Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity

BACKGROUND Anthracycline-induced cardiotoxicity is a major clinical problem, and early cardiotoxicity markers are needed. OBJECTIVES The purpose of this study was to identify early doxorubicin-induced cardiotoxicity by serial multiparametric cardiac magnetic resonance (CMR) and its pathological corr...

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Autores: Galán-Arriola, Carlos, Lobo, Manuel, Vílchez-Tschischke, Jean Paul, López, Gonzalo J., Molina-Iracheta, Antonio de, Pérez-Martínez, Claudia, Agüero, Jaume, Fernández-Jiménez, Rodrigo, Martín-García, Ana, Oliver, Eduardo, Villena-Gutierrez, Rocío, Pizarro, Gonzalo, Sánchez, Pedro L., Fuster Carulla, Valentí, Sánchez-González, Javier, Ibáñez, Borja
Tipo de recurso: artículo
Fecha de publicación:2019
País:España
Institución:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/692243
Acceso en línea:http://hdl.handle.net/10486/692243
https://dx.doi.org/10.1016/j.jacc.2018.11.046
Access Level:acceso abierto
Palabra clave:Anthracycline
Cardiooncology
Cardiotoxicity
CMR
Doxorubicin
Medicina
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spelling Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicityGalán-Arriola, CarlosLobo, ManuelVílchez-Tschischke, Jean PaulLópez, Gonzalo J.Molina-Iracheta, Antonio dePérez-Martínez, ClaudiaAgüero, JaumeFernández-Jiménez, RodrigoMartín-García, AnaOliver, EduardoVillena-Gutierrez, RocíoPizarro, GonzaloSánchez, Pedro L.Fuster Carulla, ValentíSánchez-González, JavierIbáñez, BorjaAnthracyclineCardiooncologyCardiotoxicityCMRDoxorubicinMedicinaBACKGROUND Anthracycline-induced cardiotoxicity is a major clinical problem, and early cardiotoxicity markers are needed. OBJECTIVES The purpose of this study was to identify early doxorubicin-induced cardiotoxicity by serial multiparametric cardiac magnetic resonance (CMR) and its pathological correlates in a large animal model. METHODS Twenty pigswere included.Of these, 5 received 5 biweekly intracoronary doxorubicindoses (0.45mg/kg/injection) and were followed until sacrifice at 16 weeks. Another 5 pigs received 3 biweekly doxorubicin doses and were followed to 16weeks.Athird groupwas sacrificed after the third dose.All groups underwentweekly CMRexaminations including anatomical and T2 and T1mapping (including extracellular volume [ECV] quantification).A control groupwas sacrificed after the initialCMR. RESULTS The earliest doxorubicin-cardiotoxicity CMR parameter was T2 relaxation-time prolongation at week 6 (2 weeks after the third dose). T1 mapping, ECV, and left ventricular (LV) motion were unaffected. At this early time point, isolated T2 prolongation correlated with intracardiomyocyte edema secondary to vacuolization without extracellular space expansion. Subsequent development of T1 mapping and ECV abnormalities coincided with LV motion defects: LV ejection fraction declined from week 10 (2 weeks after the fifth and final doxorubicin dose). Stopping doxorubicin therapy upon detection of T2 prolongation halted progression to LV motion deterioration and resolved intracardiomyocyte vacuolization, demonstrating that early T2 prolongation occurs at a reversible disease stage. CONCLUSIONS T2 mapping during treatment identifies intracardiomyocyte edema generation as the earliest marker of anthracycline-induced cardiotoxicity, in the absence of T1 mapping, ECV, or LV motion defects. The occurrence of these changes at a reversible disease stage shows the clinical potential of this CMR marker for tailored anthracycline therapyElsevier on behalf of the American College of Cardiology FoundationDepartamento de MedicinaFacultad de Medicina20192019-02-18research articlehttp://purl.org/coar/resource_type/c_2df8fbb1VoRhttp://purl.org/coar/version/c_970fb48d4fbd8a85info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10486/692243https://dx.doi.org/10.1016/j.jacc.2018.11.046reponame:Biblos-e Archivo. Repositorio Institucional de la UAMinstname:Universidad Autónoma de MadridInglésengopen accesshttp://purl.org/coar/access_right/c_abf2info:eu-repo/semantics/openAccessoai:repositorio.uam.es:10486/6922432026-06-23T12:46:27Z
dc.title.none.fl_str_mv Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
title Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
spellingShingle Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
Galán-Arriola, Carlos
Anthracycline
Cardiooncology
Cardiotoxicity
CMR
Doxorubicin
Medicina
title_short Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
title_full Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
title_fullStr Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
title_full_unstemmed Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
title_sort Serial magnetic resonance imaging to identify early stages of anthracycline-induced cardiotoxicity
dc.creator.none.fl_str_mv Galán-Arriola, Carlos
Lobo, Manuel
Vílchez-Tschischke, Jean Paul
López, Gonzalo J.
