Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression
Drug eluting stents are associated with late stent thrombosis (LST), delayed healing and prolonged exposure of stent struts to blood flow. Using macroscale disturbed and undisturbed fluid flow waveforms, we numerically and experimentally determined the effects of microscale model strut geometries up...
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Veröffentlicht in: | Journal of the Royal Society interface 2014-05, Vol.11 (94), p.20131079-20131079 |
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creator | Jiménez, Juan M. Prasad, Varesh Yu, Michael D. Kampmeyer, Christopher P. Kaakour, Abdul-Hadi Wang, Pei-Jiang Maloney, Sean F. Wright, Nathan Johnston, Ian Jiang, Yi-Zhou Davies, Peter F. |
description | Drug eluting stents are associated with late stent thrombosis (LST), delayed healing and prolonged exposure of stent struts to blood flow. Using macroscale disturbed and undisturbed fluid flow waveforms, we numerically and experimentally determined the effects of microscale model strut geometries upon the generation of prothrombotic conditions that are mediated by flow perturbations. Rectangular cross-sectional stent strut geometries of varying heights and corresponding streamlined versions were studied in the presence of disturbed and undisturbed bulk fluid flow. Numerical simulations and particle flow visualization experiments demonstrated that the interaction of bulk fluid flow and stent struts regulated the generation, size and dynamics of the peristrut flow recirculation zones. In the absence of endothelial cells, deposition of thrombin-generated fibrin occurred primarily in the recirculation zones. When endothelium was present, peristrut expression of anticoagulant thrombomodulin (TM) was dependent on strut height and geometry. Thinner and streamlined strut geometries reduced peristrut flow recirculation zones decreasing prothrombotic fibrin deposition and increasing endothelial anticoagulant TM expression. The studies define physical and functional consequences of macro- and microscale variables that relate to thrombogenicity associated with the most current stent designs, and particularly to LST. |
doi_str_mv | 10.1098/rsif.2013.1079 |
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Using macroscale disturbed and undisturbed fluid flow waveforms, we numerically and experimentally determined the effects of microscale model strut geometries upon the generation of prothrombotic conditions that are mediated by flow perturbations. Rectangular cross-sectional stent strut geometries of varying heights and corresponding streamlined versions were studied in the presence of disturbed and undisturbed bulk fluid flow. Numerical simulations and particle flow visualization experiments demonstrated that the interaction of bulk fluid flow and stent struts regulated the generation, size and dynamics of the peristrut flow recirculation zones. In the absence of endothelial cells, deposition of thrombin-generated fibrin occurred primarily in the recirculation zones. When endothelium was present, peristrut expression of anticoagulant thrombomodulin (TM) was dependent on strut height and geometry. Thinner and streamlined strut geometries reduced peristrut flow recirculation zones decreasing prothrombotic fibrin deposition and increasing endothelial anticoagulant TM expression. The studies define physical and functional consequences of macro- and microscale variables that relate to thrombogenicity associated with the most current stent designs, and particularly to LST.</description><identifier>ISSN: 1742-5689</identifier><identifier>EISSN: 1742-5662</identifier><identifier>DOI: 10.1098/rsif.2013.1079</identifier><identifier>PMID: 24554575</identifier><language>eng</language><publisher>England: The Royal Society</publisher><subject>Cells, Cultured ; Coronary Stent Thrombosis ; Fibrin ; Fibrin - metabolism ; Gene Expression Regulation ; Haemodynamics ; Hemodynamics ; Human Umbilical Vein Endothelial Cells - metabolism ; Human Umbilical Vein Endothelial Cells - pathology ; Humans ; Models, Cardiovascular ; Stent Geometry ; Stent Streamlining ; Stents ; Thrombomodulin ; Thrombomodulin - biosynthesis ; Thrombosis - etiology ; Thrombosis - metabolism ; Thrombosis - pathology</subject><ispartof>Journal of the Royal Society interface, 2014-05, Vol.11 (94), p.20131079-20131079</ispartof><rights>2014 The Author(s) Published by the Royal Society. All rights reserved.</rights><rights>2014 The Author(s) Published by the Royal Society. All rights reserved. