Abstract 1338 18F-FDG uptake in the pulmonary artery in sarcoidosis detected by PET/MR correlates with pulmonary hypertension

Clin Res Cardiol (2022). https://doi.org/10.1007/s00392-022-02002-5
18F-FDG uptake in the pulmonary artery in sarcoidosis detected by PET/MR correlates with pulmonary hypertension
A. Maier¹, S. L. Liao², T. Lescure², P. M. Robson², S. Sartori², J. Narula², A. Jacobi², Z. A. Fayad², M. G. Trivieri²
¹Klinik für Kardiologie und Angiologie I, Universitäts-Herzzentrum Freiburg - Bad Krozingen GmbH, Freiburg im Breisgau; ²BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, New York, US;
Introduction: Sarcoidosis is a systemic granulomatous disease of unknown etiology that mostly affects the lung and skin and commonly the heart. Pulmonary hypertension (PH) can be found in patients with sarcoidosis and its presence carries a worse prognosis. This work evaluated the prevalence of pulmonary artery (PA) inflammation using FDG-PET/MRI in a cohort of subjects referred to our institution for cardiac sarcoid screening; in addition, it investigated the association between PA uptake and PH as detected by right heart catheterization (RHC) and/or transthoracic echocardiography (TTE). Materials and Methods: 175 patients with suspected active cardiac sarcoidosis underwent hybrid thoracic PET/ MRI. FDG uptake in the PA was quantified using maximum standardized uptake value (SUVmax) and target-to-background ratio (TBRmax). PA pressures and RV function data were acquired either by RHC or TTE. Results: FDG uptake in the PA was detected in 33 scans. In those subjects, the signal in the pulmonary arterial wall was distinct from blood pool and the artery was clearly and diffusely delineated by the PET tracer. 144 patients had no visible PA uptake. Except for a higher rate of systemic hypertension and greater use of beta-blockers in the non-uptake group, baseline characteristics were similar. 86.8 % of the patients with PA FDG uptake had concomitant FDG uptake in the aorta. Conversely, in the absence of increased PA signal, only 44.2% had FDG uptake uptake in the aorta (p < 0.01). RHC data was available for 10 patients in the FDG uptake group and 40 in the non-uptake group. PA mean pressure was significantly higher in the PA FDG uptake group compared to the non-uptake group (34.4 +/- 7.2 mmHg vs. 25.6 +/- 9.3 mmHg). When a mean PA of 25 mmHg was used as cut-off, 90 % of the patients with PA FDG uptake had PH vs. 45 % in the non-uptake group (p < 0.05). However, when a cut off of 20 mmHg was used, 100% of patients with PA uptake had PH. Signs of PH on TTE were present in a significant higher number of patients with PA FDG uptake (p < 0.05). Lastly, SUVmax and TBRmax correlated with PA pressure derived from RHC and/or TTE. Conclusions: This is the first study to demonstrate that PET/MRI with FDG can detect PA wall uptake in sarcoidosis and that the intensity of FDG uptake correlates with PA pressure and with the diagnosis of PH. Albeit our work was conducted using PET/MR, we expect that our results could be easily extrapolated to PET/CT thus providing a quick and powerful tool for the diagnosis of PH. Further studies will need to be conducted to evaluate for changes in PA inflammation in response to therapy for Sarcoidosis or PH, or to assess to elevated PA uptake in patients with other form of PH.
https://dgk.org/kongress_programme/jt2022/aV1343.html