Molina-Iracheta, Antonio de
Pérez-Martínez, Claudia
Agüero, Jaume
Fernández-Jiménez, Rodrigo
Martín-García, Ana
Oliver, Eduardo
Villena-Gutierrez, Rocío
Pizarro, Gonzalo
Sánchez, Pedro L.
Fuster Carulla, Valentí
Sánchez-González, Javier
Ibáñez, Borja
author Galán-Arriola, Carlos
author_facet Galán-Arriola, Carlos
Lobo, Manuel
Vílchez-Tschischke, Jean Paul
López, Gonzalo J.
Molina-Iracheta, Antonio de
Pérez-Martínez, Claudia
Agüero, Jaume
Fernández-Jiménez, Rodrigo
Martín-García, Ana
Oliver, Eduardo
Villena-Gutierrez, Rocío
Pizarro, Gonzalo
Sánchez, Pedro L.
Fuster Carulla, Valentí
Sánchez-González, Javier
Ibáñez, Borja
author_role author
author2 Lobo, Manuel
Vílchez-Tschischke, Jean Paul
López, Gonzalo J.
Molina-Iracheta, Antonio de
Pérez-Martínez, Claudia
Agüero, Jaume
Fernández-Jiménez, Rodrigo
Martín-García, Ana
Oliver, Eduardo
Villena-Gutierrez, Rocío
Pizarro, Gonzalo
Sánchez, Pedro L.
Fuster Carulla, Valentí
Sánchez-González, Javier
Ibáñez, Borja
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Departamento de Medicina
Facultad de Medicina
dc.subject.none.fl_str_mv Anthracycline
Cardiooncology
Cardiotoxicity
CMR
Doxorubicin
Medicina
topic Anthracycline
Cardiooncology
Cardiotoxicity
CMR
Doxorubicin
Medicina
description BACKGROUND Anthracycline-induced cardiotoxicity is a major clinical problem, and early cardiotoxicity markers are needed. OBJECTIVES The purpose of this study was to identify early doxorubicin-induced cardiotoxicity by serial multiparametric cardiac magnetic resonance (CMR) and its pathological correlates in a large animal model. METHODS Twenty pigswere included.Of these, 5 received 5 biweekly intracoronary doxorubicindoses (0.45mg/kg/injection) and were followed until sacrifice at 16 weeks. Another 5 pigs received 3 biweekly doxorubicin doses and were followed to 16weeks.Athird groupwas sacrificed after the third dose.All groups underwentweekly CMRexaminations including anatomical and T2 and T1mapping (including extracellular volume [ECV] quantification).A control groupwas sacrificed after the initialCMR. RESULTS The earliest doxorubicin-cardiotoxicity CMR parameter was T2 relaxation-time prolongation at week 6 (2 weeks after the third dose). T1 mapping, ECV, and left ventricular (LV) motion were unaffected. At this early time point, isolated T2 prolongation correlated with intracardiomyocyte edema secondary to vacuolization without extracellular space expansion. Subsequent development of T1 mapping and ECV abnormalities coincided with LV motion defects: LV ejection fraction declined from week 10 (2 weeks after the fifth and final doxorubicin dose). Stopping doxorubicin therapy upon detection of T2 prolongation halted progression to LV motion deterioration and resolved intracardiomyocyte vacuolization, demonstrating that early T2 prolongation occurs at a reversible disease stage. CONCLUSIONS T2 mapping during treatment identifies intracardiomyocyte edema generation as the earliest marker of anthracycline-induced cardiotoxicity, in the absence of T1 mapping, ECV, or LV motion defects. The occurrence of these changes at a reversible disease stage shows the clinical potential of this CMR marker for tailored anthracycline therapy
publishDate 2019
dc.date.none.fl_str_mv 2019
2019-02-18
dc.type.none.fl_str_mv research article
http://purl.org/coar/resource_type/c_2df8fbb1
VoR
http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10486/692243
https://dx.doi.org/10.1016/j.jacc.2018.11.046
url http://hdl.handle.net/10486/692243
https://dx.doi.org/10.1016/j.jacc.2018.11.046
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Elsevier on behalf of the American College of Cardiology Foundation
publisher.none.fl_str_mv Elsevier on behalf of the American College of Cardiology Foundation
dc.source.none.fl_str_mv reponame:Biblos-e Archivo. Repositorio Institucional de la UAM
instname:Universidad Autónoma de Madrid
instname_str Universidad Autónoma de Madrid
reponame_str Biblos-e Archivo. Repositorio Institucional de la UAM
collection Biblos-e Archivo. Repositorio Institucional de la UAM
repository.name.fl_str_mv
repository.mail.fl_str_mv
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