Abstract

Structural valve degeneration (SVD) of bioprostheses is a common and serious complication in patients undergoing aortic valve replacement. SVD pathophysiology remains unclear.18F-sodium fluoride (NaF) and 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) have respectively shown that an active metabolic phenomenon of calcification rather than an inflammatory process contribute to native aortic valve stenosis. We studied the respective value of NaF and FDG PET to explore the potential mechanisms involved in SVD. SVD patients underwent NaF PET to explore potential active calcification process, FDG PET to explore potential inflammatory process and thoracic CT. Tracer uptake was quantitatively measured by the bioprosthesis tissue-to-background ratio of standardized uptake values (TBR). Echocardiographic parameters, bioprosthesis calcium scoring on CT, and qualitative pattern of NaF and FDG activity on bioprostheses were analyzed. Twenty-one patients were included. Calcium score was higher in patients with significant NaF visual uptake versus patients without (1065 ± 505 vs. 462 ± 320, P = 0.015). The median NaF TBR (3.49, [2.33–5.04]) was significantly higher than FDG (1.34, [1.20–1.47]). Patients with NaF TBR greater than the median value had a higher calcium score (1059 ± 550 vs. 566 ± 363, P = 0.05), and showed a tendency to have more severe hemodynamic stenosis. Picture shows an example of patient with SVD (A); CT (B) established localizations of calcium deposits; NaF PET/CT (C) show intense uptake adjacent to calcifications; FDG PET/CT (D) show no uptake ( Fig. 1 ). These results suggest a link between SVD severity and active calcification activity and opens new perspectives on the assessment of SVD pathophysiology through NaF PET quantification of ongoing mineral burden.

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