| Direction and magnitude of blood flow shear stresses on the leaflets of aortic valves: is there a link with valve calcification? | |
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MedLine Citation:
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PMID: 20524753 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Aortic stenosis caused by valve calcification is a major cause of death around the world. Hemodynamic factors have been suggested to be major players in the development of valve calcification, yet a detailed knowledge of the blood flow dynamics as experienced by endothelial cells on valve surfaces is still lacking. In this study we carry out high-resolution numerical simulations of the blood flow through a polymeric trileaflet valve in order to elucidate the differential flow dynamics on the aortic and ventricular sides of the valve leaflets. Limiting streamlines and surface shear stress contours are used to probe and quantify the blood flows on its side. Complicated flow patterns were only observed on the aortic side of the valve near the region where focalized distribution of valve calcification is typically observed. |
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Authors:
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Liang Ge; Fotis Sotiropoulos |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of biomechanical engineering Volume: 132 ISSN: 1528-8951 ISO Abbreviation: J Biomech Eng Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-06-07 Completed Date: 2010-09-30 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7909584 Medline TA: J Biomech Eng Country: United States |
Other Details:
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Languages: eng Pagination: 014505 Citation Subset: IM |
Affiliation:
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Department of Surgery, University of California, San Francisco, CA, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aortic Valve
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physiopathology* Aortic Valve Stenosis / complications*, physiopathology* Blood Flow Velocity Blood Pressure Calcinosis / complications*, physiopathology* Computer Simulation Humans Models, Cardiovascular* Shear Strength |
| Grant Support | |
ID/Acronym/Agency:
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R01-HL-07262/HL/NHLBI NIH HHS |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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