0127: Atrial fibrillation is associated with a marker of endothelial function and oxidative stress in patients with acute myocardial infarction

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• 作者：Karim Stamboul⁽¹⁾ ; Julie Lorin⁽²⁾ ; Luc Lorgis⁽²⁾ ; Jean-Claude Beer⁽²⁾ ; Claude Touzery⁽²⁾ ; Luc Rochette⁽²⁾ ; Catherine Vergely⁽²⁾ ; Yves Cottin⁽²⁾ ; Marianne Zeller ; ⁽²⁾ ; ^{marianne.zeller@u-bourgogne.fr" class="auth_mail" title="E-mail the corresponding author}
• 刊名：Archives of Cardiovascular Diseases Supplements
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：8
• 期：1
• 页码：15
• 全文大小：50 K

文摘

Atrial fibrillation (AF), whether silent or symptomatic, is a frequent and severe complication of acute myocardial infarction (AMI). Asymmetric dimethylarginine (ADMA), an endogenous eNOS inhibitor, is a risk factor for endothelial dysfunction. We addressed the relationship between ADMA plasma levels and AF occurrence in AMI.

Methods

273 patients hospitalized for AMI were included. Continuous electrocardiographic monitoring (CEM) ≥48 hours was recorded and ADMA was measured by High Performance Liquid Chromatography on admission blood sample.

Results

The incidence of silent and symptomatic AF was 39(14%) and 29 (11%), respectively. AF patients were markedly older than patients without AF (≈20y). There was a trend towards higher ADMA levels in patients with symptomatic AF than in patients with silent AF or no AF (0.53 vs 0.49 and 0.49 µmol/L, respectively). After matching on age, we found that patients with symptomatic AF had a higher heart rate on admission and a higher rate of patients with LV dysfunction (28% vs. 3%, p=0.025). Patients who developed symptomatic AF had a higher ADMA level (0.53 vs. 0.43 µmol/L; p=0.001). Multivariate logistic regression analysis to estimate symptomatic AF occur-rence showed that ADMA was independently associated with symptomatic AF (OR: 2.46 [1.21-5.00], p=0.013) beyond history of AF, LVEF<40% and elevated HR.

Conclusion

We show that high ADMA level is associated with the occur-rence of AF. Although no causative role can be concluded from our observational study, our work further supports the hypothesis that endothelial dysfunction is involved in the pathogenesis of AF in AMI.