Immune checkpoint inhibition increases aortic inflammation on 18F-FDG PET/CT: a retrospective cohort study in patients with Merkel cell carcinoma receiving avelumab

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Abstract Background Patients with cancer treated with immune checkpoint inhibitors are at increased risk of cardiovascular events. Preclinical studies suggest that this may be driven by inflammation-induced acceleration of atherosclerosis. Objective We aimed to evaluate changes in vessel wall inflammation assessed using 18F-FDG positron emission tomography/computed tomography (PET/CT) after initiation of immune checkpoint inhibitors. Methods This was a single-center retrospective cohort study of patients with Merkel cell carcinoma who received at least one cycle of the programmed death ligand 1 (PD-L1) inhibitor avelumab and underwent 18F-FDG PET/CT before initiation and after 3 months of treatment. The primary outcome was the change in the target-to-background ratio (TBRmax) in the descending aorta between baseline and first follow-up scan. Secondary outcomes included the change in TBRmax in the carotid arteries, spleen, and bone marrow, and the incidence of major cardiovascular events. Results Fifty-three patients were included (66% male; median age 75 years). Most patients had established risk factors for cardiovascular disease (62%). The 18F-FDG TBRmax in the descending aorta increased 1.52 (IQR, 1.39-1.70) at baseline to 1.64 (IQR, 1.41-1.97) after 3 months of avelumab treatment (change, 7.8%; p=0.022). No significant changes in TBRmax were observed in the carotid arteries, bone marrow, and spleen. Statin use was not associated with change in TBRmax. During the median follow-up of 50 months (IQR, 32-65), one patient developed nonfatal ischemic stroke. Conclusion Treatment with avelumab was associated with an increase in 18F-FDG uptake in the descending aorta after 3 months, which supports the concept of inflammation-driven accelerated atherosclerosis in patients receiving immune checkpoint inhibitors.

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