London, United Kingdom 2013 Cerebrovasc Dis 2013; 35 (suppl 3)1-854 181 8:30-10:00 Oral Session Room 9,10 Vascular imaging Chairs: R. Herzig, Czech Pepublic and R. Kern, Germany 1 Vascular imaging 8:30 - 8:40 Dynamic Contract-Enhanced MRI determined neovascularisation and 18F-FDG PET/CT determined inflammation in symptomatic carotid plaques are weakly correlated M.T.B. Truijman1, R.M. Kwee2, R.H.M. van Hoof3, E Hermeling4, A.H. Schreuder5, N.P. van Orshoven6, B Meems7, R.J. van Oostenbrugge8, W.H. Mess9, W.H. Backes10, M.J. Daemen11, J.A. Bucerius12, J.E. Wildberger13, M.E. Kooi14 Maastricht University Medical Center, Maastricht, THE NETHERLANDS1,Maastricht University Medical Center, Maastricht, THE NETHERLANDS2, Maastricht University Medi-cal Center, Maastricht, THE NETHERLANDS3, Maastricht University Medical Center, Maas-tricht, THE NETHERLANDS4, Atrium Medical Center, Heerlen, THE NETHERLANDS5, Orbis Medical Center, Sittard-Geleen, THE NETHERLANDS6, Viecuri Medical Center, Venlo, THE NETHERLANDS7, Maastricht University Medical Center, Maastricht, THE NETHER-LANDS8, Maastricht University Medical Center, Maastricht, THE NETHERLANDS9, Maastricht University Medical Center, Maastricht, THE NETHERLANDS10, Academic Med-ical Center, Amsterdam, THE NETHERLANDS11, Maastricht University Medical Center, Maastricht, THE NETHERLANDS12, Maastricht University Medical Center, Maastricht, THE NETHERLANDS13, Maastricht University Medical Center, Maastricht, THE NETHER-LANDS14 Background Identifying vulnerable atherosclerotic plaques can contribute to clinical decision making. Hall-marks of plaque vulnerability are inflammation, which can be assessed with 18F-FDG PET and increased neovascularisation, which can be assesses with DCE-MRI. Thus far, it remains unclear to which extent these processes are correlated or represent independent pathophysiolog-ical processes in time, that contribute to plaque vulnerability. Methods Fifty-eight patients with transient ischemic attack or minor stroke, in the carotid territory and ipsilateral carotid artery stenosis of 30 – 69% due to plaque were included. All patients under-went DCE-MRI of the carotid plaque on a 1.5T MRI system. Quantification of neovascularisa-tion was done by pixel-wise pharmacokinetic modelling of the dynamic enhancement curves and quantification of the mean transfer constant Ktrans and its 75 percentile for the heteroge-neity characterisation. In addition, a 3D PET/CT scan was performed on all patients one hour after injection of 2.75 MBq/kg body weight 18F-FDG. Dedicated fusion software was used to calculate mean blood-normalized 18F-FDG standard uptake values (SUV), known as the tar-get- to-background ratio (TBR) of the plaque. A spearman’s rank correlation coefficient was cal-culated to correlate Ktrans with TBR. Results In 49/58 patients, suitable images for further analysis were obtained. Mean time interval be-tween 18F-FDG PET and MRI was 2.9+/-5.5 days. The values of Ktrans, 75 percentile Ktrans and TBR were 0.110 +/- 0.027 min-1, 0.146 +/- 0.042 min-1 and 1.446 +/- 0.255, respectively. We found a weak but significant positive correlation between the TBR and the mean Ktrans/75 percentile Ktrans (Spearman’s r=0.30 respectively r=0.29, p=0<0.05). Conclusion There is a weak but significant positive correlation between Ktrans, a marker for neovasculari-sation, and inflammation as assessed by 18F-FDG PET/CT. 18F-FDG PET/CT and DCE-MRI are therefore not interchangeable. 2 Vascular Imaging 8:40 - 8:50 Early Blood Lipid Values are Associated with Carotid Inflammation on 18FDG-PET in Patients with Acutely Symptomatic Carotid Stenosis D. Ní Chróinín1, M. Marnane2, L. Akijian3, E. Fallon4, G. Horgan5, S. Murphy6, K. O’Ro-urke7, K. O’Malley8, M. O’Donohoe9, C. McDonnell10, I. Noone11, M. Barry12, M. Crowe13, M. O’Connell14, P.J. Kelly15 Neurovascular Unit for Translational and Therapeutics Research, Mater University Hos-pital/ University College Dublin, Dublin, IRELAND1,Neurovascular Unit for Translational and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND2, Neurovascular Unit for Translational and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND3, Neurovascular Unit for Translation-al and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND4, Neurovascular Unit for Translational and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND5, Neurovascular Unit for Translation-al and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND6, Neurovascular Unit for Translational and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND7, Department of Vascular Surgery, Ma-ter University Hospital, Dublin, IRELAND8, Department of Vascular Surgery, Mater University Hospital, Dublin, IRELAND9, Department of Vascular Surgery, Mater University Hospital, Dublin, IRELAND10, St Vin-cent’s University Hospital, Dublin, IRELAND11, St Vincent’s University Hospital, Dublin, IRELAND12, St Vincent’s University Hospital, Dublin, IRELAND13, Department of Radiolo-gy, Mater University Hospital, Dublin, Ireland, Dublin, IRELAND14, Neurovascular Unit for Translational and Therapeutics Research, Mater University Hospital/University College Dublin, Dublin, IRELAND15 Background: Factors stimulating carotid plaque inflammation and destabilisation are not well-understood. Although recent experimental data suggest diet-related lipids may be key initiators of inflammation leading to plaque rupture and stroke/TIA, no clinical studies have been performed. We hypothesised that serum lipids would be associated with plaque inflam-mation on fluorodeoxyglucose18 (FDG) PET in patients with acutely symptomatic carotid stenosis. Methods: PET-CT was performed on consecutive patients with acute symptomatic internal carotid artery (ICA) stenosis (≥50%). Symptomatic plaque FDG uptake was quantified as: (1) average maximum standardized uptake values (SUVmax) across 10 regions of interest (ROI); (2) highest single ROI SUV measure (SUVROImax); (3) averaged mean SUVs across 10 ROIs (SUVmean) Results: In 65 patients, median time to PET-CT was 7 days (IQR 4-9), to phlebotomy 2 days (IQR 1-4). Plaque inflammatory FDG SUVmax was associated with in-creasing tertiles of LDL (trend p=0.004), total cholesterol (p=0.009), triglycerides (p=0.01) and inversely associated with HDL (p=0.005). When analysed as continuous variables, LDL was associated with symptomatic ICA plaque SUVmax (Spearman rho 0.35, p=0.06), SUVmean (rho 0.44, p=0.009), and SUVROImax (rho 0.33, p=0.01). Total cholesterol was associated with SUVmean (rho 0.33, p=0.009), with trends for SUVmax (rho 0.24, p=0.059) and SUV-ROImax (rho 0.23, p=0.08). Triglycerides were associated with SUVmax (rho 0.32, p=0.01) and SUVROImax (rho 0.35, p=0.005). HDL was inversely associated with SUVmax (rho -0.37, p=0.004) and SUVROImax (rho -0.44, p=0.0004). Adjusting for age, gender, degree of stenosis and smoking, LDL (p=0.002) and total cholesterol (p=0.01) were independently associated with SUVmax. Conclusion: Serum lipids were associated with acutely symptomatic carotid plaque FDG uptake, supporting experimental data suggesting lipids may promote plaque inflammation, leading to rupture and clinical events.
Karger_ESC London_2013
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