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Article: Injury of the coronary endothelium at implantation increases endothelial dysfunction and intimal hyperplasia after heart transplantation

TitleInjury of the coronary endothelium at implantation increases endothelial dysfunction and intimal hyperplasia after heart transplantation
Authors
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/healun
Citation
Journal Of Heart And Lung Transplantation, 2005, v. 24 n. 3, p. 251-258 How to Cite?
AbstractBackground: Coronary endothelial dysfunction occurs early after heart transplantation and predicts the development of intimal thickening characteristic of cardiac allograft vasculopathy. Objectives: To assess the effects of removal of the endothelium by balloon injury of coronary arteries of allografts without rupture of the internal elastic lamina at the time of implantation and on coronary endothelial dysfunction, and to assess the development of accelerated atherosclerosis after heart transplantation. Methods: A porcine model of heterotopic heart transplantation with preoperative immunologic typing, enabling progressive rejection without immunosuppression, was used to study the effect of endothelial removal on these 2 end points. Endothelium-dependent relaxations of epicardial coronary arteries from allografts submitted to endothelial denudation after harvest, arteries from allografts not undergoing denudation, and native coronary arteries were compared 30 days after graft implantation by using standard organ chamber experiments. Intimal thickening was measured by light microscopy with a semiquantitative scale (0 to 4+ grading). Results: Relaxations to serotonin and to bradykinin were significantly decreased in denuded arteries compared with nondenuded allograft arteries. There was a significant increase in the incidence of severe intimal hyperplasia in denuded arteries compared with nondenuded arteries, which were both significantly increased compared to native coronary arteries. Conclusions: Endothelial injury at implantation worsens the endothelial dysfunction as a result of rejection after heart transplantation and compounds the intimal thickening leading to cardic allograft vasculopathy. All efforts should be deployed to maintain a morphologically intact and functional endothelium at the time of graft implantation. Copyright © 2005 by the International Society for Heart and Lung Transplantation.
Persistent Identifierhttp://hdl.handle.net/10722/80245
ISSN
2015 Impact Factor: 7.509
2015 SCImago Journal Rankings: 3.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorElHamamsy, Ien_HK
dc.contributor.authorStevens, LMen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorPerrault, LPen_HK
dc.date.accessioned2010-09-06T08:04:09Z-
dc.date.available2010-09-06T08:04:09Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Heart And Lung Transplantation, 2005, v. 24 n. 3, p. 251-258en_HK
dc.identifier.issn1053-2498en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80245-
dc.description.abstractBackground: Coronary endothelial dysfunction occurs early after heart transplantation and predicts the development of intimal thickening characteristic of cardiac allograft vasculopathy. Objectives: To assess the effects of removal of the endothelium by balloon injury of coronary arteries of allografts without rupture of the internal elastic lamina at the time of implantation and on coronary endothelial dysfunction, and to assess the development of accelerated atherosclerosis after heart transplantation. Methods: A porcine model of heterotopic heart transplantation with preoperative immunologic typing, enabling progressive rejection without immunosuppression, was used to study the effect of endothelial removal on these 2 end points. Endothelium-dependent relaxations of epicardial coronary arteries from allografts submitted to endothelial denudation after harvest, arteries from allografts not undergoing denudation, and native coronary arteries were compared 30 days after graft implantation by using standard organ chamber experiments. Intimal thickening was measured by light microscopy with a semiquantitative scale (0 to 4+ grading). Results: Relaxations to serotonin and to bradykinin were significantly decreased in denuded arteries compared with nondenuded allograft arteries. There was a significant increase in the incidence of severe intimal hyperplasia in denuded arteries compared with nondenuded arteries, which were both significantly increased compared to native coronary arteries. Conclusions: Endothelial injury at implantation worsens the endothelial dysfunction as a result of rejection after heart transplantation and compounds the intimal thickening leading to cardic allograft vasculopathy. All efforts should be deployed to maintain a morphologically intact and functional endothelium at the time of graft implantation. Copyright © 2005 by the International Society for Heart and Lung Transplantation.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/healunen_HK
dc.relation.ispartofJournal of Heart and Lung Transplantationen_HK
dc.rightsThe Journal of Heart and Lung Transplantation. Copyright © Elsevier Inc.en_HK
dc.titleInjury of the coronary endothelium at implantation increases endothelial dysfunction and intimal hyperplasia after heart transplantationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1053-2498&volume=24&spage=251&epage=258&date=2006&atitle=Injury+of+the+coronary+endothelium+at+implantation+increases+endothelial+dysfunction+and+intimal+hyperplasia+after+heart+transplantationen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.healun.2003.12.012en_HK
dc.identifier.pmid15737750-
dc.identifier.scopuseid_2-s2.0-14644420863en_HK
dc.identifier.hkuros136338en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-14644420863&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue3en_HK
dc.identifier.spage251en_HK
dc.identifier.epage258en_HK
dc.identifier.isiWOS:000227463800003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridElHamamsy, I=6507972699en_HK
dc.identifier.scopusauthoridStevens, LM=7202311548en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridPerrault, LP=7004370552en_HK

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