| Passive stiffness of myocardium from congenital heart disease and implications for diastole. | |
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MedLine Citation:
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PMID: 20159832 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Rajiv R Chaturvedi; Todd Herron; Robert Simmons; Darryl Shore; Pankaj Kumar; Babulal Sethia; Felix Chua; Efstathios Vassiliadis; Jonathan C Kentish |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2010-02-16 |
Journal Detail:
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Title: Circulation Volume: 121 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2010 Mar |
Date Detail:
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Created Date: 2010-03-02 Completed Date: 2010-03-31 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
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Languages: eng Pagination: 979-88 Citation Subset: AIM; IM |
Affiliation:
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Division of Cardiology, Hospital for Sick Children, 555 University Ave, Toronto M5G 1X8, Canada. rajiv.chaturvedi@sickkids.ca |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adolescent Adult Aged Biopsy Child Child, Preschool Collagen / metabolism 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:
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//British Heart Foundation |
| Chemical | |
Reg. No./Substance:
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0/Muscle Proteins; 0/connectin; 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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