G/5G polymorphism and risk of stroke: Replicated findings in two nested case-control studies based on independent cohorts2005In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 36, no 8, p. 1661-1665Article in journal (Refereed)
    Abstract [en]

    Background and Purpose - Impaired fibrinolytic function secondary to elevated plasminogen activator inhibitor-1 (PAI-1) levels has been implicated in ischemic stroke. PAI-1 levels are determined by genetic factors and environmental factors, triglyceride levels in particular. The aim of this study was to investigate the common functional 4/5 guanosine (4G/5G) polymorphism in the promoter region of the PAI-1 gene and the risk of stroke. Methods - A nested case-control study design was applied, using baseline data for 2 independent cohorts obtained at population-based surveys in northern Sweden. In study A, there were 113, and in study B, there were 275 individuals without major concomitant disease at baseline who later experienced a first-ever stroke. Blood samples obtained at baseline were analyzed for potential risk factors, including the 4G/5G polymorphism of the PAI-1 gene. Results - The 4G allele of the PAI-1 polymorphism was associated with an increased risk of future ischemic stroke in both studies (odds ratio [OR] of 4G homozygosity, 1.87, 95% CI, 1.12 to 3.15 in study A, OR of 4G homozygosity, 1.56, 95% CI, 1.12 to 2.16 in study B). Individuals with the combination of hypertriglyceridemia and 4G homozygosity were at the greatest risk of developing stroke. Multiple logistic regression analysis identified 4G homozygosity, systolic blood pressure, and diabetes as independent predictors of ischemic stroke. Conclusions - Identical findings in 2 independent studies strongly suggest a true and clinically important association between PAI-1 4G/5G genotype and risk of future ischemic stroke. The observed modification of the genotype effect by triglycerides may be interpreted as a gene-environment interaction. © 2005 American Heart Association. Inc.

  • 5.
    Yuan, Ximing
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Ward, Liam
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences.
    Forssell, Claes
    Region Östergötland, Heart and Medicine Center, Department of Thoracic and Vascular Surgery.
    Siraj, Nabeel
    Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center. Univ Alberta, Dept Internal Med, Edmonton, AB, Canada.
    Li, Wei
    Linköping University, Department of Clinical and Experimental Medicine, Division of Children's and Women's health. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Gynaecology and Obstetrics in Linköping.
    Carotid Atheroma From Men Has Significantly Higher Levels of Inflammation and Iron Metabolism Enabled by Macrophages2018In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 49, no 2, p. 419-425Article in journal (Refereed)
    Abstract [en]

    Background and Purpose-Men differ from women in the manifestation of atherosclerosis and iron metabolism. Intraplaque hemorrhage and hemoglobin (Hb) catabolism by macrophages are associated with atherosclerotic lesion instability. The study aims were to investigate sex differences in (1) lesion severity in relation to blood Hb, (2) iron homeostasis in human carotid plaques, and (3) macrophage polarization within atheroma. Methods-The carotid artery samples from 39 men and 23 women were immunostained with cell markers for macrophages, smooth muscle cells, ferritin, and TfR1 (transferrin receptor 1), which were further analyzed according to sex in relation to iron, Hb, and lipids in circulation. Additionally, samples of predefined regions from human carotid atherosclerotic lesions, including internal controls, were used for proteomic analysis by mass spectrometry. Results-Male patients, compared with women, had larger necrotic cores and more plaque rupture, which were associated with higher levels of Hb. Atheroma of male patients had significantly higher levels of Hb in circulation and CD68 macrophages, ferritin, and TfR1 in lesions. CD68 macrophages were significantly correlated with ferritin and TfR1. Plaques from male patients comparatively possessed higher levels of inflammatory macrophage subsets, CD86 (M1) and CD163 (M2), but lower levels of STF (serotransferrin) and HPX (hemopexin). Conclusions-Male patients with carotid atheroma had more advanced and ruptured lesions associated with significantly higher levels of inflammatory macrophage infiltration and high iron stores in the blood and in their plaques. These findings help to understand sex differences and iron metabolism in atherosclerosis and factors related to atheroma progression.

