Abstract
PurposeBone-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. MethodsWe 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. ResultsWe 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). ConclusionAlthough 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.
Highlights
Cardiac amyloidosis (CA) is nowadays recognized as a major cause of heart failure (HF) with high mortality rates.[1]
Protein-independent binding is supported by our results, the diagnostic yield of Positron emission tomography (PET) was low
We demonstrate here for the first time the low sensitivity of PET for CA. (J Nucl Cardiol 2020)
Summary
Cardiac amyloidosis (CA) is nowadays recognized as a major cause of heart failure (HF) with high mortality rates.[1]. Transthyretin amyloidosis (ATTR) was shown to be highly prevalent among older patients with left ventricular hypertrophy, HF with preserved ejection fraction and severe aortic valve stenosis, and represents probably the most underdiagnosed heart disease to date.[2,3,4,5] These two distinct disease phenotypes account for the overwhelming majority of CA cases and both are associated with a dismal prognosis. In AL-CA median survival can be \ 6 months from the time of diagnosis depending on the severity of cardiac involvement.[6] ATTR amyloidosis has a longer disease course with a median survival of 3.6 years for the acquired, wild-type disease and varying prognosis for the hereditary type of disease, depending on the underlying transthyretin gene mutation.[7]
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