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Understanding Vulnerable Plaques: Current Status and Future Directions

The main cause of acute myocardial infarction is plaque rupture accompanied by superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested as a type of lesion with a vulnerability that can cause plaque rupture. However, not only the existence of a TCFA but also the fine and...

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Autores principales: Lee, Kwan Yong, Chang, Kiyuk
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Cardiology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875591/
https://www.ncbi.nlm.nih.gov/pubmed/31760703
http://dx.doi.org/10.4070/kcj.2019.0211
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author Lee, Kwan Yong
Chang, Kiyuk
author_facet Lee, Kwan Yong
Chang, Kiyuk
author_sort Lee, Kwan Yong
collection PubMed
description The main cause of acute myocardial infarction is plaque rupture accompanied by superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested as a type of lesion with a vulnerability that can cause plaque rupture. However, not only the existence of a TCFA but also the fine and complex interactions of other anatomical and hemodynamic factors, such as microcalcification in the fibrous cap, cholesterol crystal-induced inflammasome activation, the apoptosis of intraplaque macrophages, and endothelial shear stress distribution should precede a clinical event caused by plaque rupture. Recent studies are being conducted to identify these mechanisms through molecular imaging and hemodynamic assessment using computational fluid dynamics, which will result in better clinical results through selective coronary interventions.
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spelling pubmed-68755912019-12-04 Understanding Vulnerable Plaques: Current Status and Future Directions Lee, Kwan Yong Chang, Kiyuk Korean Circ J Review Article The main cause of acute myocardial infarction is plaque rupture accompanied by superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested as a type of lesion with a vulnerability that can cause plaque rupture. However, not only the existence of a TCFA but also the fine and complex interactions of other anatomical and hemodynamic factors, such as microcalcification in the fibrous cap, cholesterol crystal-induced inflammasome activation, the apoptosis of intraplaque macrophages, and endothelial shear stress distribution should precede a clinical event caused by plaque rupture. Recent studies are being conducted to identify these mechanisms through molecular imaging and hemodynamic assessment using computational fluid dynamics, which will result in better clinical results through selective coronary interventions. The Korean Society of Cardiology 2019-11-05 /pmc/articles/PMC6875591/ /pubmed/31760703 http://dx.doi.org/10.4070/kcj.2019.0211 Text en Copyright © 2019. The Korean Society of Cardiology https://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Lee, Kwan Yong
Chang, Kiyuk
Understanding Vulnerable Plaques: Current Status and Future Directions
title Understanding Vulnerable Plaques: Current Status and Future Directions
title_full Understanding Vulnerable Plaques: Current Status and Future Directions
title_fullStr Understanding Vulnerable Plaques: Current Status and Future Directions
title_full_unstemmed Understanding Vulnerable Plaques: Current Status and Future Directions
title_short Understanding Vulnerable Plaques: Current Status and Future Directions
title_sort understanding vulnerable plaques: current status and future directions
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6875591/
https://www.ncbi.nlm.nih.gov/pubmed/31760703
http://dx.doi.org/10.4070/kcj.2019.0211
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