Clinical Chemistry 56: 111-120, 2010. First published November 5, 2009; 10.1373/clinchem.2009.136200
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Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
(Clinical Chemistry. 2010;56:111-120.)
© 2010 American Association for Clinical Chemistry, Inc.

Lipids, Lipoproteins, and Cardiovascular Risk Factors

Distribution of Asymmetric Dimethylarginine among 980 Healthy, Older Adults of Different Ethnicities

Karsten Sydow1,4, Stephen P. Fortmann2, Joan M. Fair2, Ann Varady2, Mark A. Hlatky3, Alan S. Go5,6, Carlos Iribarren5, Philip S. Tsao1,a for the ADVANCE Investigators7

1 Division of Cardiovascular Medicine, 2 Stanford Prevention Research Center, and 3 Department of Health Research and Policy, Stanford University School of Medicine, Stanford, CA; 4 Department of Cardiology, Hamburg University Heart Center, Hamburg, Germany; 5 Division of Research, Kaiser Permanente of Northern California, Oakland, CA; 6 Department of Epidemiology and Department of Biostatistics and Medicine, University of California, San Francisco, CA.
7 The Atherosclerotic Disease, Vascular Function, and Genetic Epidemiology (ADVANCE) Study is a collaboration between investigators at Stanford University Medical School and Kaiser Permanente Division of Research and was funded in part by a grant from the Donald W. Reynolds Foundation (Las Vegas, NV).

aAddress correspondence to this author at: Stanford University School of Medicine, Division of Cardiovascular Medicine, 300 Pasteur Drive, Stanford, CA 94305-5406. Fax 650-725-2178; e-mail ptsao{at}stanford.edu.

Background: Endothelium-derived nitric oxide plays a crucial role in the regulation of vascular tone and the development of cardiovascular disease. The endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) has emerged as a novel cardiovascular risk factor. ADMA appears to be an independent predictor for cardiovascular and overall mortality. However, the majority of studies investigating the clinical role of ADMA were performed in European study populations with few individuals of other ethnicities.

Methods: We performed a cross-sectional study of 980 healthy, older (age 60–72 years) individuals of different ethnicities living in the San Francisco Bay area and analyzed ADMA plasma concentrations and their relationship to other cardiovascular risk factors. Plasma ADMA concentrations were measured using a recently developed, highly sensitive ELISA.

Results: In our entire sample, we were able to define a reference interval for ADMA plasma concentrations of 0.47 (90% CI 0.46–0.48) µmol/L to 0.85 (0.84–0.89) µmol/L. The mean ADMA concentration was 0.63 (SD 0.11) µmol/L (median 0.61 µmol/L). Mean ADMA concentrations were significantly lower in African Americans (0.60 µmol/L; P < 0.01) and mixed non-Hispanics (0.60 µmol/L; P < 0.05) compared with whites (0.63 µmol/L). ADMA was positively correlated with cystatin-C in both men ({rho} = 0.29) and women ({rho} = 0.37), and median plasma ADMA concentrations increased across cystatin-C quintiles.

Conclusions: ADMA varies nearly 2-fold across a healthy sample of older men and women, correlates with age, body mass index, and renal function, and is different across ethnic groups. Additional studies in a wider age range and including larger ethnic subgroups would be useful.