Background:Giant cell arteritis (GCA) and Takayasu’s arteritis (TAK) are the two main forms of large-vessel vasculitis (LVV). Although angiography is essential to detect vascular disease in patients with LVV, there is limited prospective data characterizing change in arterial lesions over time, and factors that predict angiographic change remain unknown.Objectives:The objectives of this study were to: 1) describe longitudinal change in angiographic studies in patients with GCA and TAK and 2) determine whether FDG-PET activity predicts angiographic progression of disease.Methods:Patients with GCA or TAK were recruited into a prospective, observational cohort. All patients underwent baseline magnetic resonance (MR) or computed tomography (CT) angiography and a follow-up study (same modality) ≥6 months after baseline per a standardized imaging protocol. For patients who had multiple angiograms, the baseline and most recent images were compared. Arterial lesions, defined as stenosis, occlusion, or aneurysm, were evaluated by visual inspection in 4 segments of the aorta and 13 branch arteries by a single reader blinded to clinical status. On follow up angiography, the development of new lesions in these same territories was recorded, and existing lesions were characterized as improved, worsened, or unchanged by visual inspection, with confirmation by an independent reader.All patients underwent FDG-PET on the same date as angiography. Qualitative assessment of FDG uptake was performed in each corresponding arterial territory evaluated by angiography. Active vasculitis was defined as greater FDG uptake in the arterial wall compared to the liver by visual inspection.Results:At the baseline visit, there were 248 arterial lesions (21%) out of 1162 arterial territories evaluated from 70 patients with LVV (TAK=38; GCA=32). Baseline characteristics were as follows: Age [TAK=29.5 years (18.4-39.5), GCA=69.6 years (60.7-75.5)], Female gender [TAK=30 patients (79%), GCA=23 patients (72%)], Disease duration [TAK=2.2 years (0.6-5.5), GCA=0.7 years (0.1-2.6)], Active clinical disease [TAK=17 patients (45%), GCA=20 patients (63%)].Over 1.6 years (1.0-2.7) of median follow-up, no angiographic change was observed in 1,132 (97%) arterial territories. New lesions developed in 8 arterial territories, exclusively in 5 patients with TAK. Arterial lesions improved in 16 territories (GCA = 7, TAK = 9) and worsened in 6 territories (GCA = 1, TAK = 5). Patients with angiographic improvement were initially imaged earlier in the disease course compared to patients with new/worsening lesions (median 1.1 vs 16.4 months, p=0.09). Patients with angiographic improvement had significantly lower acute phase reactants at follow-up compared to patients with new/worsening arterial lesions [median ESR 3.0 (2.0-15.0) vs. 27.0 (7.3-39) mm/h, p<0.01; median CRP 0.7 (0.3-1.4) vs. 6.1 (3.1-19.6) mg/L, p<0.01]. Seventy-nine percent of patients with new/worsening arterial lesions had received increased treatment over the follow-up interval compared to 100% patients with improved arterial lesions, p=0.09.FDG-PET activity was evaluated in 1091/1162 (94%) of corresponding arterial territories. PET activity in an arterial territory at baseline was significantly associated with change in that arterial territory (either new/worsening or improvement) on follow-up angiography (p<0.01) (FIGURE 1). PET activity had a sensitivity of 80% and specificity of 74% for predicting change in arterial lesions. Most arterial territories without PET activity at baseline remained unchanged over time by angiography, yielding a negative predictive value of 99%. (FIGURE 1).Conclusion:Development of new arterial lesions is infrequent in LVV. Change in arterial lesions is dynamic, and improvement can occur. FDG-PET activity predicts change in angiographic lesions, and lack of PET activity is strongly associated with stable angiographic disease. These data may inform guideline recommendations for imaging monitoring in LVV.Figure 1.Disclosure of Interests:None declared
Clinical Factors Associated with Time-Specific Distribution of 18F-Fluorodeoxyglucose in Large-Vessel Vasculitis
