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Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail

Patients with coronary disease remain at high risk for future cardiovascular events, even with optimal risk factor modification, lipid-lowering drugs and antithrombotic regimens. A myriad of inflammatory pathways contribute to progression of the atherosclerotic burden in these patients. Only in the...

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Autores principales: Fiolet, A. T. L., Opstal, T. S. J., Silvis, M. J. M., Cornel, J. H., Mosterd, A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bohn Stafleu van Loghum 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8724334/
https://www.ncbi.nlm.nih.gov/pubmed/34403066
http://dx.doi.org/10.1007/s12471-021-01605-3
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author Fiolet, A. T. L.
Opstal, T. S. J.
Silvis, M. J. M.
Cornel, J. H.
Mosterd, A.
author_facet Fiolet, A. T. L.
Opstal, T. S. J.
Silvis, M. J. M.
Cornel, J. H.
Mosterd, A.
author_sort Fiolet, A. T. L.
collection PubMed
description Patients with coronary disease remain at high risk for future cardiovascular events, even with optimal risk factor modification, lipid-lowering drugs and antithrombotic regimens. A myriad of inflammatory pathways contribute to progression of the atherosclerotic burden in these patients. Only in the last few years has the inflammatory biology of atherosclerosis translated into clinical therapeutic options. Low-dose colchicine can provide a clinically relevant reduction in the risk for composite and individual major cardiovascular outcomes in patients with acute and chronic coronary syndromes. Among others, its anti-inflammatory effects in atherosclerosis seem to be related to neutrophil recruitment and adhesion, inflammasome inhibition, and morphological changes in platelets and platelet aggregation. Future research is aimed at further elucidating its particular mechanism of action, as well as identifying patients with the highest expected benefit and evaluating efficacy in other vascular beds. These data will help to formulate the role of colchicine and other anti-inflammatory drugs in patients with coronary disease and atherosclerosis in general in the near future.
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spelling pubmed-87243342022-01-18 Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail Fiolet, A. T. L. Opstal, T. S. J. Silvis, M. J. M. Cornel, J. H. Mosterd, A. Neth Heart J Review Article Patients with coronary disease remain at high risk for future cardiovascular events, even with optimal risk factor modification, lipid-lowering drugs and antithrombotic regimens. A myriad of inflammatory pathways contribute to progression of the atherosclerotic burden in these patients. Only in the last few years has the inflammatory biology of atherosclerosis translated into clinical therapeutic options. Low-dose colchicine can provide a clinically relevant reduction in the risk for composite and individual major cardiovascular outcomes in patients with acute and chronic coronary syndromes. Among others, its anti-inflammatory effects in atherosclerosis seem to be related to neutrophil recruitment and adhesion, inflammasome inhibition, and morphological changes in platelets and platelet aggregation. Future research is aimed at further elucidating its particular mechanism of action, as well as identifying patients with the highest expected benefit and evaluating efficacy in other vascular beds. These data will help to formulate the role of colchicine and other anti-inflammatory drugs in patients with coronary disease and atherosclerosis in general in the near future. Bohn Stafleu van Loghum 2021-08-17 2022-01 /pmc/articles/PMC8724334/ /pubmed/34403066 http://dx.doi.org/10.1007/s12471-021-01605-3 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Review Article
Fiolet, A. T. L.
Opstal, T. S. J.
Silvis, M. J. M.
Cornel, J. H.
Mosterd, A.
Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
title Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
title_full Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
title_fullStr Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
title_full_unstemmed Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
title_short Targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
title_sort targeting residual inflammatory risk in coronary disease: to catch a monkey by its tail
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8724334/
https://www.ncbi.nlm.nih.gov/pubmed/34403066
http://dx.doi.org/10.1007/s12471-021-01605-3
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