## 2 Materials and Methods  
The present study is a pre-specified subanalysis of a study aimed at evaluating the relationship between aortic inflammation as assessed using \({}^{18}\)F-FDG-PET and features of coronary plaque vulnerability as assessed using OCT [12]. Briefly, we prospectively enrolled consecutive patients with NSTE-ACS referred to the S. Orsola/Malpighi Hospital Catheterization Laboratory and scheduled for percutaneous coronary intervention (PCI) for at least 1 coronary obstruction in one of the main three epicardial vessels. Inclusion and exclusion criteria have been previously described in detail [12]. Of note, although diabetes mellitus is one of the major cardiovascular risk factors, it was included in the exclusion criteria since it is known that high levels of prescan glucose value reduce aortic \({}^{18}\)F-FDG uptake and increase blood pool activity [13]. In addition to the evaluation of routine hematological and biochemical profiles, for the purpose of this sub-study an additional tube was drawn for the determination of serum Cystatin C. Serum levels of C-reactive protein (CRP) were measured using the immunoblotting-photimetric method [14] (AU 5800, Beckman Coulter, Brea, California, United States). Intra- and inter-individual coefficients of variation were 3.22% and 3.79%, respectively. Serum levels of cystatin C were measured using the nephelometric method [15] (Image 800, Beckman Coulter, Brea, California, United States). Intra- and inter-individual coefficients of variation ranged from 1.6% to 1.8% and 2.3% to 2.9%, respectively. Coronary angiography and angioplasty was performed either via the trans-radial or the trans-femoral approach with the use of a 6F sheath [16]. Standard techniques and medications were used. Three vessel OCT acquisition and analyses were previously described [12,17,18]. For each patient the number of lipid-rich plaques and lipid-rich plaques with macrophages and thin cap fibroatheromas (TCFAs) were established. All patients underwent \({}^{18}\)F-FDG-PET/Computed tomography (CT) >24 h after successful PCI procedure and before discharge. Patients preparation and \({}^{18}\)F-FDG-PET/CT protocol were previouslydescribed [12]. 18F-FDG uptake was measured within the wall of both the ascending aorta (AA) and thoracic descending aorta (DA). Superior vena cava was used to calculate the blood pool background SUV with a 1 cm standard region of interest. SUV values (maximum and mean) were calculated on an axial plane slice by slice (every 3.75 mm) around the wall of both the AA and DA. For each aortic slice, the mean and maximum target to background ratio (TBR\({}_{\text{mean}}\) and TBR\({}_{\text{max}}\), respectively) was calculated by dividing the SUV\({}_{\text{mean}}\) and SUV\({}_{\text{max}}\) of the aorta with the SUV\({}_{\text{mean}}\) of the superior vena cava. Subsequently, TBR\({}_{\text{mean}}\) and TBR\({}_{\text{max}}\) were averaged for both the AA and DA [19]. We also calculated the number of active slices in both the AA and DA. 18F-FDG-PET slices were defined as active if TBR\({}_{\text{max}}\) was \(\geq\)1.6, as previously described [19]. Coronary calcification was evaluated using standardized methods as previously described [20]. Low attenuation CT scanning was performed using a tube voltage of 120 kV and 80 mA and slice thickness of 3.75 mm. Previous studies have demonstrated that CAC scores measured on CT scan images obtained from a hybrid PET-CT scanner are comparable with those obtained on a dedicated CT scanner [21]. CAC score was measured in a blind fashion by a separate investigator (F.B.) from those who performed the PET analyses. Categorical data are expressed as proportions and continuous variables reported as medians (25 th-75 th percentiles). Patients were divided into low cystatin C group and high cystatin C group, on the basis of the median value of serum cystatin C. For comparisons between groups, the [PERSON] chi-square test and [PERSON]'s test were used for categorical and continuous variables, respectively.