PMC10017927_01
(A) Cardiac MRI showing late gadolinium enhancement. Arrows pointing to focal areas of midmyocardial enhancement in the interventricular septum, lateral ventricular wall, and wall of the right ventricle. The myocardium is diffusely lighter in color despite adequate nulling using an appropriate inversion time. This suggests that there is diffuse iron uptake and that the midmyocardial enhancement and color of the myocardium is not a technical artifact, particularly when taken in the context of T1 images (Figure 1B). (B) Cardiac MRI panel showing severely decreased pre-contrast T1 values. This 4-paneled figure demonstrates the regions of myocardium that were selected for T1 mapping in the left-sided panels before (top left panel) and after (bottom left panel) the injection of contrast. The top right panel demonstrates the numeric values for T1 time, wherein a significant decrease in T1 relaxation time both before (690 ms; reference value ~950 +- 20 ms at our center) and after (400 ms) the injection of contrast compared to what would be expected for normal myocardium is seen. The bottom right panel demonstrates the obtained values in a graphical format. Collectively, this 4-paneled figure corroborates the presence of significant cardiac iron deposition on the T1 mapping sequence. This is also supported by the dramatic increase in extracellular volume (49.4%; reference range 25% +- 4% at our center).
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Stress cardiac magnetic resonance imaging (MRI) revealed no evidence of ischemia but demonstrated moderately reduced LV systolic function with LVEF of 38% due to IOC as evidenced by late gadolinium enhancement showing diffuse enhancement globally and T1 mapping with severely decreased pre-contrast T1 values (Figure 1A, B).
Cardiac biopsy Prussian blue iron stain highlights hemosiderin deposition. (B) High power view of a hematoxylin and eosin stain showing hypertrophic cardiac myocytes with numerous golden brown pigment granules.
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A cardiac biopsy 6 months post-LT confirmed cardiac myocyte hemosiderosis and associated myocyte hypertrophy (Figure 2A, B).