Source:http://linkedlifedata.com/resource/pubmed/id/21148762
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2011-2-1
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pubmed:abstractText |
Congestive heart failure (CHF) predisposes to ventricular fibrillation (VF) in association with electrical remodeling of the ventricle. However, much remains unknown about the rate-dependent electrophysiological properties in a failing heart. Action potential properties in the left ventricular subepicardial muscles during dynamic pacing were examined with optical mapping in pacing-induced CHF (n=18) and control (n=17) rabbit hearts perfused in vitro. Action potential durations (APDs) in CHF were significantly longer than those observed for controls at basic cycle lengths (BCLs)>1,000 ms but significantly shorter at BCLs<400 ms. Spatial APD dispersions were significantly increased in CHF versus control (by 17-81%), and conduction velocity was significantly decreased in CHF (by 6-20%). In both groups, high-frequency stimulation (BCLs<150 ms) always caused spatial APD alternans; spatially concordant alternans and spatially discordant alternans (SDA) were induced at 60% and 40% in control, respectively, whereas 18% and 82% in CHF. SDA in CHF caused wavebreaks followed by reentrant excitations, giving rise to VF. Incidence of ventricular tachycardia/VFs elicited by high-frequency dynamic pacing (BCLs<150 ms) was significantly higher in CHF versus control (93% vs. 20%). In CHF, left ventricular subepicardial muscles show significant APD shortenings at short BCLs favoring reentry formations following wavebreaks in association with SDA. High-frequency excitation itself may increase the vulnerability to VF in CHF.
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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 |
Feb
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pubmed:issn |
1522-1539
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pubmed:author |
pubmed-author:HaradaMasahideM,
pubmed-author:HonjoHaruoH,
pubmed-author:IndenYasuyaY,
pubmed-author:IshiguroYuko SYS,
pubmed-author:KamiyaKaichiroK,
pubmed-author:KodamaItsuoI,
pubmed-author:LeeJong-KookJK,
pubmed-author:MuroharaToyoakiT,
pubmed-author:OkunoYusukeY,
pubmed-author:SakumaIchiroI,
pubmed-author:TakanariHirokiH,
pubmed-author:TsujiYukiomiY
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pubmed:issnType |
Electronic
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pubmed:volume |
300
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H565-73
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pubmed:meshHeading |
pubmed-meshheading:21148762-Action Potentials,
pubmed-meshheading:21148762-Animals,
pubmed-meshheading:21148762-Arrhythmias, Cardiac,
pubmed-meshheading:21148762-Calcium Channels, L-Type,
pubmed-meshheading:21148762-Cardiac Pacing, Artificial,
pubmed-meshheading:21148762-Electrophysiological Phenomena,
pubmed-meshheading:21148762-Heart Failure,
pubmed-meshheading:21148762-Heart Ventricles,
pubmed-meshheading:21148762-Microelectrodes,
pubmed-meshheading:21148762-Rabbits,
pubmed-meshheading:21148762-Ventricular Fibrillation
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pubmed:year |
2011
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pubmed:articleTitle |
Rate-dependent shortening of action potential duration increases ventricular vulnerability in failing rabbit heart.
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pubmed:affiliation |
Department of Electrophysiology, Research Center of Montreal Heart Institute, Montreal, QC, Canada. mharada@riem.nagoya-u.ac.jp
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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