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. 2020 Sep 30;29(2):741–749. doi: 10.1007/s12350-020-02356-1

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© The Author(s) 2020

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/.

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Patterns of 18F-fluoride uptake between cohorts. Columns represent each cohort and rows imaging modality in the short axis view. Panel A shows a delayed enhanced image of a control subject with normal myocardial mass and no LGE. The corresponding fused PET/MR image (E) shows uptake only in the blood pool. Panel B is a patient with aortic stenosis and elevated LV mass. Note the absence of myocardial 18F-fluoride uptake on panel F and similar to the healthy control, uptake is greater in the blood pool than myocardium. Panel C shows a patient with AL amyloid displaying the characteristic myocardial nulling difficulties with LGE found in cardiac amyloidosis. Panel G shows patchy lateral wall uptake greater than the blood pool. Panel D shows similar LGE findings, but this time in TTR amyloid. Note the striking and extensive biventricular uptake in panel H, much greater than the blood pool and what was seen in AL