Document Detail


Passive stiffness of myocardium from congenital heart disease and implications for diastole.
MedLine Citation:
PMID:  20159832     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: In ventricular dilatation or hypertrophy, an elevated end-diastolic pressure is often assumed to be secondary to increased myocardial stiffness, but stiffness is rarely measured in vivo because of difficulty. We measured in vitro passive stiffness of volume- or pressure-overloaded myocardium mainly from congenital heart disease.
METHODS AND RESULTS: Endocardial ventricular biopsies were obtained at open heart surgery (n=61; pressure overload, 36; volume-overload, 19; dilated cardiomyopathy, 4; normal donors, 2). In vitro passive force-extension curves and the stiffness modulus were measured in skinned tissue: muscle strips, strips with myofilaments extracted (mainly extracellular matrix), and myocytes. Collagen content (n=38) and titin isoforms (n=16) were determined. End-diastolic pressure was measured at cardiac catheterization (n=14). Pressure-overloaded tissue (strips, extracellular matrix, myocytes) had a 2.6- to 7.0-fold greater force and stiffness modulus than volume-overloaded tissue. Myocyte force and stiffness modulus at short stretches (0.05 resting length, L(0)) was pressure-overloaded >normal approximately volume-overloaded>dilated cardiomyopathy. Titin N2B:N2BA isoform ratio varied little between conditions. The extracellular matrix contributed more to force at 0.05 L(0) in pressure-overloaded (35.1%) and volume-overloaded (17.4%) strips than normal myocardium. Stiffness modulus increased with collagen content in pressure-overloaded but not volume-overloaded strips. In vitro stiffness modulus at 0.05 L(0) was a good predictor of in vivo end-diastolic pressure for pressure-overloaded but not volume-overloaded ventricles and estimated normal end-diastolic pressure as 5 to 7 mm Hg.
CONCLUSIONS: An elevated end-diastolic pressure in pressure-overloaded, but not volume-overloaded, ventricles was related to increased myocardial stiffness. The greater stiffness of pressure-overloaded compared with volume-overloaded myocardium was due to the higher stiffness of both the extracellular matrix and myocytes. The transition from normal to very-low stiffness myocytes may mark irreversible dilatation.
Authors:
Rajiv R Chaturvedi; Todd Herron; Robert Simmons; Darryl Shore; Pankaj Kumar; Babulal Sethia; Felix Chua; Efstathios Vassiliadis; Jonathan C Kentish
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-16
Journal Detail:
Title:  Circulation     Volume:  121     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-02     Completed Date:  2010-03-31     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  979-88     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Biopsy
Child
Child, Preschool
Collagen / metabolism
Connectin
Diastole / physiology*
Dilatation, Pathologic / metabolism,  physiopathology
Elasticity / physiology*
Extracellular Matrix / metabolism
Female
Heart / physiopathology*
Heart Diseases / congenital*,  metabolism,  physiopathology*
Humans
Hypertrophy, Left Ventricular / metabolism,  physiopathology
Infant
Male
Middle Aged
Muscle Proteins / metabolism
Myocardium / metabolism,  pathology
Protein Kinases / metabolism
Ventricular Dysfunction, Left / metabolism,  physiopathology
Young Adult
Grant Support
ID/Acronym/Agency:
G0001112//Medical Research Council; //British Heart Foundation
Chemical
Reg. No./Substance:
0/Connectin; 0/Muscle Proteins; 0/TTN protein, human; 9007-34-5/Collagen; EC 2.7.-/Protein Kinases

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


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