gms | German Medical Science

33rd International Congress on Electrocardiology

International Society of Electrocardiology

Asymmetrical dimethylarginine levels in acute onset and chronic atrial fibrillation

Meeting Abstract

  • A. Cengel - Gazi University Medical School, Ankara, Türkei
  • corresponding author presenting/speaker A. Sahinarslan - Gazi University Medical School, Ankara, Türkei
  • G. Biberoglu - Gazi University Medical School, Ankara, Türkei
  • A. Hasanoglu - Gazi University Medical School, Ankara, Türkei
  • Y. Tavil - Gazi University Medical School, Ankara, Türkei
  • M. Ozdemir - Gazi University Medical School, Ankara, Türkei

33rd International Congress on Electrocardiology. Cologne, 28.06.-01.07.2006. Düsseldorf, Köln: German Medical Science; 2007. Doc06ice120

The electronic version of this article is the complete one and can be found online at:

Published: February 8, 2007

© 2007 Cengel et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Question: It is known that atrial fibrillation (AF) is 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.

Method: 17 patients with the first detected attack of AF within the first 24 hours of presentation (Group I), 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, 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.

Results: 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 groups as pairs we also found a significant difference ( p=0.003 for comparison of Group I and Group II, p<0.001 for comparison of Group I and Group III, p=0.045 for comparison of Group II and Group III).

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