Source:http://linkedlifedata.com/resource/pubmed/id/10525245
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
4
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| pubmed:dateCreated |
1999-12-23
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| pubmed:abstractText |
The local dispersion of conduction and refractoriness has been considered essential for induction of atrial arrhythmias. This study sought to determine whether a difference of refractoriness and vulnerability for induction of atrial fibrillation between trabeculated and smooth as well as high and low right atrium may contribute to initiation of atrial fibrillation in dogs. In 14 healthy mongrel dogs weighing 22.4 +/- 1 kg, closed-chest endocardial programmed stimulation was performed from four distinct right atrial sites. Atrial refractory periods and vulnerability for induction of atrial fibrillation or premature atrial complexes were determined during a basic cycle length of 400 and 300 ms and an increasing pacing current strength. For a pacing cycle length of 300 ms, atrial refractory periods were longer on the smooth, as compared to the trabeculated right atrium (102 +/- 25 vs. 97 +/- 17 ms, p < 0.05), whereas for a pacing cycle length of 400 ms, there was no significant difference. The duration of the vulnerability zone for induction of atrial fibrillation was longer on the smooth right atrium, for a cycle length of both 400 ms (40 +/- 30 vs. 31 +/- 22 ms; p < 0.05) and 300 ms (33 +/- 25 vs. 23 +/- 21 ms; p < 0. 01). When comparing high and low right atrium, refractory periods were longer on the the low right atrium, for a cycle length of both 400 ms (111 +/- 23 vs. 94 +/- 24 ms; p < 0.01) and 300 ms (104 +/- 20 vs. 96 +/- 23 ms; p < 0.01). For a pacing cycle length of 300 ms, the duration of the atrial fibrillation vulnerability zone was longer for the high, as compared to the low right atrium (34 +/- 22 vs. 22 +/- 22, p < 0.01). Seven dogs with easily inducible episodes of atrial fibrillation demonstrated significantly shorter refractory periods as compared to 7 non-vulnerable dogs, regardless of pacing site and current strength. In conclusion, significant differences in refractoriness and vulnerability for induction of atrial fibrillation can be observed in the area of the crista terminalis in healthy dogs. Thus, local anatomic factors may play a role in the initiation of atrial fibrillation.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
1383-875X
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
3
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
311-9
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| pubmed:dateRevised |
2009-11-3
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| pubmed:meshHeading |
pubmed-meshheading:10525245-Animals,
pubmed-meshheading:10525245-Atrial Fibrillation,
pubmed-meshheading:10525245-Atrial Function, Right,
pubmed-meshheading:10525245-Cardiac Pacing, Artificial,
pubmed-meshheading:10525245-Disease Susceptibility,
pubmed-meshheading:10525245-Dogs,
pubmed-meshheading:10525245-Refractory Period, Electrophysiological
|
| pubmed:year |
1999
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| pubmed:articleTitle |
The spatial dispersion of atrial refractoriness and atrial fibrillation vulnerability.
|
| pubmed:affiliation |
Section of Cardiac Electrophysiology, Department of Medicine and Cardiovascular Research Institute, University of California, San Francisco, 94143-1354, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|