Levels of asymmetrical dimethylarginine are predictive of brachial artery flow-mediated dilation 6 years later. The Cardiovascular Risk in Young Finns Study
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.
aDivision of Emergency, University Hospital of Tampere, Tampere, Finland
bDepartment of Clinical Chemistry, Tampere University Hospital and University of Tampere Medical School, Tampere, Finland
cDepartment of Clinical Physiology, University of Tampere and Tampere University Hospital, Tampere, Finland
dMedical School, University of Tampere, Tampere, Finland
eNational Institute of Health and Welfare, Helsinki, Finland
fDepartment of Medicine, University of Turku and Turku University Hospital, Turku, Finland
gDepartment of Clinical Pharmacology, University of Helsinki, Helsinki, Finland
hDepartment of Pediatrics, University of Tampere and Tampere University Hospital, Tampere, Finland
iDepartment of Clinical Physiology, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland
jDepartment of Pediatrics, Vaasa Central Hospital, Vaasa, Finland
kDepartment of Clinical Physiology, Turku University Hospital and Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland
Corresponding 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.
ABSTRACT
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