18F-flutemetamol positron emission tomography in cardiac amyloidosis

Maria Papathanasiou, Lukas Kessler, Alexander Carpinteiro, Tim Hagenacker, Felix Nensa, Lale Umutlu, Michael Forsting, Alexandra Brainman, Christoph Kleinschnitz, Gerald Antoch, Ulrich Dührsen, Thomas-Wilfried Schlosser, Ken Herrmann, Tienush Rassaf, Peter Luedike, Christoph Rischpler, Maria Papathanasiou, Lukas Kessler, Alexander Carpinteiro, Tim Hagenacker, Felix Nensa, Lale Umutlu, Michael Forsting, Alexandra Brainman, Christoph Kleinschnitz, Gerald Antoch, Ulrich Dührsen, Thomas-Wilfried Schlosser, Ken Herrmann, Tienush Rassaf, Peter Luedike, Christoph Rischpler

Abstract

Purpose: Bone-tracer scintigraphy has an established role in diagnosis of cardiac amyloidosis (CA) as it detects transthyretin amyloidosis (ATTR). Positron emission tomography (PET) with amyloid tracers has shown high sensitivity for detection of both ATTR and light-chain (AL) CA. We aimed to investigate the accuracy of 18F-flutemetamol in CA.

Methods: We enrolled patients with CA or non-amyloid heart failure (NA-HF), who underwent cardiac 18F-flutemetamol PET/MRI or PET/CT. Myocardial and blood pool standardized tracer uptake values (SUV) were estimated. Late gadolinium enhancement (LGE) and T1 mapping/ extracellular volume (ECV) estimation were performed.

Results: We included 17 patients (12 with CA, 5 with NA-HF). PET/MRI was conducted in 13 patients, while PET/CT was conducted in 4. LGE was detected in 8 of 9 CA patients. Global relaxation time and ECV were higher in CA (1448 vs. 1326, P = 0.02 and 58.9 vs. 33.7%, P = 0.006, respectively). Positive PET studies were demonstrated in 2 of 12 patients with CA (AL and ATTR). Maximal and mean SUV did not differ between groups (2.21 vs. 1.69, P = 0.18 and 1.73 vs. 1.30, P = 0.13).

Conclusion: Although protein-independent binding is supported by our results, the diagnostic yield of PET was low. We demonstrate here for the first time the low sensitivity of PET for CA.

Keywords: Cardiac amyloidosis; amyloid-binding tracers; light-chain; molecular imaging; positron emission tomography; transthyretin.

© 2020. The Author(s).

Figures

Fig. 1
Fig. 1
Diagram depicting the imaging modality used in the amyloidosis and heart failure groups (18F-flutemetamol PET/MRI or 18F-flutemetamol PET/CT)
Fig. 2
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)
Fig. 3
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

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