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. 2020 Jan 21;9(2):e013755. doi: 10.1161/JAHA.119.013755

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© 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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A, (Left) Velocity vector imaging tracking endomyocardial border throughout the cardiac cycle. (Right) Bull's‐eye plot of average peak systolic global longitudinal strain in a normal subject compared with that of a patient with chemotherapy‐induced cardiotoxicity. Adapted from Mele et al17 under the Creative Commons Attribution Non‐Commercial‐NoDerivs (CC‐BY‐NC‐ND) license. B, Objective increase in myocardial T2 mapping values (a marker of inflammation/edema) after cardiotoxic anthracycline therapy exposure (A through E), even before cardiac fibrosis (F; yellow arrow, LGE) and clinical heart failure (with left ventricular ejection fraction decline) development among breast cancer patients via use of T2 mapping. Note: maximum T2 plateaus and actually declines after cancer therapy cessation (A, D, and E; black arrow in D, high T2). Adapted with permission from Lustberg et al18 Copyright ©2019, Wolters Kluwer Health, Inc. LGE indicates late gadolinium enhancement.