4.7 Article

Coronary Arterial 18F-Sodium Fluoride Uptake A Novel Marker of Plaque Biology

Journal

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 59, Issue 17, Pages 1539-1548

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2011.12.037

Keywords

acute coronary syndrome; calcification; inflammation; positron emission tomography; risk prediction

Funding

  1. National Health Service Research Scotland through National Health Service Lothian
  2. British Heart Foundation [FS/10/026, CH/09/002]
  3. British Heart Foundation Centre of Research Excellence
  4. Chief Scientist Office [ETM/160]
  5. Scottish Imaging Network-a Platform of Scientific Excellence
  6. Toshiba
  7. HEFCE
  8. Cambridge NIHR Biomedical Research Centre
  9. Academy of Medical Sciences (AMS) [AMS-SGCL1-Rudd] Funding Source: researchfish
  10. British Heart Foundation [FS/11/14/28692, FS/12/29/29463, FS/10/026/28209, PG/09/083/27667] Funding Source: researchfish
  11. Chief Scientist Office [ETM/160] Funding Source: researchfish
  12. Medical Research Council [G0701127] Funding Source: researchfish
  13. MRC [G0701127] Funding Source: UKRI

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Objectives With combined positron emission tomography and computed tomography (CT), we investigated coronary arterial uptake of 18F-sodium fluoride (18F-NaF) and 18F-fluorodeoxyglucose (18F-FDG) as markers of active plaque calcification and inflammation, respectively. Background The noninvasive assessment of coronary artery plaque biology would be a major advance particularly in the identification of vulnerable plaques, which are associated with specific pathological characteristics, including micro-calcification and inflammation. Methods We prospectively recruited 119 volunteers (72 +/- 8 years of age, 68% men) with and without aortic valve disease and measured their coronary calcium score and 18F-NaF and 18F-FDG uptake. Patients with a calcium score of 0 were used as control subjects and compared with those with calcific atherosclerosis (calcium score >0). Results Inter-observer repeatability of coronary 18F-NaF uptake measurements (maximum tissue/background ratio) was excellent (intra-class coefficient 0.99). Activity was higher in patients with coronary atherosclerosis (n = 106) versus control subjects (1.64 +/- 0.49 vs. 1.23 +/- 0.24; p = 0.003) and correlated with the calcium score (r = 0.652, p < 0.001), although 40% of those with scores >1,000 displayed normal uptake. Patients with increased coronary 18F-NaF activity (n = 40) had higher rates of prior cardiovascular events (p = 0.016) and angina (p = 0.023) and higher Framingham risk scores (p = 0.011). Quantification of coronary 18F-FDG uptake was hampered by myocardial activity and was not increased in patients with atherosclerosis versus control subjects (p = 0.498). Conclusions 18F-NaF is a promising new approach for the assessment of coronary artery plaque biology. Prospective studies with clinical outcomes are now needed to assess whether coronary 18F-NaF uptake represents a novel marker of plaque vulnerability, recent plaque rupture, and future cardiovascular risk. (An Observational PET/CT Study Examining the Role of Active Valvular Calcification and Inflammation in Patients With Aortic Stenosis; NCT01358513) (J Am Coll Cardiol 2012;59:1539-48) (C) 2012 by the American College of Cardiology Foundation

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