Published Online
on January 4, 2007

A more recent version of this article appeared on February 1, 2007

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Submitted on August 17, 2006
Accepted on September 13, 2006

Asymmetric Dimethylarginine in Cerebral Small Vessel Disease

Usman Khan MRCP; Ahamad Hassan MRCP; Patrick Vallance FRCP; and Hugh S. Markus FRCP^*

From Centre for Clinical Neuroscience, St George’s University of London, London, UK.

^* To whom correspondence should be addressed. E-mail: hmarkus{at}sgul.ac.uk.

Background and Purpose--Endothelial dysfunction may play a causal role in cerebral small vessel disease (SVD). Asymmetric dimethylarginine (ADMA), a circulating endogenous inhibitor of nitric oxide, has been implicated in endothelial dysfunction, particularly in hyperhomocystinemia, a known risk factor for SVD. We determined if ADMA was elevated in SVD, correlated with disease severity, and interacted with homocysteine.

Methods--ADMA and homocysteine levels were determined in 47 consecutive symptomatic SVD patients and 38 controls. SVD was graded by leukoariosis severity and number of lacunar infarcts.

Results--Mean (and SD) ADMA was higher in SVD patients compared with controls (0.814 [0.145] versus 0.747 [0.184] µmol/L; P=0.014) after controlling for age, gender, vascular risk factors, and creatinine clearance. Additionally controlling for homocysteine had only a small effect on this relationship (P=0.055). Mean homocysteine was higher in SVD cases compared with controls (15.14 [5.59] versus 12.49 [4.15] µmol/L; P=0.035). Leukoariosis grade correlated positively with ADMA (P=0.026) and homocysteine (P=0.003). Lacunar grade correlated with homocysteine (P=0.017), but not ADMA.

Conclusions--ADMA is independently associated with SVD and correlates with leukoariosis severity.

Key words: ADMA • endothelial dysfunction • homocysteine • lacunar • leukoaraiosis • stroke

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