Case Report: From metabolic normalization to incidental type A aortic dissection in immune checkpoint inhibitor–associated aortitis

Abstract

Immune checkpoint inhibitors can precipitate large-vessel vasculitis. It remains unknown whether metabolic remission on 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) reliably indicates long-term structural stability or absence of later complications. A 58-year-old man with KRAS-G12C–mutated stage IVB lung adenocarcinoma initiated first-line treatment with carboplatin + pemetrexed + pembrolizumab. After the fourth cycle he developed persistent fever with normal procalcitonin and negative cultures. Contrast-enhanced computed tomography showed concentric thickening of the aorta and major branches; 18F-FDG PET/CT demonstrated increased inflammatory uptake consistent with large-vessel vasculitis. Testing for autoimmune and infectious etiologies yielded no diagnostic findings. Given the strong clinicoradiologic agreement and the unfavorable risk–benefit profile of deep arterial biopsy, histologic confirmation was not pursued. Intravenous methylprednisolone led to rapid defervescence and biochemical improvement. On follow-up, 18F-FDG PET/CT demonstrated complete metabolic normalization. Subsequent surveillance imaging incidentally identified an asymptomatic Stanford type A aortic dissection. In the absence of indications for elective repair (diameter below surgical thresholds, no rapid expansion, malperfusion, or significant regurgitation) and after discussion within the multidisciplinary Heart Team, management consisted of structured imaging surveillance and optimal medical therapy. Thereafter, he initiated adagrasib, achieving a durable partial response. This case illustrates discordance between metabolic quiescence and later structural damage in immune checkpoint inhibitor-associated aortitis. This supports long-term structural surveillance, as 18F-FDG PET/CT normalization does not guarantee structural safety.