Chronic Amiodarone Therapy Impairs the Function of the Superior Sinoatrial Node in Patients With Atrial Fibrillation

DOI Web Site PubMed 被引用文献3件 参考文献23件
  • Mun Hee-Sun
    Division of Cardiology, Department of Medicine, Yonsei University College of Medicine Division of Cardiology, Department of Internal Medicine, Kangnam Sacred Heart Hospital, Hallym University Medical Center
  • Shen Changyu
    the Department of Biostatistics, the Division of Cardiology, Department of Medicine, Indiana University School of Medicine
  • Pak Hui-Nam
    Division of Cardiology, Department of Medicine, Yonsei University College of Medicine
  • Lee Moon-Hyoung
    Division of Cardiology, Department of Medicine, Yonsei University College of Medicine
  • Lin Shien-Fong
    the Krannert Institute of Cardiology, the Division of Cardiology, Department of Medicine, Indiana University School of Medicine
  • Chen Peng-Sheng
    the Krannert Institute of Cardiology, the Division of Cardiology, Department of Medicine, Indiana University School of Medicine
  • Joung Boyoung
    Division of Cardiology, Department of Medicine, Yonsei University College of Medicine

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Background: The mechanisms underlying amiodarone-induced sinoatrial node (SAN) dysfunction remain unclear, so we used 3-dimensional endocardial mapping of the right atrium (RA) to investigate. Methods and Results: In a matched-cohort design, 18 patients taking amiodarone before atrial fibrillation (AF) ablation (amiodarone group) were matched for age, sex and type of AF with 18 patients who had undergone AF ablation without taking amiodarone (no-amiodarone group). The amiodarone group had a slower heart rate than the no-amiodarone group at baseline and during isoproterenol infusion. Only the amiodarone group had sick sinus syndrome (n=4, 22%, P=0.03) and abnormal (>550ms) corrected SAN recovery time (n=5, 29%; P=0.02). The median distance from the junction of the superior vena cava (SVC) and RA to the most cranial earliest activation site (EAS) was longer in the amiodarone group than in the no-amiodarone group at baseline (20.5 vs. 10.6mm, P=0.04) and during isoproterenol infusion (12.8 vs. 6.3mm, P=0.03). The distance from the SVC-RA junction to the EAS negatively correlated with the P-wave amplitudes of leads II (r=–0.47), III (r=–0.60) and aVF (r=–0.56) (P<0.001 for all). Conclusions: In a quarter of the AF patients, amiodarone causes superior SAN dysfunction, which results in a downward shift of the EAS and reduced P-wave amplitude in leads II, III and aVF at baseline and during isoproterenol infusion.  (Circ J 2013; 77: 2255–2263)<br>

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  • Circulation Journal

    Circulation Journal 77 (9), 2255-2263, 2013

    一般社団法人 日本循環器学会

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