  • 6.
    Zhou, Zien
    et al.
    Univ New South Wales, Australia; Shanghai Jiao Tong Univ, Peoples R China.
    Lindley, Richard I.
    George Inst Global Hlth, Australia; Univ Sydney, Australia.
    Rådholm, Karin
    Linköping University, Department of Medical and Health Sciences, Division of Community Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Primary Care Center, Primary Health Care Center Ödeshög. George Inst Global Hlth, Australia; Univ Sydney, Australia.
    Jenkins, Bronwyn
    Royal North Shore Hosp, Australia.
    Watson, John
    Univ New South Wales, Australia.
    Perkovic, Vlado
    Univ New South Wales, Australia; Univ Sydney, Australia; Royal North Shore Hosp, Australia.
    Mahaffey, Kenneth W.
    Stanford Univ, CA 94305 USA.
    de Zeeuw, Dick
    Univ Groningen, Netherlands.
    Fulcher, Greg
    Univ Sydney, Australia; Royal North Shore Hosp, Australia.
    Shaw, Wayne
    Janssen Res and Dev LLC, NJ USA.
    Oh, Richard
    Janssen Res and Dev LLC, NJ USA.
    Desai, Mehul
    Janssen Res and Dev LLC, NJ USA.
    Matthews, David R.
    Univ Oxford, England; Univ Oxford, England.
    Neal, Bruce
    Univ New South Wales, Australia; Univ New South Wales, Australia; Univ Sydney, Australia; Imperial Coll London, England.
    Canagliflozin and Stroke in Type 2 Diabetes Mellitus Results From the Randomized CANVAS Program Trials2019In: Stroke, ISSN 0039-2499, E-ISSN 1524-4628, Vol. 50, no 2, p. 396-404Article in journal (Refereed)
    Abstract [en]

    Background and Purpose-This study reports the detailed effects of canagliflozin on stroke, stroke subtypes, and vascular outcomes in participants with and without cerebrovascular disease (stroke or transient ischemic attack) at baseline from the CANVAS (Canagliflozin Cardiovascular Assessment Study) Program. Methods-The CANVAS Program, comprising 2 similarly designed and conducted clinical trials, randomly assigned 10 142 participants with type 2 diabetes mellitus and high cardiovascular risk to canagliflozin or placebo. Its primary outcome was a composite of major adverse cardiovascular events. The main outcome of interest for this report was fatal or nonfatal stroke. Additional exploratory outcomes were stroke subtypes and other vascular outcomes defined according to standard criteria. Results-There were 1 958 (19%) participants with prior stroke or transient ischemic attack at baseline. These individuals were older, more frequently women, and had higher rates of heart failure, atrial fibrillation, and microvascular disease (all Pamp;lt;0.001) compared with those without such a history. There were 309 participants with stroke events during followup (123 had prior stroke or transient ischemic attack at baseline and 186 did not), at a rate of 7.93/1000 patient-years among those assigned canagliflozin and 9.62/1000 patient-years among placebo (hazard ratio, 0.87; 95% CI, 0.691.09). Analysis of stroke subtypes found no effect on ischemic stroke (n=253, hazard ratio, 0.95; 95% CI, 0.74-1.22), a significant reduction for hemorrhagic stroke (n=30, hazard ratio, 0.43; 95% CI, 0.20-0.89) and no effect on undetermined stroke (n=29, hazard ratio, 1.04; 95% CI, 0.48-2.22). Effects on other cardiovascular outcomes were comparable among participants with and without stroke or transient ischemic attack at baseline. Conclusions-There were too few events in the CANVAS Program to separately define the effects of canagliflozin on stroke, but benefit is more likely than harm. The observed possible protective effect for hemorrhagic stroke was based on small numbers but warrants further investigation.

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