Document Detail


Extracellular matrix and left ventricular mechanics in overload hypertrophy.
MedLine Citation:
PMID:  17582942     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In all conditions altering wall stress and mechanical stretching, LV performance becomes insufficient at the distance, due to a number of structural and functional alterations ultimately impairing pump function, but not invariably due to reduced inotropic state. Among them, structural alteration of the normal myocardial architectures might play a key role to explain the early events of cardiac dysfunction. Abnormalities of the collagen scaffold facilitate alteration of the physiological orientation of muscular fibers and consequent impaired transmission of the contraction force through the myocardial wall toward the endocardium. Further adaptations are promoted by neurohormonal activation eventually yielding abnormal gene expression of contractile proteins. In the alterations of normal myocardial architecture, the turnover of ECM and the architecture of the scaffold is possibly as important as the organization of the cardiomyocyte layers which contributes with their normal orientation to the developed strength at the chamber level.
Authors:
Giovanni de Simone; Oreste de Divitiis
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Advances in clinical pathology : the official journal of Adriatic Society of Pathology     Volume:  6     ISSN:  1125-5552     ISO Abbreviation:  Adv Clin Path     Publication Date:  2002 Jan 
Date Detail:
Created Date:  2007-06-22     Completed Date:  2007-07-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9709997     Medline TA:  Adv Clin Path     Country:  Italy    
Other Details:
Languages:  eng     Pagination:  3-10     Citation Subset:  IM    
Affiliation:
Giovanni de Simone Echocardiography Laboratory, Department of Clinical and Experimental Medicine Federico II, University Hospital, School of Medicine, Via S. Pansini 5, 1-80131 Naples, Italy. simogi@unina.it
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MeSH Terms
Descriptor/Qualifier:
Animals
Biomechanics
Collagen / genetics,  metabolism
Contractile Proteins / genetics,  metabolism
Extracellular Matrix / metabolism*,  pathology
Gene Expression Regulation
Humans
Hypertrophy, Left Ventricular / pathology,  physiopathology*
Myocardial Contraction / physiology
Myocytes, Cardiac / metabolism,  pathology*
Chemical
Reg. No./Substance:
0/Contractile Proteins; 9007-34-5/Collagen

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


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