Author + information
- Jacek Kwiecinski, MDa,b,
- Damini Dey, PhDa,
- Sebastien Cadet, MSa,
- Sang-Eun Lee, MDc,
- Yuka Otaki, MDa,
- Phi T. Huynh, BSa,
- Mhairi K. Doris, MDb,
- Evann Eisenberg, MDa,
- Mijin Yun, MDc,
- Maurits A. Jansen, PhDb,
- Michelle C. Williams, MDb,
- Balaji K. Tamarappoo, MDa,
- John D. Friedman, MDa,
- Marc R. Dweck, MD, PhDa,
- David E. Newby, MD, PhDb,
- Hyuk-Jae Chang, MDc,
- Piotr J. Slomka, PhDa and
- Daniel S. Berman, MDa,∗ ()
- aDepartment of Imaging (Division of Nuclear Medicine), Medicine, and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California
- bBHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom
- cSeverance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, South Korea
- ↵∗Address for correspondence:
Dr. Daniel S. Berman, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, California 90048.
Objectives This study aimed to assess the association between increased lesion peri-coronary adipose tissue (PCAT) density and coronary 18F-sodium fluoride (18F-NaF) uptake on positron emission tomography (PET) in stable patients with high-risk coronary plaques (HRPs) shown on coronary computed tomography angiography (CTA).
Background Coronary 18F-NaF uptake reflects the rate of calcification of coronary atherosclerotic plaque. Increased PCAT density is associated with vascular inflammation. Currently, the relationship between increased PCAT density and 18F-NaF uptake in stable patients with HRPs on coronary CTA has not been characterized.
Methods Patients who underwent coronary CTA were screened for HRP, which was defined by 3 concurrent plaque features: positive remodeling; low attenuation plaque (LAP; <30 Hounsfield units [HU]) and spotty calcification; and obstructive coronary stenosis ≥50% (plaque volume >100 mm3). Patients with HRPs were recruited to undergo 18F-NaF PET/CT. In lesions with stenosis ≥25%, quantitative plaque analysis, mean PCAT density, maximal coronary motion−corrected 18F-NaF standard uptake values (SUVmax), and target-to-background ratios (TBR) were measured.
Results Forty-one patients (age 65 ± 6 years; 68% men) were recruited. Fifty-one lesions in 23 patients (56%) showed increased coronary 18F-NaF activity. Lesions with 18F-NaF uptake had higher surrounding PCAT density than those without 18F-NaF uptake (−73 HU; interquartile range −79 to −68 vs. −86 HU; interquartile range −94 to −80 HU; p < 0.001). 18F-NaF TBR and SUVmax were correlated with PCAT density (r = 0.63 and r = 0.68, respectively; all p < 0.001). On adjusted multiple regression analysis, increased lesion PCAT density and LAP volume were associated with 18F-NaF TBR (β = 0.25; 95% confidence interval: 0.17 to 0.34; p < 0.001 for PCAT, and β = 0.07; 95% confidence interval: 0.03 to 0.11; p = 0.002 for LAP).
Conclusions In patients with HRP features on coronary CTA, increased density of PCAT was associated with focal 18F-NaF PET uptake. Simultaneous assessment of these imaging biomarkers by 18F-NaF PET and CTA might refine cardiovascular risk prediction in stable patients with HRP features.
- 18F-sodium fluoride
- coronary computed tomography angiography
- coronary imaging
- high-risk plaque
- peri-coronary adipose tissue density
This research was supported in part by the National Heart, Lung, and Blood Institute/National Institute of Health (NHLBI/NIH) (grants R01HL135557 and R01HL133616) and by a grant from the Miriam and Sheldon G. Adelson Medical Research Foundation. Dr. Doris was supported by the British Heart Foundation (FS/14/78/31020). Dr. Williams is supported by The Chief Scientist Office of the Scottish Government Health and Social Care Directorates (PCL/17/04). Dr. Newby was supported by the British Heart Foundation (CH/09/002, RE/13/3/30183) and received a Wellcome Trust Senior Investigator Award (WT103782AIA). Dr. Dweck was supported by the British Heart Foundation (FS/17/79/33226). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Drs. Dey, Slomka, and Berman have received software royalties from Cedars-Sinai Medical Center and have a patent (US8885905B2 in U.S. and WO patent WO2011069120A1 worldwide). Mr. Cadet has received software royalties from Cedars-Sinai Medical. Dr. Williams has been a consultant for GE Healthcare. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 28, 2018.
- Revision received November 12, 2018.
- Accepted November 15, 2018.
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