Short-term changes in arterial inflammation predict long-term changes in atherosclerosis progression

• Published in: European journal of nuclear medicine and molecular imaging 2017-01, Vol.44 (1), p.141-150
• Main Authors: Joseph, Philip, Ishai, Amorina, Mani, Venkatesh, Kallend, David, Rudd, James H. F., Fayad, Zahi A., Tawakol, Ahmed
• Format: Article
• Language: English
• Subjects: Arteritis - complications; Arteritis - diagnostic imaging; Atherosclerosis; Cardiology; Carotid Arteries - diagnostic imaging; Carotid Artery Diseases - diagnostic imaging; Carotid Artery Diseases - etiology; Disease Progression; Female; Fluorodeoxyglucose F18; Humans; Imaging; Inflammation; Longitudinal Studies; Magnetic Resonance Imaging - methods; Male; Medical imaging; Medicine; Medicine & Public Health; Middle Aged; Nuclear Medicine; Oncology; Original Article; Orthopedics; Positron Emission Tomography Computed Tomography - methods; Prognosis; Radiology; Radiopharmaceuticals; Reproducibility of Results; Sensitivity and Specificity; Tomography
• ISSN: 1619-7070; 1619-7089
• DOI: 10.1007/s00259-016-3524-0

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.