Fabian Demeure1, Caroline Bouzin1, Véronique Roelants1, Anne Bol1, Robert Verhelst1, Parla Astarci1, Bernhard L Gerber1, Anne-Catherine Pouleur1, Agnès Pasquet1, Christophe de Meester1, Jean-Louis J Vanoverschelde1, David Vancraeynest2. 1. From the Pôle de Recherche Cardiovasculaire (CARD), Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain, Brussels, Belgium (F.D., R.V., P.A., B.L.G., A.-C.P., A.P., C.d.M., J.-L.J.V., D.V.); Cardiovascular Department, Institut Cardiovasculaire, Cliniques Universitaires Saint-Luc, Brussels, Belgium (F.D., R.V., P.A., B.L.G., A.-C.P., A.P., C.d.M., J.-L.J.V., D.V.); IREC Imaging Platform, Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain, Brussels, Belgium (C.B.); Pôle d'Imagerie Médicale, Radiothérapie et Oncologie (MIRO), Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain, Brussels, Belgium (V.R., A.B.); and Division of Nuclear Medicine, Internal Medicine Department, Cliniques Universitaires Saint-Luc, Brussels, Belgium (V.R., A.B.). 2. From the Pôle de Recherche Cardiovasculaire (CARD), Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain, Brussels, Belgium (F.D., R.V., P.A., B.L.G., A.-C.P., A.P., C.d.M., J.-L.J.V., D.V.); Cardiovascular Department, Institut Cardiovasculaire, Cliniques Universitaires Saint-Luc, Brussels, Belgium (F.D., R.V., P.A., B.L.G., A.-C.P., A.P., C.d.M., J.-L.J.V., D.V.); IREC Imaging Platform, Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain, Brussels, Belgium (C.B.); Pôle d'Imagerie Médicale, Radiothérapie et Oncologie (MIRO), Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain, Brussels, Belgium (V.R., A.B.); and Division of Nuclear Medicine, Internal Medicine Department, Cliniques Universitaires Saint-Luc, Brussels, Belgium (V.R., A.B.). david.vancraeynest@uclouvain.be.
Abstract
BACKGROUND: Inflammation and intraplaque neovascularization are acknowledged to be 2 features of plaque vulnerability, although their temporal expression and their respective value in predicting clinical events are poorly understood. To determine their respective temporal associations, we conducted a comprehensive assessment of inflammation and intraplaque neovascularization in the carotid plaque of symptomatic and asymptomatic patients. METHODS AND RESULTS: Thirty patients with severe carotid stenosis underwent 18F-fluorodeoxyglucose-positron emission tomography/computed tomographic imaging. Plaque 18F-fluorodeoxyglucose-uptake, indicative of inflammation, was measured by calculating the target:background ratio. The presence of intraplaque neovascularization during contrast-enhanced ultrasound was judged semiquantitatively; low-grade contrast enhancement (CE) suggested its absence, and high-grade CE, the presence of neovascularization. Carotid surgery was performed 1.6±1.8 days after completing both imaging modalities in all patients, and the presence of macrophages and neovessels was quantified by immunohistochemistry. We identified a significant correlation between the target:background ratio and macrophage quantification (R=0.78; P<0.001). The number of vessels was also significantly higher in carotid plaque with high-CE (P<0.001). Surprisingly, immunohistochemistry showed that high-CE and vessel number were neither associated with an elevated target:background ratio (P=0.28 and P=0.60, respectively) nor macrophage infiltration (P=0.59 and P=0.40, respectively). Finally, macrophage infiltration and target:background ratio were higher in the carotid plaque of symptomatic patients (P=0.021 and P=0.05, respectively), whereas CE grade and the presence of neovessels were not. CONCLUSIONS: Inflammation and intraplaque neovascularization are not systematically associated in carotid plaques, suggesting a temporal separation between the 2 processes. Inflammation seems more pronounced when symptoms are present. These data highlight the challenges that face any imaging strategy designed to assess plaque vulnerability.
BACKGROUND:Inflammation and intraplaque neovascularization are acknowledged to be 2 features of plaque vulnerability, although their temporal expression and their respective value in predicting clinical events are poorly understood. To determine their respective temporal associations, we conducted a comprehensive assessment of inflammation and intraplaque neovascularization in the carotid plaque of symptomatic and asymptomatic patients. METHODS AND RESULTS: Thirty patients with severe carotid stenosis underwent 18F-fluorodeoxyglucose-positron emission tomography/computed tomographic imaging. Plaque 18F-fluorodeoxyglucose-uptake, indicative of inflammation, was measured by calculating the target:background ratio. The presence of intraplaque neovascularization during contrast-enhanced ultrasound was judged semiquantitatively; low-grade contrast enhancement (CE) suggested its absence, and high-grade CE, the presence of neovascularization. Carotid surgery was performed 1.6±1.8 days after completing both imaging modalities in all patients, and the presence of macrophages and neovessels was quantified by immunohistochemistry. We identified a significant correlation between the target:background ratio and macrophage quantification (R=0.78; P<0.001). The number of vessels was also significantly higher in carotid plaque with high-CE (P<0.001). Surprisingly, immunohistochemistry showed that high-CE and vessel number were neither associated with an elevated target:background ratio (P=0.28 and P=0.60, respectively) nor macrophage infiltration (P=0.59 and P=0.40, respectively). Finally, macrophage infiltration and target:background ratio were higher in the carotid plaque of symptomatic patients (P=0.021 and P=0.05, respectively), whereas CE grade and the presence of neovessels were not. CONCLUSIONS:Inflammation and intraplaque neovascularization are not systematically associated in carotid plaques, suggesting a temporal separation between the 2 processes. Inflammation seems more pronounced when symptoms are present. These data highlight the challenges that face any imaging strategy designed to assess plaque vulnerability.
Authors: L Saba; S Zucca; A Gupta; G Micheletti; J S Suri; A Balestrieri; M Porcu; P Crivelli; G Lanzino; Y Qi; V Nardi; G Faa; R Montisci Journal: AJNR Am J Neuroradiol Date: 2020-07-30 Impact factor: 3.825