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dc.contributor.authorConnell, Patrick S.
Azimuddin, Anam F.
Kim, Seulgi E.
Ramirez, Fernando
Jackson, Matthew S.
Little, Stephen H.
Grande-Allen, K. Jane
dc.date.accessioned 2017-05-03T18:24:05Z
dc.date.available 2017-05-03T18:24:05Z
dc.date.issued 2016
dc.identifier.citation Connell, Patrick S., Azimuddin, Anam F., Kim, Seulgi E., et al.. "Regurgitation Hemodynamics Alone Cause Mitral Valve Remodeling Characteristic of Clinical Disease States In Vitro." Annals of Biomedical Engineering, 44, no. 4 (2016) Springer: 954-967. https://doi.org/10.1007/s10439-015-1398-0.
dc.identifier.urihttps://hdl.handle.net/1911/94138
dc.description.abstract Mitral valve regurgitation is a challenging clinical condition that is frequent, highly varied, and poorly understood. While the causes of mitral regurgitation are multifactorial, how the hemodynamics of regurgitation impact valve tissue remodeling is an understudied phenomenon. We employed a pseudo-physiological flow loop capable of long-term organ culture to investigate the early progression of remodeling in living mitral valves placed in conditions resembling mitral valve prolapse (MVP) and functional mitral regurgitation (FMR). Valve geometry was altered to mimic the hemodynamics of controls (no changes from native geometry), MVP (5ᅠmm displacement of papillary muscles towards the annulus), and FMR (5ᅠmm apical, 5ᅠmm lateral papillary muscle displacement, 65% larger annular area). Flow measurements ensured moderate regurgitant fraction for regurgitation groups. After 1-week culture, valve tissues underwent mechanical and compositional analysis. MVP conditioned tissues were less stiff, weaker, and had elevated collagen III and glycosaminoglycans. FMR conditioned tissues were stiffer, more brittle, less extensible, and had more collagen synthesis, remodeling, and crosslinking related enzymes and proteoglycans, including decorin, matrix metalloproteinase-1, and lysyl oxidase. These models replicate clinical findings of MVP (myxomatous remodeling) and FMR (fibrotic remodeling), indicating that valve cells remodel extracellular matrix in response to altered mechanical homeostasis resulting from disease hemodynamics.
dc.language.iso eng
dc.publisher Springer
dc.rights This is an author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by Springer.
dc.title Regurgitation Hemodynamics Alone Cause Mitral Valve Remodeling Characteristic of Clinical Disease States In Vitro
dc.type Journal article
dc.citation.journalTitle Annals of Biomedical Engineering
dc.subject.keywordMitral valve regurgitation
Mitral valve prolapse
Functional mitral regurgitation
Organ culture
Myxomatous remodeling
dc.citation.volumeNumber 44
dc.citation.issueNumber 4
dc.type.dcmi Text
dc.identifier.doihttps://doi.org/10.1007/s10439-015-1398-0
dc.identifier.pmcid PMC4733442
dc.identifier.pmid 26224524
dc.type.publication post-print
dc.citation.firstpage 954
dc.citation.lastpage 967


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