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Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies

Chimeric antigen receptor (CAR)-T cell therapy is the next revolutionary advance in cancer therapy. By using ex vivo engineered T cells to specifically target antigens, a targeted immune reaction is induced. Chimeric antigen receptor-T cell therapy is approved for patients suffering from advanced an...

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Autores principales: Totzeck, Matthias, Michel, Lars, Lin, Yi, Herrmann, Joerg, Rassaf, Tienush
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9123242/
https://www.ncbi.nlm.nih.gov/pubmed/35257157
http://dx.doi.org/10.1093/eurheartj/ehac106
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author Totzeck, Matthias
Michel, Lars
Lin, Yi
Herrmann, Joerg
Rassaf, Tienush
author_facet Totzeck, Matthias
Michel, Lars
Lin, Yi
Herrmann, Joerg
Rassaf, Tienush
author_sort Totzeck, Matthias
collection PubMed
description Chimeric antigen receptor (CAR)-T cell therapy is the next revolutionary advance in cancer therapy. By using ex vivo engineered T cells to specifically target antigens, a targeted immune reaction is induced. Chimeric antigen receptor-T cell therapy is approved for patients suffering from advanced and refractory B cell and plasma cell malignancies and is undergoing testing for various other haematologic and solid malignancies. In the process of triggering an anticancer immune reaction, a systemic inflammatory response can emerge as cytokine release syndrome (CRS). The severity of CRS is highly variable across patients, ranging from mild flu-like symptoms to fulminant hyperinflammatory states with excessive immune activation, associated multiorgan failure and high mortality risk. Cytokine release syndrome is also an important factor for adverse cardiovascular (CV) events. Sinus tachycardia and hypotension are the most common reflections, similar to what is seen with other systemic inflammatory response syndromes. Corrected QT interval prolongation and tachyarrhythmias, including ventricular arrhythmias and atrial fibrillation, also show a close link with CRS. Events of myocardial ischaemia and venous thromboembolism can be provoked during CAR-T cell therapy. Although not as closely related to CRS, changes in cardiac function can be observed to the point of heart failure and cardiogenic shock. This may also be encountered in patients with severe valvular heart disease in the setting of CRS. This review will discuss the pertinent CV risks of the growing field of CAR-T cell therapy for today’s cardiologists, including incidence, characteristics, and treatment options, and will conclude with an integrated management algorithm.
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spelling pubmed-91232422022-05-23 Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies Totzeck, Matthias Michel, Lars Lin, Yi Herrmann, Joerg Rassaf, Tienush Eur Heart J State of the Art Review Chimeric antigen receptor (CAR)-T cell therapy is the next revolutionary advance in cancer therapy. By using ex vivo engineered T cells to specifically target antigens, a targeted immune reaction is induced. Chimeric antigen receptor-T cell therapy is approved for patients suffering from advanced and refractory B cell and plasma cell malignancies and is undergoing testing for various other haematologic and solid malignancies. In the process of triggering an anticancer immune reaction, a systemic inflammatory response can emerge as cytokine release syndrome (CRS). The severity of CRS is highly variable across patients, ranging from mild flu-like symptoms to fulminant hyperinflammatory states with excessive immune activation, associated multiorgan failure and high mortality risk. Cytokine release syndrome is also an important factor for adverse cardiovascular (CV) events. Sinus tachycardia and hypotension are the most common reflections, similar to what is seen with other systemic inflammatory response syndromes. Corrected QT interval prolongation and tachyarrhythmias, including ventricular arrhythmias and atrial fibrillation, also show a close link with CRS. Events of myocardial ischaemia and venous thromboembolism can be provoked during CAR-T cell therapy. Although not as closely related to CRS, changes in cardiac function can be observed to the point of heart failure and cardiogenic shock. This may also be encountered in patients with severe valvular heart disease in the setting of CRS. This review will discuss the pertinent CV risks of the growing field of CAR-T cell therapy for today’s cardiologists, including incidence, characteristics, and treatment options, and will conclude with an integrated management algorithm. Oxford University Press 2022-03-08 /pmc/articles/PMC9123242/ /pubmed/35257157 http://dx.doi.org/10.1093/eurheartj/ehac106 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of European 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-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle State of the Art Review
Totzeck, Matthias
Michel, Lars
Lin, Yi
Herrmann, Joerg
Rassaf, Tienush
Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies
title Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies
title_full Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies
title_fullStr Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies
title_full_unstemmed Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies
title_short Cardiotoxicity from chimeric antigen receptor-T cell therapy for advanced malignancies
title_sort cardiotoxicity from chimeric antigen receptor-t cell therapy for advanced malignancies
topic State of the Art Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9123242/
https://www.ncbi.nlm.nih.gov/pubmed/35257157
http://dx.doi.org/10.1093/eurheartj/ehac106
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