Asymmetrical dimethylarginine level in atrial fibrillation

Atrial fibrillation (AF) is known to be related with increased risk of thromboembolic events. Asymmetrical dimethylarginine (ADMA), which is an endogenous inhibitor of nitric oxide synthase (NOS), can cause endothelial dysfunction by decreasing nitric oxide (NO) and lead to increased risk of thrombosis. In the present study our aim was to compare plasma levels of ADMA in patients with acute onset (< 24 hours) and chronic AF (> 1 year) to determine the risk of thrombosis.

17 patients with the first detected attack of AF within the first 24 hours of presentation (group 1), 25 patients who had permanent chronic AF lasting at least 1 year or more (group II) and 18 healthy persons as the control group (group III) were included in the study. For each patient the plasma ADMA, L-arginine, symmetrical dimethylarginine (SDMA) concentrations were measured by high-performance liquid chromatography in venous blood samples collected before cardioversion. We compared the plasma ADMA, L-arginine and SDMA concentrations between the groups.

Plasma L-arginine (78.18 +/- 28.29 vs. 73.14 +/- 14.11 vs. 71.03 +/- 21.31, P = 0.549) and plasma SDMA concentrations (0.38 +/-0.18 vs. 0.42 +/- 0.21 vs. 0.32 +/- 0.24, P = 0.224) were similar in all groups. There was a significant difference between plasma ADMA concentrations (0.76 +/- 0.27 vs. 0.50 +/- 0.26 vs. 0.36 +/- 0.20, P < 0.001) among the groups. When we compared plasma ADMA levels between the subgroups, we also found a significant difference (P = 0.002 when comparing group I and group II, P < 0.001 when comparing of group I and group III, P = 0.042 when compareng of group II and group III).

ADMA levels in patients with acute onset AF were significantly increased when compared with patients with chronic AF and the healthy control group indicating the presence of endothelial dysfunction and a prothrombotic state even in a very early phase of AF.