Document Detail


Changes in myofibrillar content and Mg-ATPase activity in ventricular tissues from patients with heart failure caused by coronary artery disease, cardiomyopathy, or mitral valve insufficiency.
MedLine Citation:
PMID:  2969307     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Force development and shortening by cardiac muscle occur as a result of the interaction between actin and myosin within the myofibrillar lattice. This interaction is dependent upon intracellular ionized calcium and is controlled by the troponin-tropomyosin regulatory proteins situated along the actin filament. In this study, we compared the myofibrillar content and myofibrillar Mg-ATPase activity of normal human ventricular muscle with that of ventricular muscle from patients in end-stage failure caused by coronary artery disease or cardiomyopathy and ventricular muscle from patients with heart failure due to mitral valve insufficiency. The results show that the amount of myofibrillar protein (mg/g wet wt ventricle) in hearts in end-stage failure (coronary artery disease and cardiomyopathy) is significantly lower compared with normal hearts and hearts in failure due to mitral valve insufficiency. However, the Mg-ATPase activity of myofibrils from hearts in both end-stage failure and failure due to mitral valve insufficiency is significantly lower compared with myofibrils from normal hearts. The data suggest that the reduction in the amount of myofibrillar protein in ventricular tissue is a pivotal event that may be responsible for the progression of heart disease to the point of end-stage failure.
Authors:
E D Pagani; A A Alousi; A M Grant; T M Older; S W Dziuban; P D Allen
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Circulation research     Volume:  63     ISSN:  0009-7330     ISO Abbreviation:  Circ. Res.     Publication Date:  1988 Aug 
Date Detail:
Created Date:  1988-08-31     Completed Date:  1988-08-31     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  380-5     Citation Subset:  IM    
Affiliation:
Molecular Cardiology Unit, Sterling-Winthrop Research Institute, Rensselaer, New York 12144.
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MeSH Terms
Descriptor/Qualifier:
Ca(2+) Mg(2+)-ATPase / metabolism*
Cardiomyopathies / complications*
Coronary Disease / complications*
Heart Catheterization
Heart Failure / etiology,  metabolism*,  pathology
Humans
Mitral Valve Insufficiency / complications*
Muscle Proteins / metabolism
Myocardium / enzymology,  metabolism*,  ultrastructure
Myofibrils / metabolism*
Reference Values
Chemical
Reg. No./Substance:
0/Muscle Proteins; EC 3.6.1.-/Ca(2+) Mg(2+)-ATPase

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


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