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Recurrent atherosclerosis complications as a mechanism for stent failure.

Authors
  • Andreou, Ioannis1
  • Stone, Peter H2
  • Ikonomidis, Ignatios3
  • Alexopoulos, Dimitrios3
  • Sabaté, Manel4
  • 1 Department of Cardiology, Cardiovascular Institute (ICCV), Hospital Clínic, University of Barcelona, Barcelona 08036, Spain; Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; 2nd Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens Medical School, Athens 12462, Greece. Electronic address: [email protected] , (Spain)
  • 2 Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
  • 3 2nd Department of Cardiology, Attikon University Hospital, National and Kapodistrian University of Athens Medical School, Athens 12462, Greece. , (Greece)
  • 4 Department of Cardiology, Cardiovascular Institute (ICCV), Hospital Clínic, University of Barcelona, Barcelona 08036, Spain. , (Spain)
Type
Published Article
Journal
Hellenic journal of cardiology : HJC = Hellenike kardiologike epitheorese
Publication Date
Jan 01, 2020
Volume
61
Issue
1
Pages
9–14
Identifiers
DOI: 10.1016/j.hjc.2019.04.007
PMID: 31034959
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Stents are an indispensable tool in the percutaneous treatment of symptomatic coronary artery disease. Yet, stent failure due to restenosis or thrombosis may compromise their clinical benefit, carrying substantial morbidity and mortality. Despite improvements in device design and adjunctive medical treatment, stent failure still occurs during long-term follow-up, suggesting that this may be an issue that persists for many years, perhaps indefinitely. Numerous studies during the last decade have highlighted the previously underappreciated pivotal role of atherosclerosis in stent failure. We review evolving evidence on the role of atherosclerosis in stent restenosis and thrombosis, differentiating between de novo in-stent atherosclerosis development (i.e., neoatherosclerosis) and progression of pre-existing underlying atherosclerosis (i.e., paleoatherosclerosis), a distinction with potentially important clinical implications. We conclude with a concept that provides a unifying pathophysiology for these significant problems in the field of interventional cardiology based on the progression and destabilization of atherosclerosis. Copyright © 2019 Hellenic Society of Cardiology. Published by Elsevier B.V. All rights reserved.

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