4.3 Article

Early detection of anthracycline-mediated cardiotoxicity: the value of considering both global longitudinal left ventricular strain and twist

Journal

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 91, Issue 8, Pages 601-607

Publisher

CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
DOI: 10.1139/cjpp-2012-0398

Keywords

anthracycline-mediated cardiomyopathy; left ventricular function; left ventricular ejection fraction; bidimensional-strain imaging; left ventricular deformation; global longitudinal strain; twist

Funding

  1. CNCSIS-UEFISCU [PD 526/2010]

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Anthracyclines are important anticancer drugs, but their use is limited by cardiotoxicity. Left ventricular ejection fraction (LVEF) is often inadequate to detect myocardial disease induced by chemotherapy. Tissue Doppler and bidimensionalstrain imaging could detect LV myocardial dysfunction earlier than LVEF. In drug-induced cardiotoxicity, torsional and longitudinal LV deformations [LV twist (LVtw), radial strain (GRS), global longitudinal strain (GLS)] are damaged. We assessed whether a new index, GLSxLVtw, could predict future anthracycline-induced cardiomyopathy. Echocardiography, troponin, and natriuretic peptide determination were prospectively performed in 74 patients before and after 6, 12, 24, and 52 weeks of anthracycline treatment. These patients were treated for breast cancer, Hodgkin's or non-Hodgkin's lymphoma, acute lymphoblastic or myeloblastic leukaemia, or osteosarcoma. At 6 weeks after initiation of chemotherapy, isovolumic relaxation time, systolic mitral annular velocity, LVGLS, LVGRS, LV apical rotation, LVtw, and GLSxLVtw deteriorated, and troponin levels became elevated (all p < 0.05 by ANOVA) before LVEF decreased. The receiver operating characteristic curves identified early deterioration of GLSxLVtw as the best predictor of later cardiotoxicity (area under curve = 0.93), followed by GLS (0.84) and LV apical rotation (0.81) deterioration. In conclusion, early change in the GLSxLVtw index seems to be a good predictor of future development of anthracycline-induced cardiotoxicity.

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