Source:http://linkedlifedata.com/resource/pubmed/id/12736484
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2003-5-8
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| pubmed:abstractText |
The aims of this study were to evaluate the changes in the electrophysiological characteristics of the right atrium after the administration of flecainide and to clarify whether flecainide has a selective effect on human atrial tissue. Electrophysiological measurements were made in 38 patients, before and after intravenous administration of flecainide (2 mg/kg per 10 min). The effective refractory period of the right atrium (ERP-A), maximum conduction delay (Max.CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAAZ), and conduction delay zone (CDZ) were studied in the patients who were divided into 2 groups based on whether repetitive atrial firing (RAF) was induced in the baseline study. Flecainide significantly prolonged the ERP-A (202+/-22 to 238+/-33 ms, p<0.001) and shortened Max.CD (77+/-17 to 63+/-32 ms, p<0.05) in the patients with RAF, but not in those without RAF in the baseline study. After flecainide administration, there were significant reductions in the RAFZ (43+/-22 to 13+/-19 ms, p<0.0001), FAAZ (51+/-22 to 28+/-26 ms, p<0.001) and CDZ (70+/-21 to 48+/-30 ms, p<0.01) in the patients with RAF. However, atrial fibrillation (AF) was induced by stimulation after flecainide in 2 patients without RAF in the baseline study. There was a significant negative correlation between the ERP-A in the baseline study and the change in the ERP-A upon flecainide administration (r=0.45, p<0.01). Flecainide may preferentially activate the substrate for AF and RAF, but that action is mainly based on the electrophysiological characteristics found in the baseline study.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1346-9843
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| pubmed:author |
pubmed-author:DoiMasahiroM,
pubmed-author:EsatoMasahiroM,
pubmed-author:ItagakiKazuoK,
pubmed-author:KakugawaHiroyukiH,
pubmed-author:KimuraMasayasuM,
pubmed-author:MatsuzakiMasunoriM,
pubmed-author:OhmuraMasatoM,
pubmed-author:ShimizuAkihikoA,
pubmed-author:UeyamaTakeshiT,
pubmed-author:YamagataToshihikoT,
pubmed-author:YoshigaYasuhiroY
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| pubmed:issnType |
Print
|
| pubmed:volume |
67
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
437-42
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| pubmed:dateRevised |
2004-11-17
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| pubmed:meshHeading |
pubmed-meshheading:12736484-Anti-Arrhythmia Agents,
pubmed-meshheading:12736484-Atrial Fibrillation,
pubmed-meshheading:12736484-Electrocardiography,
pubmed-meshheading:12736484-Electrophysiology,
pubmed-meshheading:12736484-Female,
pubmed-meshheading:12736484-Flecainide,
pubmed-meshheading:12736484-Heart Atria,
pubmed-meshheading:12736484-Heart Conduction System,
pubmed-meshheading:12736484-Humans,
pubmed-meshheading:12736484-Male,
pubmed-meshheading:12736484-Middle Aged,
pubmed-meshheading:12736484-Regression Analysis
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| pubmed:year |
2003
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| pubmed:articleTitle |
Effects of flecainide on the electrophysiological properties of atrial vulnerability in humans.
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| pubmed:affiliation |
The Department of Medical Bioregulation, Faculty of Science, Yamaguchi University School of Medicine, Ube, Japan.
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| pubmed:publicationType |
Journal Article
|