Leticia Fernández-Friera1, Valentín Fuster2, Beatriz López-Melgar3, Belén Oliva4, Javier Sánchez-González5, Angel Macías4, Braulio Pérez-Asenjo4, Daniel Zamudio4, Juan C Alonso-Farto6, Samuel España4, José Mendiguren7, Héctor Bueno8, Jose M García-Ruiz9, Borja Ibañez10, Antonio Fernández-Ortiz11, Javier Sanz12. 1. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Hospital Universitario HM Montepríncipe-CIEC, Madrid, Spain; CIBERV, Madrid, Spain; Universidad CEU San Pablo, Madrid, Spain. 2. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: vfuster@cnic.es. 3. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Hospital Universitario HM Montepríncipe-CIEC, Madrid, Spain; Universidad CEU San Pablo, Madrid, Spain. 4. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain. 5. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Philips Healthcare, Iberia, Spain. 6. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Hospital General Universitario Gregorio Marañón, Madrid, Spain. 7. Banco de Santander, Madrid, Spain. 8. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Hospital Universitario 12 de Octubre and Instituto de Investigación Sanitaria Hospital 12 de Octubre (imas12), Madrid, Spain; Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain. 9. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; CIBERV, Madrid, Spain; Hospital Universitario de Cabueñes Gijón, Instituto de Investigación Sanitaria del Principado de Asturias, Oviedo, Spain. 10. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; CIBERV, Madrid, Spain; IIS-Fundación Jiménez Díaz University Hospital, Madrid, Spain. 11. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; CIBERV, Madrid, Spain; Hospital Clínico San Carlos, Universidad Complutense, IdISSC, Madrid, Spain. 12. Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain; Icahn School of Medicine at Mount Sinai, New York, New York.
Abstract
BACKGROUND: Atherosclerosis is a chronic inflammatory disease, but data on arterial inflammation at early stages is limited. OBJECTIVES: The purpose of this study was to characterize vascular inflammation by hybrid 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/magnetic resonance imaging (PET/MRI). METHODS: Carotid, aortic, and ilio-femoral 18F-FDG PET/MRI was performed in 755 individuals (age 40 to 54 years; 83.7% men) with known plaques detected by 2-/3-dimensional vascular ultrasound and/or coronary calcification in the PESA (Progression of Early Subclinical Atherosclerosis) study. The authors evaluated the presence, distribution, and number of arterial inflammatory foci (increased 18F-FDG uptake) and plaques with or without inflammation (coincident 18F-FDG uptake). RESULTS: Arterial inflammation was present in 48.2% of individuals (24.4% femorals, 19.3% aorta, 15.8% carotids, and 9.3% iliacs) and plaques in 90.1% (73.9% femorals, 55.8% iliacs, and 53.1% carotids). 18F-FDG arterial uptakes and plaques significantly increased with cardiovascular risk factors (p < 0.01). Coincident 18F-FDG uptakes were present in 287 of 2,605 (11%) plaques, and most uptakes were detected in plaque-free arterial segments (459 of 746; 61.5%). Plaque burden, defined by plaque presence, number, and volume, was significantly higher in individuals with arterial inflammation than in those without (p < 0.01). The number of plaques and 18F-FDG uptakes showed a positive albeit weak correlation (r = 0.25; p < 0.001). CONCLUSIONS: Arterial inflammation is highly prevalent in middle-aged individuals with known subclinical atherosclerosis. Large-scale multiterritorial PET/MRI allows characterization of atherosclerosis-related arterial inflammation and demonstrates 18F-FDG uptake in plaque-free arterial segments and, less frequently, within plaques. These findings suggest an arterial inflammatory state at early stages of atherosclerosis. (Progression of Early Subclinical Atherosclerosis [PESA]; NCT01410318).
BACKGROUND:Atherosclerosis is a chronic inflammatory disease, but data on arterial inflammation at early stages is limited. OBJECTIVES: The purpose of this study was to characterize vascular inflammation by hybrid 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/magnetic resonance imaging (PET/MRI). METHODS: Carotid, aortic, and ilio-femoral 18F-FDG PET/MRI was performed in 755 individuals (age 40 to 54 years; 83.7% men) with known plaques detected by 2-/3-dimensional vascular ultrasound and/or coronary calcification in the PESA (Progression of Early Subclinical Atherosclerosis) study. The authors evaluated the presence, distribution, and number of arterial inflammatory foci (increased 18F-FDG uptake) and plaques with or without inflammation (coincident 18F-FDG uptake). RESULTS:Arterial inflammation was present in 48.2% of individuals (24.4% femorals, 19.3% aorta, 15.8% carotids, and 9.3% iliacs) and plaques in 90.1% (73.9% femorals, 55.8% iliacs, and 53.1% carotids). 18F-FDG arterial uptakes and plaques significantly increased with cardiovascular risk factors (p < 0.01). Coincident 18F-FDG uptakes were present in 287 of 2,605 (11%) plaques, and most uptakes were detected in plaque-free arterial segments (459 of 746; 61.5%). Plaque burden, defined by plaque presence, number, and volume, was significantly higher in individuals with arterial inflammation than in those without (p < 0.01). The number of plaques and 18F-FDG uptakes showed a positive albeit weak correlation (r = 0.25; p < 0.001). CONCLUSIONS:Arterial inflammation is highly prevalent in middle-aged individuals with known subclinical atherosclerosis. Large-scale multiterritorial PET/MRI allows characterization of atherosclerosis-related arterial inflammation and demonstrates 18F-FDG uptake in plaque-free arterial segments and, less frequently, within plaques. These findings suggest an arterial inflammatory state at early stages of atherosclerosis. (Progression of Early Subclinical Atherosclerosis [PESA]; NCT01410318).
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
Authors: Milena Aksentijevich; Sundus S Lateef; Paula Anzenberg; Amit K Dey; Nehal N Mehta Journal: Trends Cardiovasc Med Date: 2019-11-20 Impact factor: 6.677
Authors: Nicholas R Evans; Jason M Tarkin; Elizabeth Pv Le; Rouchelle S Sriranjan; Andrej Corovic; Elizabeth A Warburton; James Hf Rudd Journal: Br J Radiol Date: 2020-04-03 Impact factor: 3.039