## 1 Introduction  
Infective endocarditis (IE) is a pathological condition in the heart derived from the proliferation of microorganisms causing inflammatory disease involving the heart valves [1]. It is a diagnostic challenge due to the high variability of the presentation of clinical signs. The current diagnosis is a compendium of microbiological information and medical imaging, interpreted in combination with clinical signs and symptoms. This information is included as part of the criteria that define the gold standard of diagnosis, the modified Duke criteria. These criteria classify endocarditis into three subcategories based on the aforementioned findings: rejected, possible, and definite IE [2; 3]. However, these criteria exhibit limited sensitivity and specificity [4; 5; 6], as reported in the most recent AHA/IDSA and ESC guidelines [3; 7]. Despite the vast comprehension of IE clinical management, the morphiortality of this disease is still unacceptably high (20% at 30 days and 40-50% at subsequent follow-up) due to consequent complications [8]. The early identification of signs is crucial in preventing future complications and thus reducing the associated morbidity and mortality. The transthoracic (TTE) and transesophageal ultrasound (TEE) are usually employed as the gold standard in the diagnosis of IE. However, TTE especially fails to identify approximately 30% of the cases with prosthetic valve endocarditis (PVE) or infections in implantable electronic devices (CIED) [8]. In fact, when echocardiography fails to detect infective valve endocarditis, the Duke criteria show reduced diagnostic sensitivity [8]. Moreover, the sensitivity of echocardiography is still limited depending on several factors related to the stage of the disease, the clinician's expertise, or even the prosthetic material-related imaging artifacts. This limited sensitivity of diagnostic procedures leads to an important delay in the early diagnosis and consequent structural damage due to the infection [4; 9]. Precisely because of the limitations found in the modified Duke criteria, especially in the context of PVE and cardiovascular device-related infective endocarditis (CDRIE), additional imaging modalities were introduced as part of the ESC guideline criteria. In particular, the AHA guidelines recently highlighted the potential of the [18]FFDG PET/CT imaging in the diagnosis of PVE and native valve endocarditis (NVE) [7]. [18F]FDG PET/CT imaging has demonstrated a major role in PVE for the identification of valvular and perivalvular involvement [2; 10; 11; 12; 13]. In fact, [18F]FDG PET/CT imaging maintained a sensitivity and specificity of 86% and 84%, respectively, in those patients who demonstrated limited echocardiography sensitivity [14]. The major contribution of this imaging modality occurs in those cases where there is a high suspicion of IE and with a diagnosis of \"Possible IE\" or even \"IE rejected\" based on the other diagnostic criteria [6; 10; 15; 16; 17]. The inclusion of the [18F]FDG PET/CT imaging modality in the Duke criteria increased sensitivity from 57.1% to 83.5% [8]. The standardized uptake value (SUV)-related metrics have been widely used to analyze the metabolic patterns associated with cardiovascular infectious disease [2; 9; 17; 18; 19; 20; 21; 22; 23; 24; 25]. Although experience with SUV-based semiquantitative metrics has shown extensive use in oncologic applications, their use is less widespread in infective endocarditis and there is not yet a standard to obtain consistent values across studies [9; 26; 27; 28]. Despite some promising results in this regard, further technical developments are needed to consolidate the potential value of [18F]FDG PET/CT in the diagnosis of IE [28; 29]. In addition, recent advances have shown that the uptake pattern could play a relevant role in decreasing false positives. In fact, a homogeneous uptake pattern is related to reactive inflammatory activity and not to infection.