Author + information
- Received April 10, 2019
- Accepted April 12, 2019
- Published online August 14, 2019.
- Mohammed M. Chowdhury, MB, ChB, MRes, MSca,b,∗ (, )
- Jason M. Tarkin, MBBS, PhDb,
- Mazen S. Albaghdadi, MD, MScc,
- Nicholas R. Evans, MB, BChir, PhDf,
- Elizabeth P.V. Le, BAb,
- Thomas B. Berrett, PhDd,
- Umar Sadat, MD, PhDa,
- Francis R. Joshi, MD, PhDe,
- Elizabeth A. Warburton, DMf,
- John R. Buscombe, MDg,
- Paul D. Hayes, MDa,
- Marc R. Dweck, MD, PhDh,
- David E. Newby, MD, PhDh,
- James H.F. Rudd, MD, PhDb,† and
- Patrick A. Coughlin, MDa,†
- aDivision of Vascular Surgery, Department of Surgery, Addenbrooke’s Hospital, University of Cambridge, United Kingdom
- bDepartment of Cardiovascular Medicine, Addenbrooke’s Hospital, University of Cambridge, United Kingdom
- cCardiovascular Research Center, Division of Cardiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- dStatistical Laboratory, Department of Pure Mathematics and Mathematical Sciences, University of Cambridge, United Kingdom
- eHeart Center, Rigshospitalet, Denmark
- fDepartment of Clinical Neurosciences, University of Cambridge, United Kingdom
- gDepartment of Nuclear Medicine, Addenbrooke’s Hospital, University of Cambridge, United Kingdom
- hBritish Heart Foundation for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom
- ↵∗Address for correspondence:
Mr. Mohammed M. Chowdhury, Divisions of Vascular Surgery and Cardiovascular Medicine, University of Cambridge, Box 212, Addenbrooke’s Cambridge University Hospital, Hills Road, Cambridge CB2 2QQ, United Kingdom.
Objectives This study determined whether in vivo positron emission tomography (PET) of arterial inflammation (18F-fluorodeoxyglucose [18F-FDG]) or microcalcification (18F-sodium fluoride [18F-NaF]) could predict restenosis following PTA.
Background Restenosis following lower limb percutaneous transluminal angioplasty (PTA) is common, unpredictable, and challenging to treat. Currently, it is impossible to predict which patient will suffer from restenosis following angioplasty.
Methods In this prospective observational cohort study, 50 patients with symptomatic peripheral arterial disease underwent 18F-FDG and 18F-NaF PET/computed tomography (CT) imaging of the superficial femoral artery before and 6 weeks after angioplasty. The primary outcome was arterial restenosis at 12 months.
Results Forty subjects completed the study protocol with 14 patients (35%) reaching the primary outcome of restenosis. The baseline activities of femoral arterial inflammation (18F-FDG tissue-to-background ratio [TBR] 2.43 [interquartile range (IQR): 2.29 to 2.61] vs. 1.63 [IQR: 1.52 to 1.78]; p < 0.001) and microcalcification (18F-NaF TBR 2.61 [IQR: 2.50 to 2.77] vs. 1.69 [IQR: 1.54 to 1.77]; p < 0.001) were higher in patients who developed restenosis. The predictive value of both 18F-FDG (cut-off TBRmax value of 1.98) and 18F-NaF (cut-off TBRmax value of 2.11) uptake demonstrated excellent discrimination in predicting 1-year restenosis (Kaplan Meier estimator, log-rank p < 0.001).
Conclusions Baseline and persistent femoral arterial inflammation and micro-calcification are associated with restenosis following lower limb PTA. For the first time, we describe a method of identifying complex metabolically active plaques and patients at risk of restenosis that has the potential to select patients for intervention and to serve as a biomarker to test novel interventions to prevent restenosis.
- computed tomography
- 18F-sodium fluoride
- peripheral arterial disease
- positron emission tomography
↵† Drs. Rudd and Coughlin are joint senior authors.
This work was supported by the NIHR Cambridge Biomedical Research Centre and the Cambridge Clinical Trials Unit. This study and Dr. Chowdhury were funded by Fellowships from the Royal College of Surgeons of England and the British Heart Foundation (BHF) (FS/16/29/31957). Dr. Tarkin is supported by a Wellcome Trust research training fellowship (104492/Z/14/Z). Dr. Evans is supported by a fellowship the Dunhill Medical Trust (RTF44/0114). Dr. Berrett is supported by Engineering and Physical Sciences Research Council (ESPRC) program grant StatScale (EP/N031938/1). Dr. Rudd is supported by the National Institute of Health Research (NIHR), BHF, Wellcome Trust, and Higher Education Funding Council for England (HEFCE). Dr. Dweck is supported by the BHF (FS/14/78/31020); and is the recipient of Sir Jules Thorn Award for Biomedical Research (15/JTA). Dr. Newby is supported by the BHF (CH/09/002, RE/13/3/30183, RM/13/2/30158); and is the recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA). Dr. Le is undertaking a PhD funded by the Cambridge School of Clinical Medicine, Frank Edward Elmore Fund, and the Medical Research Council; and has received a Doctoral Training Partnership (Award Reference: 1966157). Dr. Hayes has provided consultancy with endovascular companies that are not relevant to this publication. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received April 10, 2019.
- Accepted April 12, 2019.
- 2019 The Authors