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-e25cf62eec00bd38c5f298260d553321678d60f32a3ac6a444bab48eb77f6f883</citedby><cites>FETCH-LOGICAL-c538t-e25cf62eec00bd38c5f298260d553321678d60f32a3ac6a444bab48eb77f6f883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973357/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973357/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24554575$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiménez, Juan M.</creatorcontrib><creatorcontrib>Prasad, Varesh</creatorcontrib><creatorcontrib>Yu, Michael D.</creatorcontrib><creatorcontrib>Kampmeyer, Christopher P.</creatorcontrib><creatorcontrib>Kaakour, Abdul-Hadi</creatorcontrib><creatorcontrib>Wang, Pei-Jiang</creatorcontrib><creatorcontrib>Maloney, Sean F.</creatorcontrib><creatorcontrib>Wright, Nathan</creatorcontrib><creatorcontrib>Johnston, Ian</creatorcontrib><creatorcontrib>Jiang, Yi-Zhou</creatorcontrib><creatorcontrib>Davies, Peter F.</creatorcontrib><title>Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression</title><title>Journal of the Royal Society interface</title><addtitle>J. R. Soc. Interface</addtitle><addtitle>J. R. Soc. Interface</addtitle><description>Drug eluting stents are associated with late stent thrombosis (LST), delayed healing and prolonged exposure of stent struts to blood flow. Using macroscale disturbed and undisturbed fluid flow waveforms, we numerically and experimentally determined the effects of microscale model strut geometries upon the generation of prothrombotic conditions that are mediated by flow perturbations. Rectangular cross-sectional stent strut geometries of varying heights and corresponding streamlined versions were studied in the presence of disturbed and undisturbed bulk fluid flow. Numerical simulations and particle flow visualization experiments demonstrated that the interaction of bulk fluid flow and stent struts regulated the generation, size and dynamics of the peristrut flow recirculation zones. In the absence of endothelial cells, deposition of thrombin-generated fibrin occurred primarily in the recirculation zones. When endothelium was present, peristrut expression of anticoagulant thrombomodulin (TM) was dependent on strut height and geometry. Thinner and streamlined strut geometries reduced peristrut flow recirculation zones decreasing prothrombotic fibrin deposition and increasing endothelial anticoagulant TM expression. The studies define physical and functional consequences of macro- and microscale variables that relate to thrombogenicity associated with the most current stent designs, and particularly to LST.</description><subject>Cells, Cultured</subject><subject>Coronary Stent Thrombosis</subject><subject>Fibrin</subject><subject>Fibrin - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Haemodynamics</subject><subject>Hemodynamics</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells - pathology</subject><subject>Humans</subject><subject>Models, Cardiovascular</subject><subject>Stent Geometry</subject><subject>Stent Streamlining</subject><subject>Stents</subject><subject>Thrombomodulin</subject><subject>Thrombomodulin - biosynthesis</subject><subject>Thrombosis - etiology</subject><subject>Thrombosis - metabolism</subject><subject>Thrombosis - pathology</subject><issn>1742-5689</issn><issn>1742-5662</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1v1DAQxS0EoqVw5Yhy5EAWx44_ckGCCFqgiAsfR2vijLsuSbzYSdX973HYsoIDJ8_o_eZ5NI-QpxXdVLTRL2PybsNoxXOrmnvktFI1K4WU7P6x1s0JeZTSNaVccSEekhNWC1ELJU7J-AlsDGUBU1-MPpfJwoDFDUQP3YCpiHi1DDBjkWac5mILOIZ-P0GG04vC-S76qehxF5KffZh-G83bGMYuZHAZsoq3u4gpZfUxeeBgSPjk7j0jX9-9_dJelJefz9-3ry9LK7ieS2TCOskQLaVdz7UVjjWaSdoLwTmrpNK9pI4z4GAl1HXdQVdr7JRy0mnNz8irg-9u6Ubsbd48wmB20Y8Q9yaAN_8qk9-aq3BjeKM4FyobPL8ziOHngmk2o08WhwEmDEsylcgnV0qqFd0c0PV4KaI7flNRs2Zk1ozMmpFZM8oDz_5e7oj_CSUD_ADEsM9XCtbjvDfXYYlTbv9vWx6mfE7q9ugK8YeRiithvunatG_Yh-Zj-920_Bfb2LHG</recordid><startdate>20140506</startdate><enddate>20140506</enddate><creator>Jiménez, Juan M.</creator><creator>Prasad, Varesh</creator><creator>Yu, Michael D.</creator><creator>Kampmeyer, Christopher P.</creator><creator>Kaakour, Abdul-Hadi</creator><creator>Wang, Pei-Jiang</creator><creator>Maloney, Sean F.</creator><creator>Wright, Nathan</creator><creator>Johnston, Ian</creator><creator>Jiang, Yi-Zhou</creator><creator>Davies, Peter F.