Abstract
241356
Introduction: Aortic stenosis (AS), prevalent in developed countries, shares pathophysiological similarities with atherosclerosis, involving endothelial damage, lipid infiltration, and progressive calcification leading to valvular fibrosis, stiffening, and stenosis. This progression can result in left ventricular hypertrophy, heart failure, and potentially fatal outcomes without valve replacement. While echocardiography remains the diagnostic standard, CT calcium scoring and cardiac MRI offer additional insights into stenosis severity and myocardial condition. Given the limitations of conventional imaging in early detection and the potential mismatch between disease severity and echocardiographic findings, there's increasing interest in exploring molecular imaging, particularly PET/CT and PET/MRI, in AS evaluation. Our focus is to assess the effectiveness of these modalities in AS.
Methods: Utilizing keywords "PET/CT, PET/MRI, Aortic Stenosis, 18F-FDG, and 18F-NaF," we conducted a focused search on Google Scholar and PubMed for literature on AS evaluation via PET/CT and PET/MRI. Our analysis centered on highly cited articles from the past five years, synthesizing their results and conclusions for a comprehensive understanding.
Results: PET/CT and PET/MRI are becoming crucial in the comprehensive assessment of Aortic Stenosis (AS), blending anatomical and molecular data. While CT and MRI components provide detailed images of the aortic valve and myocardium, PET adds a unique dimension by using tracers like 18F-fluorodeoxyglucose (18F-FDG) and 18F-sodium fluoride (18F-NaF) to highlight areas of active inflammation and calcification. 18F-FDG is particularly adept at identifying inflammation, as it accumulates in glucose-dependent macrophages present in inflamed tissues.18F-FDG baseline SUVmax was significantly higher in patients who subsequently developed (2.28 ± 0.42 vs. 1.73 ± 0.36) or had increased (2.03 ± 0.52 vs.1.74 ± 0.36) AV calcification as compared to patients who did not have a change in calcification. However, its utility in AS is somewhat hindered by its physiological uptake in the myocardium and a lack of specificity. Additionally, 18F-FDG uptake does not consistently align with AS severity, limiting its diagnostic value. Contrastingly, 18F-NaF shines in detecting valve calcification, closely correlating with AS severity and progression. In patients with aortic sclerosis and stenosis, 18F-NaF uptake, as measured by TBRmax, is significantly higher compared to the control group. This is substantiated by its alignment with echocardiographic findings and CT calcium scores. 18F-NaF's ability to detect early microcalcifications makes it a powerful tool for early diagnosis and prognostication of potential adverse outcomes in AS. PET/MRI, in particular, offers superior tissue characterization, effective motion correction, and reduced radiation exposure compared to PET/CT. Despite these advantages, the application of PET/MRI in AS remains limited. Factors like high cost, limited availability, and technical challenges constrain its widespread adoption in the clinical assessment of AS, suggesting a need for further development and accessibility improvements in this technology.
Conclusions: 18F-FDG and 18F-NaF PET/CT are emerging as complementary imaging modalities in Aortic Stenosis (AS), offering insights into valve inflammation and calcification and aiding in diagnosis, progression assessment, and adverse event prediction. PET/MRI further enhances this evaluation with detailed valve and myocardial analysis, coupled with lower radiation exposure. However, defining the specific clinical roles and integration of PET/CT and PET/MRI in AS requires further research to optimize their use in clinical practice.