Philip Joseph1,2, Amorina Ishai1, Venkatesh Mani3, David Kallend4, James H F Rudd5, Zahi A Fayad6,7, Ahmed Tawakol8. 1. Cardiology Division and Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Suite 400-165 Cambridge St, Boston, MA, 02114, USA. 2. Population Health Research Institute, Department of Medicine, and Department of Radiology, McMaster University, Hamilton, ON, Canada. 3. Translational and Molecular Imaging Institute and Department of Radiology, Icahn School of Medicine at Mount Sinai School of Medicine, New York, NY, USA. 4. The Medicines Company, Parsippany, NJ, USA. 5. Division of Cardiovascular Medicine, University of Cambridge, Cambridge, UK. 6. Translational and Molecular Imaging Institute and Department of Radiology, Icahn School of Medicine at Mount Sinai School of Medicine, New York, NY, USA. zahi.fayad@mssm.edu. 7. Translational and Molecular Imaging Institute and Department of Radiology, Icahn School of Medicine at Mount Sinai School of Medicine, Hess CSM Building Floor TMII, Rm S1-104, 1470 Madison Avenue, New York, NY, 10029, USA. zahi.fayad@mssm.edu. 8. Cardiology Division and Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Suite 400-165 Cambridge St, Boston, MA, 02114, USA. atawakol@mgh.harvard.edu.
Abstract
PURPOSE: It remains unclear whether changes in arterial wall inflammation are associated with subsequent changes in the rate of structural progression of atherosclerosis. METHODS: In this sub-study of the dal-PLAQUE clinical trial, multi-modal imaging was performed using 18-fludeoxyglucose (FDG) positron emission tomography (PET, at 0 and 6 months) and magnetic resonance imaging (MRI, at 0 and 24 months). The primary objective was to determine whether increasing FDG uptake at 6 months predicted atherosclerosis progression on MRI at 2 years. Arterial inflammation was measured by the carotid FDG target-to-background ratio (TBR), and atherosclerotic plaque progression was defined as the percentage change in carotid mean wall area (MWA) and mean wall thickness (MWT) on MRI between baseline and 24 months. RESULTS: A total of 42 participants were included in this sub-study. The mean age of the population was 62.5 years, and 12 (28.6 %) were women. In participants with (vs. without) any increase in arterial inflammation over 6 months, the long-term changes in both MWT (% change MWT: 17.49 % vs. 1.74 %, p = 0.038) and MWA (% change MWA: 25.50 % vs. 3.59 %, p = 0.027) were significantly greater. Results remained significant after adjusting for clinical and biochemical covariates. Individuals with no increase in arterial inflammation over 6 months had no significant structural progression of atherosclerosis over 24 months as measured by MWT (p = 0.616) or MWA (p = 0.373). CONCLUSIONS: Short-term changes in arterial inflammation are associated with long-term structural atherosclerosis progression. These data support the concept that therapies that reduce arterial inflammation may attenuate or halt progression of atherosclerosis.
PURPOSE: It remains unclear whether changes in arterial wall inflammation are associated with subsequent changes in the rate of structural progression of atherosclerosis. METHODS: In this sub-study of the dal-PLAQUE clinical trial, multi-modal imaging was performed using 18-fludeoxyglucose (FDG) positron emission tomography (PET, at 0 and 6 months) and magnetic resonance imaging (MRI, at 0 and 24 months). The primary objective was to determine whether increasing FDG uptake at 6 months predicted atherosclerosis progression on MRI at 2 years. Arterial inflammation was measured by the carotid FDG target-to-background ratio (TBR), and atherosclerotic plaque progression was defined as the percentage change in carotid mean wall area (MWA) and mean wall thickness (MWT) on MRI between baseline and 24 months. RESULTS: A total of 42 participants were included in this sub-study. The mean age of the population was 62.5 years, and 12 (28.6 %) were women. In participants with (vs. without) any increase in arterial inflammation over 6 months, the long-term changes in both MWT (% change MWT: 17.49 % vs. 1.74 %, p = 0.038) and MWA (% change MWA: 25.50 % vs. 3.59 %, p = 0.027) were significantly greater. Results remained significant after adjusting for clinical and biochemical covariates. Individuals with no increase in arterial inflammation over 6 months had no significant structural progression of atherosclerosis over 24 months as measured by MWT (p = 0.616) or MWA (p = 0.373). CONCLUSIONS: Short-term changes in arterial inflammation are associated with long-term structural atherosclerosis progression. These data support the concept that therapies that reduce arterial inflammation may attenuate or halt progression of atherosclerosis.
Entities:
Keywords:
Atherosclerosis; Inflammation; Magnetic resonance imaging; Positron emission tomography
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