Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22332
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dc.contributor.authorChen, J. P.en
dc.contributor.authorHou, D.en
dc.contributor.authorPendyala, L.en
dc.contributor.authorGoudevenos, J. A.en
dc.contributor.authorKounis, N. G.en
dc.date.accessioned2015-11-24T19:23:34Z-
dc.date.available2015-11-24T19:23:34Z-
dc.identifier.issn1876-7605-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22332-
dc.rightsDefault Licence-
dc.subjectAcute Coronary Syndrome/*etiology/immunology/pathology/prevention & controlen
dc.subjectAngioplasty, Balloon, Coronary/*adverse effects/instrumentationen
dc.subjectCardiovascular Agents/adverse effectsen
dc.subjectCoronary Artery Disease/*therapyen
dc.subjectDrug Hypersensitivity/*etiology/immunology/pathology/prevention & controlen
dc.subjectDrug-Eluting Stents/*adverse effectsen
dc.subjectHumansen
dc.subjectHypersensitivity/*etiology/immunology/pathology/prevention & controlen
dc.subjectMetals/adverse effectsen
dc.subjectPractice Guidelines as Topicen
dc.subjectProsthesis Designen
dc.subjectRisk Assessmenten
dc.subjectRisk Factorsen
dc.subjectThrombosis/*etiology/immunology/pathology/prevention & controlen
dc.subjectTreatment Failureen
dc.titleDrug-eluting stent thrombosis: the Kounis hypersensitivity-associated acute coronary syndrome revisiteden
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.jcin.2009.04.017-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/19628178-
heal.identifier.secondaryhttp://ac.els-cdn.com/S1936879809003264/1-s2.0-S1936879809003264-main.pdf?_tid=dcdeee7162d334a18ba2bd51ee8a72a2&acdnat=1333519030_d19aca206d94ecd048bc535782c82540-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2009-
heal.abstractThe advent of drug-eluting stents (DES) has revolutionized the field of interventional cardiology. Their dramatic and persistent restenotic and target lesion revascularization advantages are unquestioned. However, concerns over the rare but potentially catastrophic risk of stent thrombosis (ST) have tempered universal acceptance of these devices. Although the precise mechanism of DES ST is undoubtedly multifactorial and as yet not fully elucidated, delayed or incomplete endothelial healing clearly plays a pivotal role. Detailed histopathological data have implicated a contributory allergic or hypersensitivity component, as verified by the Food and Drug Administration's Manufacturer and User Device Experience Center and the Research on Adverse Drug/device events And Reports (RADAR) project. These findings thus suggest a potential connection with the Kounis syndrome, the concurrence of acute coronary events with allergic, hypersensitivity, anaphylactic, or anaphylactoid reactions. Potential culprits responsible for this phenomenon include: arachidonic acid metabolites such as leukotrienes and thromboxane, proteolytic enzymes such as chymase and tryptase, histamine, cytokines, and chemokines. Additionally, inflammatory cells such as macrophages, T-lymphocytes, and mast cells are probably also contributory. Autopsy-confirmed infiltrates of various inflammatory cells including lymphocytes, plasma cells, macrophages, and eosinophils have been reported in all 3 vascular wall layers and are reminiscent of those associated with the Kounis syndrome. Although the concurrence of acute coronary syndromes with hypersensitivity reactions has been long established, the specific association with DES ST remains unproven. Potential incorporation of hypersensitivity suppressive agents might represent a promising paradigm shift from efficacy to safety in future DES designs.en
heal.journalNameJACC Cardiovasc Interven
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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