Article ID Journal Published Year Pages File Type
2895324 Atherosclerosis 2006 7 Pages PDF
Abstract
We examined 363 CVD patients and 48 controls. The ADMA concentration (mean ± S.D., μmol/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.
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