Trial reportCirculation journal : official journal of the Japanese Circulation Society2013
Chronic amiodarone therapy impairs the function of the superior sinoatrial node in patients with atrial fibrillation.
Trial report in Circulation journal : official journal of the Japanese Circulation Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Simple electrocardiographic index for A4-wave amplitude of the VDD leadless pacemaker.Heart rhythm O2 · 2025Article
- In silico study of the effects of anti-arrhythmic drug treatment on sinoatrial node function for patients with atrial fibrillation.Scientific reports · 2020Article
- 2018 Korean Guideline of Atrial Fibrillation Management.Korean circulation journal · 2018Review
- Function and dysfunction of human sinoatrial node.Korean circulation journal · 2015Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe 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
resultsIn 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).
conclusionsIn 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.
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