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ADMA should not yet inform clinical decisions; leaves open its causal role in CVD pending mechanistic and interventional studies.
Asymmetric dimethylarginine (ADMA) is a methylated derivative of the amino acid L-arginine that is receiving increasing attention as a cardiovascular risk factor. As a structural analog of L-arginine, ADMA can inhibit the activity of nitric oxide (NO) synthase, resulting in decreased NO production in blood vessels and other tissues. While substantial epidemiological and experimental evidence links elevated levels of ADMA with endothelial dysfunction and adverse vascular events, the causative role of ADMA in cardiovascular diseases remains still largely unproven. To definitively determine whether ADMA is a biomarker or a causative risk factor, a better understanding of the biochemistry, genetics, and pharmacology of the ADMA metabolic pathways is needed.
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Rodionov et al. (2008) studied this question.
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