</creator><general>The Royal Society</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140506</creationdate><title>Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression</title><author>Jiménez, Juan M. ; Prasad, Varesh ; Yu, Michael D. ; Kampmeyer, Christopher P. ; Kaakour, Abdul-Hadi ; Wang, Pei-Jiang ; Maloney, Sean F. ; Wright, Nathan ; Johnston, Ian ; Jiang, Yi-Zhou ; Davies, Peter F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-e25cf62eec00bd38c5f298260d553321678d60f32a3ac6a444bab48eb77f6f883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Cells, Cultured</topic><topic>Coronary Stent Thrombosis</topic><topic>Fibrin</topic><topic>Fibrin - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Haemodynamics</topic><topic>Hemodynamics</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Human Umbilical Vein Endothelial Cells - pathology</topic><topic>Humans</topic><topic>Models, Cardiovascular</topic><topic>Stent Geometry</topic><topic>Stent Streamlining</topic><topic>Stents</topic><topic>Thrombomodulin</topic><topic>Thrombomodulin - biosynthesis</topic><topic>Thrombosis - etiology</topic><topic>Thrombosis - metabolism</topic><topic>Thrombosis - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiménez, Juan M.</creatorcontrib><creatorcontrib>Prasad, Varesh</creatorcontrib><creatorcontrib>Yu, Michael D.</creatorcontrib><creatorcontrib>Kampmeyer, Christopher P.</creatorcontrib><creatorcontrib>Kaakour, Abdul-Hadi</creatorcontrib><creatorcontrib>Wang, Pei-Jiang</creatorcontrib><creatorcontrib>Maloney, Sean F.</creatorcontrib><creatorcontrib>Wright, Nathan</creatorcontrib><creatorcontrib>Johnston, Ian</creatorcontrib><creatorcontrib>Jiang, Yi-Zhou</creatorcontrib><creatorcontrib>Davies, Peter F.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the Royal Society interface</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiménez, Juan M.</au><au>Prasad, Varesh</au><au>Yu, Michael D.</au><au>Kampmeyer, Christopher P.</au><au>Kaakour, Abdul-Hadi</au><au>Wang, Pei-Jiang</au><au>Maloney, Sean F.</au><au>Wright, Nathan</au><au>Johnston, Ian</au><au>Jiang, Yi-Zhou</au><au>Davies, Peter F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression</atitle><jtitle>Journal of the Royal Society interface</jtitle><stitle>J. R. Soc. Interface</stitle><addtitle>J. R. Soc. Interface</addtitle><date>2014-05-06</date><risdate>2014</risdate><volume>11</volume><issue>94</issue><spage>20131079</spage><epage>20131079</epage><pages>20131079-20131079</pages><issn>1742-5689</issn><eissn>1742-5662</eissn><abstract>Drug eluting stents are associated with late stent thrombosis (LST), delayed healing and prolonged exposure of stent struts to blood flow. Using macroscale disturbed and undisturbed fluid flow waveforms, we numerically and experimentally determined the effects of microscale model strut geometries upon the generation of prothrombotic conditions that are mediated by flow perturbations. Rectangular cross-sectional stent strut geometries of varying heights and corresponding streamlined versions were studied in the presence of disturbed and undisturbed bulk fluid flow. Numerical simulations and particle flow visualization experiments demonstrated that the interaction of bulk fluid flow and stent struts regulated the generation, size and dynamics of the peristrut flow recirculation zones. In the absence of endothelial cells, deposition of thrombin-generated fibrin occurred primarily in the recirculation zones. When endothelium was present, peristrut expression of anticoagulant thrombomodulin (TM) was dependent on strut height and geometry. Thinner and streamlined strut geometries reduced peristrut flow recirculation zones decreasing prothrombotic fibrin deposition and increasing endothelial anticoagulant TM expression. The studies define physical and functional consequences of macro- and microscale variables that relate to thrombogenicity associated with the most current stent designs, and particularly to LST.</abstract><cop>England</cop><pub>The Royal Society</pub><pmid>24554575</pmid><doi>10.1098/rsif.2013.1079</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Cells, Cultured Coronary Stent Thrombosis Fibrin Fibrin - metabolism Gene Expression Regulation Haemodynamics Hemodynamics Human Umbilical Vein Endothelial Cells - metabolism Human Umbilical Vein Endothelial Cells - pathology Humans Models, Cardiovascular Stent Geometry Stent Streamlining Stents Thrombomodulin Thrombomodulin - biosynthesis Thrombosis - etiology Thrombosis - metabolism Thrombosis - pathology |
title | Macro- and microscale variables regulate stent haemodynamics, fibrin deposition and thrombomodulin expression |
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