Asymmetric dimethylarginine (ADMA) as a risk marker for stroke and TIA in a Swedish population.

Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, has been shown to be involved in the pathogenesis of atherosclerosis. The present study was initiated to investigate the role of ADMA as a risk marker of acute cerebrovascular disease (CVD). We examined 363 CVD patients and 48 controls. The ADMA concentration (mean+/-S.D., mumol/L) in controls was 0.50 +/- 0.06. Compared to controls, increased concentrations of ADMA were observed in cardio-embolic infarction (0.55 +/- 0.08; p < 0.001; n = 71), and TIA (0.54 +/-0 .05; p < 0.001; n = 31), but not in non-cardio-embolic infarction (0.51 +/- 0.07; p = 0.56; n = 239) and haemorrhagic stroke (0.51 +/- 0.11; p = 0.77; n = 22). In multivariate logistic regression models, CVD increased across quartiles of ADMA in all subgroups, but this association was only significant in the TIA group (odds ratio for highest versus lowest quartile 13.1; 95% CI: 2.9-58.6; p trend 0.001) A decreased arginine/ADMA ratio was significantly associated with CVD in the entire study population (p < 0.01). Our results indicate that ADMA is a weak independent marker for acute stroke and a strong marker for TIA and that relative arginine deficiency, measured as the l-arginine/ADMA ratio, is present in acute CVD.