Relation between thoracic aortic inflammation and features of plaque vulnerability in the coronary tree in patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention. An FDG-positron emission tomography and optical coherence tomography study

Purpose: To evaluate the relationship between aortic inflammation as assessed by18F–fluorodeoxyglucose-positron emission tomography (18F–FDG-PET) and features of plaque vulnerability as assessed by frequency domain-optical coherence tomography (FD-OCT). Methods: We enrolled 30 consecutive non-ST-segment elevation acute coronary syndrome patients undergoing percutaneous coronary intervention. All patients underwent three-vessel OCT before intervention and18F–FDG-PET before discharge. Univariable and C-reactive protein (CRP)-adjusted linear regression analyses were performed between features of vulnerability [namely:lipid-rich plaques with and without macrophages and thin cap fibroatheromas (TCFA)] and18F–FDG uptake in both ascending (AA) and descending aorta (DA) [measured either as averaged mean and maximum target-to-blood ratio (TBR) or as active slices (TBRmax ≥ 1.6)]. Results: Mean age was 62 years, and 26 patients were male. On univariable linear regression analysis TBRmeanand TBRmaxin DA was associated with the number of lipid-rich plaques (β = 4.22; 95%CI 0.05–8.39; p = 0.047 and β = 3.72; 95%CI 1.14–6.30; p = 0.006, respectively). TBRmaxin DA was also associated with the number of lipid-rich plaques containing macrophages (β = 2.40; 95%CI 0.07–4.72; p = 0.044). A significant CRP adjusted linear association between the TBRmaxin DA and the number of lipid-rich plaques was observed (CRP-adjusted β = 3.58; 95%CI -0.91-6.25; p = 0.01). TBRmaxin DA showed a trend towards significant CRP-adjusted association with number of lipid-rich plaques with macrophages (CRP-adjusted β = 2.30; 95%CI -0.11-4.71; p = 0.06). We also observed a CRP-adjusted (β = 2.34; 95%CI 0.22–4.47; p = 0.031) linear association between the number of active slices in DA and the number of lipid-rich plaques. No relation was found between FDG uptake in the aorta and the number of TCFAs. Conclusions: In patients with first NSTEACS, 18F–FDG uptake in DA is correlated with the number of OCT detected lipid-rich plaques with or without macrophages. This association may be independent from CRP values.