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. 2021 Jul 12;23:92. doi: 10.1186/s12968-021-00775-8

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Apart from patients with cardiac amyloidosis, there was no difference in LV ejection fraction (LVEF) between the other groups (A). Patients with HCM and amyloidosis exhibited the highest LV mass index (B). Patients with cardiac amyloidosis exhibited the highest values for T1 followed by HCM patients (p < 0.05 vs. controls). There were no significant differences in T1 however, between athletes, healthy controls and HHD patients (C). Atypical late gadolinium enhancement (LGE) score was higher in HHD and HCM vs. controls and even higher in amyloidosis (D). GLS and %normal myocardium were similar between healthy subjects and athletes, whereas values significantly decreased with HHD and further decreased with HCM and amyloidosis (E, F)