Document Detail


Connexins and cardiac arrhythmias.
MedLine Citation:
PMID:  16646589     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During cardiac remodeling, impulse conduction in the heart is altered by changes in excitability, electrical coupling, and tissue architecture. The impairment of normal impulse conduction is one of the factors that increases the propensity for arrhythmias. This chapter focuses on the relationship between electrical coupling between ventricular myocytes and arrhythmogenesis. Mouse models of decreased electrical coupling in the heart have shown that a clinically relevant 50% reduction in gap junctions in the heart has no effect on impulse conduction or arrhythmogenesis. To impair conduction and arrhythmias, coupling has to be reduced to very low levels. Apparently, there is a large conduction reserve, which can preserve normal impulse conduction even when electrical coupling is moderately reduced. However, cardiac remodeling is also associated with reduced excitability and increased levels of collagen deposition (fibrosis). It is therefore presumably the combination of, in itself ineffective, reduction of electrical coupling with other impairments like fibrosis or reduced excitability that causes the limits of conduction reserve to be exceeded, thereby resulting in abnormal impulse conduction and enhanced arrhythmogenesis.
Authors:
Harold V M van Rijen; Toon A B van Veen; Daniel Gros; Ronald Wilders; Jacques M T de Bakker
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Advances in cardiology     Volume:  42     ISSN:  0065-2326     ISO Abbreviation:  Adv Cardiol     Publication Date:  2006  
Date Detail:
Created Date:  2006-05-01     Completed Date:  2006-07-06     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0270063     Medline TA:  Adv Cardiol     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  150-60     Citation Subset:  IM    
Affiliation:
Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands. H.V.M.vanRijen@med.uu.nl
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MeSH Terms
Descriptor/Qualifier:
Animals
Arrhythmias, Cardiac / physiopathology*
Connexins / metabolism,  physiology*
Gap Junctions / metabolism
Heart Conduction System / physiopathology*
Humans
Models, Animal
Tachycardia, Ventricular / physiopathology
Ventricular Remodeling / physiology
Chemical
Reg. No./Substance:
0/Connexins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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