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Serial Magnetic Resonance Imaging to Identify Early Stages of Anthracycline-Induced Cardiotoxicity

Fecha de publicación:

Autores de IIS La Fe

Participantes ajenos a IIS La Fe

  • Galan-Arriola, C
  • Lobo, M
  • Vilchez-Tschischke, JP
  • Lopez, GJ
  • de Molina-Iracheta, A
  • Perez-Martinez, C
  • Fernandez-Jimenez, R
  • Martin-Garcia, A
  • Oliver, E
  • Villena-Gutierrez, R
  • Pizarro, G
  • Sanchez, PL
  • Fuster, V
  • Sanchez-Gonzalez, J
  • Ibanez, B

Grupos

Abstract

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 pigs were included. Of these, 5 received 5 biweekly intracoronary doxorubicin doses (0.45 mg/kg/injection) and were followed until sacrifice at 16 weeks. Another 5 pigs received 3 biweekly doxorubicin doses and were followed to 16 weeks. A third group was sacrificed after the third dose. All groups underwent weekly CMR examinations including anatomical and T-2 and T-1 mapping (including extracellular volume [ECV] quantification). A control group was sacrificed after the initial CMR. RESULTS The earliest doxorubicin cardiotoxicity CMR parameter was T-2 relaxation-time prolongation at week 6 (2 weeks after the third dose). T-1 mapping, ECV, and left ventricular (LV) motion were unaffected. At this early time point, isolated T-2 prolongation correlated with intracardiomyocyte edema secondary to vacuolization without extracellular space expansion. Subsequent development of T-1 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 T-2 prolongation halted progression to LV motion deterioration and resolved intracardiomyocyte vacuolization, demonstrating that early T-2 prolongation occurs at a reversible disease stage. CONCLUSIONS T-2 mapping during treatment identifies intracardiomyocyte edema generation as the earliest marker of anthracycline-induced cardiotoxicity, in the absence of T-1 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. (J Am Coll Cardiol 2019; 73: 77991) (c) 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/byncnd/4.0/).

Datos de la publicación

ISSN/ISSNe:
0735-1097, 1558-3597

JACC-Journal of the American College of Cardiology  ELSEVIER SCIENCE INC

Tipo:
Article
Páginas:
779-791
PubMed:
30784671
Factor de Impacto:
9,989 SCImago ℠
Cuartil:
Q1 SCImago ℠

Citas Recibidas en Web of Science: 197

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Keywords

  • anthracycline; cardio-oncology; cardiotoxicity; CMR; doxorubicin

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