18F-flutemetamol positron emission tomography in cardiac amyloidosis

Figures

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  Fig. 1. Diagram depicting the imaging modality used in the amyloidosis and heart failure groups (18F-flutemetamol PET/MRI or 18F-flutemetamol PET/CT)

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  Fig. 2. 18F-flutemetamol PET/MRIs of a PET-positive, female patient with hereditary ATTR-CA (A) and a PET-negative male patient with wild-type ATTR-CA (B). Representative short-axis images of native T1 maps (left column), late gadolinium enhancement (middle column), and F-18 flutemetamol PET (right column). While patient A demonstrates an abnormal T1 map (1448 ms), diffused LGE, and an increased tracer uptake (SUVmean myocardium: 3.1, SUVmean blood pool: 1.3), patient B does not demonstrate an increased tracer uptake (SUVmean myocardium 1.4, SUVmean blood pool: 1.5) despite an abnormal native T1 map (1460 ms), focal areas of LGE, and a positive myocardial biopsy and bone scan (Perugini 3, not shown)

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  Fig. 3. Tracer kinetics in the left ventricular myocardium and the blood. SUVs of the left ventricular myocardium and blood pool are depicted in PET-positive hereditary ATTR-CA (A), PET-positive AL-CA (B), PET-negative hereditary ATTR-CA with positive endomyocardial biopsy (C), and a healthy control (D). In the first few minutes, the mean left ventricular and blood pool SUVs are similar for all patients. While the SUVs of the left ventricular myocardium then remain above the SUVs of the blood pool in the PET-positive hereditary ATTR-CA (A) and AL-CA patients (B), the SUVs of the myocardium decrease in the PET-negative hereditary ATTR-CA (C) and the healthy control (D) and even fall below the SUVs of the blood pool after approximately 400-600 seconds. Unspecific pericardial tracer uptake can be seen in all patients