Document Detail


Atrial contractile protein content and function are preserved in patients with coronary artery disease and atrial fibrillation.
MedLine Citation:
PMID:  20657267     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
OBJECTIVES: Atrial fibrillation (AF) causes atrial contractile dysfunction. The focus of this study was to determine whether the contractile deficit of human AF is the result of altered contractile protein abundance and/or function.
METHODS: Atrial tissue from patients with chronic AF undergoing open-heart surgery was compared with the tissue from patients in normal sinus rhythm (NSR). Myosin isoform composition and content were determined. Intact native thin filament and cardiac myosin contractile protein performance were independently assessed in an in-vitro motility assay.
RESULTS: Myosin isoform expression and total myosin content were not different between AF and NSR. Calcium-activated native thin filament function was similar between AF and NSR as measured by calcium sensitivity and maximal activation. Myosin isolated from the atria of AF and NSR groups showed similar unloaded shortening speeds and isometric force generation.
CONCLUSION: Unlike human ventricular dysfunction where contractile protein function is directly affected, the contractile deficit of AF is not the result of alterations in myosin content or contractile protein function.
Authors:
Mark Hünlich; Sarah M Tremble; Kelly J Begin; Bruce J Leavitt; Frank P Ittleman; Peter VanBuren
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Coronary artery disease     Volume:  21     ISSN:  1473-5830     ISO Abbreviation:  Coron. Artery Dis.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-05     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9011445     Medline TA:  Coron Artery Dis     Country:  England    
Other Details:
Languages:  eng     Pagination:  357-62     Citation Subset:  IM    
Affiliation:
Cardiology Division, Department of Medicine, University of Vermont, Burlington, Vermont 05405, USA.
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MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
HL77637/HL/NHLBI NIH HHS

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