Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation

Hee Sun Mun, Changyu Shen, huinam pak, Moon Hyoung Lee, Shien Fong Lin, Peng Sheng Chen, Boyoung Joung

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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 (>550 ms) 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. 10.6 mm, P=0.04) and during isopro-terenol infusion (12.8 vs. 6.3 mm, 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 isoproter-enol infusion.

Original languageEnglish
Pages (from-to)2255-2263
Number of pages9
JournalCirculation Journal
Volume77
Issue number9
DOIs
Publication statusPublished - 2013 Aug 28

Fingerprint

Sinoatrial Node
Amiodarone
Atrial Fibrillation
Heart Atria
Therapeutics
Superior Vena Cava
Sick Sinus Syndrome
Isoproterenol
Research Design
Heart Rate

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Mun, Hee Sun ; Shen, Changyu ; pak, huinam ; Lee, Moon Hyoung ; Lin, Shien Fong ; Chen, Peng Sheng ; Joung, Boyoung. / Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation. In: Circulation Journal. 2013 ; Vol. 77, No. 9. pp. 2255-2263.
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title = "Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation",
abstract = "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 (>550 ms) 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. 10.6 mm, P=0.04) and during isopro-terenol infusion (12.8 vs. 6.3 mm, 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 isoproter-enol infusion.",
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Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation. / Mun, Hee Sun; Shen, Changyu; pak, huinam; Lee, Moon Hyoung; Lin, Shien Fong; Chen, Peng Sheng; Joung, Boyoung.

In: Circulation Journal, Vol. 77, No. 9, 28.08.2013, p. 2255-2263.

Research output: Contribution to journalArticle

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T1 - Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation

AU - Mun, Hee Sun

AU - Shen, Changyu

AU - pak, huinam

AU - Lee, Moon Hyoung

AU - Lin, Shien Fong

AU - Chen, Peng Sheng

AU - Joung, Boyoung

PY - 2013/8/28

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N2 - 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 (>550 ms) 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. 10.6 mm, P=0.04) and during isopro-terenol infusion (12.8 vs. 6.3 mm, 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 isoproter-enol infusion.

AB - 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 (>550 ms) 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. 10.6 mm, P=0.04) and during isopro-terenol infusion (12.8 vs. 6.3 mm, 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 isoproter-enol infusion.

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