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Levels of asymmetrical dimethylarginine are predictive of brachial artery flow-mediated dilation 6 years later. The Cardiovascular Risk in Young Finns Study

Hannu PäiväabCorresponding Author Informationemail address, Mika Kähönenc, Terho Lehtimäkibd, Georg Alfthane, Jorma Viikarif, Reijo Laaksonenbg, Nina Hutri-Kähönenh, Tomi Laitineni, Leena Taittonenj, Olli T. Raitakarifk, Markus Juonalaf

Received 9 May 2010; received in revised form 19 June 2010; accepted 21 June 2010. published online 23 July 2010.
Corrected Proof

Abstract 

Aim

Plasma asymmetric dimethylarginine (ADMA) is a novel risk factor for atherosclerosis and has been observed to associate with endothelial function in cross-section studies. In the present study our aim was to investigate whether plasma ADMA levels are predictive of brachial artery endothelial function in a prospective setting.

Methods and results

Using ultrasound we measured brachial artery flow-mediated dilation (FMD) both in 2001 and 2007 in 1808 healthy subjects aged 24–39 years at baseline. Plasma methylarginines were determined by isocratic high-pressure liquid chromatography in 2001. In a multivariable model adjusted with brachial diameter and conventional cardiovascular risk factors, baseline ADMA levels had a significant inverse association with FMD measured 6 years later (β±SE: −1.89±0.69%, P=0.006).

Conclusions

We conclude that plasma ADMA can predict brachial artery FMD in subjects without prevalent atherosclerotic disease. These data suggest that plasma ADMA may have a determinative role in predicting endothelial function.

a Division of Emergency, University Hospital of Tampere, Tampere, Finland

b Department of Clinical Chemistry, Tampere University Hospital and University of Tampere Medical School, Tampere, Finland

c Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Tampere, Finland

d Medical School, University of Tampere, Tampere, Finland

e National Institute of Health and Welfare, Helsinki, Finland

f Department of Medicine, University of Turku and Turku University Hospital, Turku, Finland

g Department of Clinical Pharmacology, University of Helsinki, Helsinki, Finland

h Department of Pediatrics, University of Tampere and Tampere University Hospital, Tampere, Finland

i Department of Clinical Physiology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland

j Department of Pediatrics, Vaasa Central Hospital, Vaasa, Finland

k Department of Clinical Physiology, Turku University Hospital and Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland

Corresponding Author InformationCorresponding author at: Division of Emergency, University Hospital of Tampere, PO Box 2000, 33521 Tampere, Finland. Tel.: +358 3 311 611; fax: +358 3 311 65346.

PII: S0021-9150(10)00498-3

doi:10.1016/j.atherosclerosis.2010.06.041

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