18 F-Sodium Fluoride Positron Emission Tomography and Computed Tomography in Acute Aortic Syndrome.

Background: Acute aortic syndrome is associated with aortic medial degeneration. ¹⁸ F-sodium fluoride ( ¹⁸ F-NaF) positron emission tomography (PET) detects microscopic tissue calcification as a marker of disease activity.
Objectives: In a proof-of-concept study, this investigation aimed to establish whether ¹⁸ F-NaF PET combined with computed tomography (CT) angiography could identify aortic medial disease activity in patients with acute aortic syndrome.
Methods: Patients with aortic dissection or intramural hematomas and control subjects underwent ¹⁸ F-NaF PET/CT angiography of the aorta. Aortic ¹⁸ F-NaF uptake was measured at the most diseased segment, and the maximum value was corrected for background blood pool activity (maximum tissue-to-background ratio [TBR _max ]). Radiotracer uptake was compared with change in aortic size and major adverse aortic events (aortic rupture, aorta-related death, or aortic repair) over 45 ± 13 months.
Results: Aortic ¹⁸ F-NaF uptake co-localized with histologically defined regions of microcalcification and elastin disruption. Compared with control subjects, patients with acute aortic syndrome had increased ¹⁸ F-NaF uptake (TBR _max : 1.36 ± 0.39 [n = 20] vs 2.02 ± 0.42 [n = 47] respectively; P < 0.001) with enhanced uptake at the site of intimal disruption (+27.5%; P < 0.001). ¹⁸ F-NaF uptake in the false lumen was associated with aortic growth (+7.1 mm/year; P = 0.011), and uptake in the outer aortic wall was associated with major adverse aortic events (HR: 8.5 [95% CI: 1.4-50.4]; P = 0.019).
Conclusions: In patients with acute aortic syndrome, ¹⁸ F-NaF uptake was enhanced at sites of disease activity and was associated with aortic growth and clinical events. ¹⁸ F-NaF PET/CT holds promise as a noninvasive marker of disease severity and future risk in patients with acute aortic syndrome. ( ¹⁸ F Sodium Fluoride PET/CT in Acute Aortic Syndrome [FAASt]; NCT03647566).
Competing Interests: Funding Support and Author Disclosure All funding support is from the United Kingdom. Mr Syed and Drs Fletcher, Dweck, Shah, and Tavares, Mr Kaczynki, and Dr Newby were supported by the British Heart Foundation (FS/18/31/33676, FS/19/15/34155, FS/11/014, FS/14/78/31020, CH/09/002, RG/16/10/32375, RE/18/5/34216). Dr Dweck has received the Sir Jules Thorn Award for Biomedical Research 2015 (15/JTA). Dr Newby has received a Wellcome Trust Senior Investigator Award (WT103782AIA). Dr van Beek has been supported by the Scottish Imaging Network—a Platform of Scientific Excellence (SINAPSE). Edinburgh Clinical Research Facility and Edinburgh Imaging Facility are supported by NHS Research Scotland. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2022. Published by Elsevier Inc.)