Atherosclerosis
Volume 185, Issue 2 , Pages 271-277, April 2006

Asymmetric dimethylarginine (ADMA) as a risk marker for stroke and TIA in a Swedish population

  • P. Wanby

      Affiliations

    • Department of Internal Medicine, County Hospital of Kalmar, SE-391 85 Kalmar, Sweden
    • Faculty of Health Sciences, Linkoping University, Linkoping, Sweden
    • Corresponding Author InformationCorresponding author. Tel.: +46 480 448204; fax +46 480 81998.
  • ,
  • T. Teerlink

      Affiliations

    • Department of Clinical Chemistry, VU University Medical Center, Amsterdam, Netherlands
  • ,
  • L. Brudin

      Affiliations

    • Department of Clinical Physiology, County Hospital of Kalmar, Sweden
  • ,
  • L. Brattström

      Affiliations

    • Department of Internal Medicine, County Hospital of Kalmar, SE-391 85 Kalmar, Sweden
    • Faculty of Health Sciences, Linkoping University, Linkoping, Sweden
  • ,
  • I. Nilsson

      Affiliations

    • Department of Clinical Chemistry, County Hospital of Kalmar, SE-391 85 Kalmar, Sweden
  • ,
  • P. Palmqvist

      Affiliations

    • Department of Internal Medicine, County Hospital of Kalmar, SE-391 85 Kalmar, Sweden
    • Faculty of Health Sciences, Linkoping University, Linkoping, Sweden
  • ,
  • M. Carlsson

      Affiliations

    • Department of Internal Medicine, County Hospital of Kalmar, SE-391 85 Kalmar, Sweden
    • Faculty of Health Sciences, Linkoping University, Linkoping, Sweden
    • Department of Clinical Chemistry, County Hospital of Kalmar, SE-391 85 Kalmar, Sweden
    • Corresponding Author InformationCorresponding author. Tel.: +46 480 81456; fax: +46 480 81025.

Received 13 April 2005; received in revised form 8 June 2005; accepted 21 June 2005. published online 01 August 2005.

Abstract 

Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has been shown to be involved in the pathogenesis of atherosclerosis. The present study was initiated to investigate the role of ADMA as a risk marker of acute cerebrovascular disease (CVD).

We examined 363 CVD patients and 48 controls. The ADMA concentration (mean±S.D., μmol/L) in controls was 0.50±0.06. Compared to controls, increased concentrations of ADMA were observed in cardio-embolic infarction (0.55±0.08; p<0.001; n=71), and TIA (0.54±0.05; p<0.001; n=31), but not in non-cardio-embolic infarction (0.51±0.07; p=0.56; n=239) and haemorrhagic stroke (0.51±0.11; p=0.77; n=22). In multivariate logistic regression models, CVD increased across quartiles of ADMA in all subgroups, but this association was only significant in the TIA group (odds ratio for highest versus lowest quartile 13.1; 95% CI: 2.9–58.6; p trend 0.001) A decreased arginine/ADMA ratio was significantly associated with CVD in the entire study population (p<0.01). Our results indicate that ADMA is a weak independent marker for acute stroke and a strong marker for TIA and that relative arginine deficiency, measured as the l-arginine/ADMA ratio, is present in acute CVD.

Keywords: Asymmetric dimethylarginine, Arginine, Atherosclerosis, Stroke, TIA

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PII: S0021-9150(05)00441-7

doi:10.1016/j.atherosclerosis.2005.06.033

Atherosclerosis
Volume 185, Issue 2 , Pages 271-277, April 2006