## 1 Introduction  
Amyloidosis is a systemic infiltrative disease caused by the formation and deposition of misfolded protein fibrils involving several organs, including the heart [1, 2, 3]. One of the most common forms of cardiac amyloidosis is transthyretin-related amyloidosis (ATTR), a tetrameric structured transport protein synthesized mainly by the liver. There are two types of amyloidosis resulting from the deposition of this protein [4]: a non-hereditary form known as \"wild type\" TTR amyloidosis (ATTRwt) that primarily involves the heart, particularly in male subjects older than 65 years, and a genetic form known as \"hereditary TTR amyloidosis\" (ATTRm), an autosomal dominant disease characterized by a particular tropism for nervous and/or cardiac tissue [2; 5]. The frequency of these two types of amyloidosis in the population is related to several factors, including specific TTR mutations (there are more than 100 genetic mutations of the TTR gene), sex, and geographic distribution [6]. The cardiac phenotypic expressions are related to Thr60 Ala, Leu111 Met, Ile68 Leu, and Val122 Ile gene mutations [2]. Another form of systemic amyloidosis that frequently affects the heart is light chain amyloidosis (AL); this is secondary to the presence of clones of plasma cells in the bone marrow that produce free light chains of immunoglobulins in the circulation, which are responsible for fibrillar deposits. The extreme clinical heterogeneity of ATTR forms makes the diagnosis and treatment a real challenge; in fact, these forms are often underdiagnosed or diagnosed late, given the non-specificity of symptoms [7], and that might lead to a poor prognosis. The need for an early diagnosis of cardiac involvement in individuals with ATTR has been highlighted in the scientific literature, as it can significantly influence patient treatment [8]. The suspicion of amyloidotic cardiomyopathy demands several diagnostic tests, including an electrocardiogram (ECG), which may detect low peripheral voltages, pseudo-necrosis patterns, conduction delays, and repolarization changes, and echocardiography, which may identify left ventricular hypertrophy, valve and interatrial septum thickening, pericardial effusion, granular sparkling appearance, diastolic dysfunction, a reduction of global longitudinal strain, and apical sparing [9]. Unfortunately, none of these provides information on the etiologic type of amyloidosis [5]; thus, the \"gold standard\" examination for a definitive diagnosis of amyloid cardiomyopathy is an endomyocardial biopsy (EMB). This investigation has good accuracy in characterizing the proteins contained in the deposits (through immunohistochemical and mass spectrometry analysis) and in confirming the presence of amyloid; nevertheless, it is an invasive procedure that is not free from complications [10]. Currently, the use of EMB has been curtailed by the increasing diagnostic accuracy offered by other non-invasive imaging methods with technetium-99m (\({}^{99\text{m}}\)Tc)-diphosphonate (DPD), \({}^{99\text{m}}\)Tc-hydroxyl-methylene-diphosphonate (HMDP), or \({}^{99\text{m}}\)Tc-pyrophosphate (PYP) bone scintigraphy [5]. In fact, according to the study by [PERSON] et al. [11] bone scintigraphy can confidently define cardiac amyloidosis due to TTR in the presence of a moderate/intense cardiac uptake when the AL form can be excluded with dedicated serum-urinary investigations. On the contrary, cardiac uptake expressed by Scintigraphic Score can vary from zero to three in AL [11; 12] and other extremely rare forms of cardiac amyloidosis. Furthermore, this diagnostic method can identify TTR deposits at a preclinical stage of the disease, when echocardiogram and biomarkers are still normal. In addition to cardiac visual score [13], several studies have evaluated the application of a semiquantitative analysis of cardiac uptake [9; 14].