Abstract 18880: Inflammation Imaged With [18F]-FDG PET/CTA is Related to 3D Ultrasound Phenotypes of High-risk Carotid Plaque: Sub-study of the Canadian Atherosclerosis Imaging Network (CAIN-2)
Background: Inflammation may contribute to plaque instability. [18F]-fluorodeoxyglucose (FDG) uptake imaged with positron emission tomography (PET) and computed tomography (CT) may serve as a biomarker of plaque inflammation.
3-dimensional ultrasound (U/S)-derived total plaque volume (TPV) and vessel wall volume (VWV) are measures of plaque volume and vessel wall thickness that are used for monitoring progression and regression of carotid atherosclerosis. Progression of TPV has been related to cardiovascular events.
The volumetric phenotype (TPV and VWV) and extent of the inflammatory burden (FDG uptake) may independently predict carotid plaque vulnerability. However, the interrelationship between FDG uptake and measures of TPV and VWV remains poorly understood.
Methods: Thirty-seven patients (67±9 years, 9 female) scheduled for carotid endarterectomy were prospectively recruited for 3D U/S and FDG PET/CT imaging of the left and right internal carotid arteries.
Maximum FDG uptake normalized to blood (tissue to blood ratio - TBR) was measured for bilateral carotid plaque.
Manual planimetry was used to measure bilateral TPV and VWV. Each 3-D image were evaluated from the bifurcation to the common carotid, and then to the internal and external carotid arteries.
Results: Maximum FDG uptake correlated with TPV (r=0.42, p<0.001) and VWV (r=0.30, p=0.015) (Figure 1). FDG uptake was greater in plaque scheduled for endarterectomy (TBR=3.6±1.3 endarterectomy vs. 3.0±1.2 contralateral, p=0.049). There was also a trend for greater TPV at the side of endarterectomy: 799±390mm3 endarterectomy vs. 672±150mm3 contralateral (p=0.088).
Conclusion: FDG uptake in high-risk carotid plaque is related to TPV and VWV. The inflammatory burden and the volumetric phenotype of plaque may synergistically provide a more robust evaluation of plaque vulnerability. Longitudinal follow-up for the assessment of plaque progression in this study cohort is currently underway.
Author Disclosures: M.S. Cocker: None. A. Fenster: None. R.R. Hammond: None. S.P. Lim: None. R.A. deKemp: None. C. Lum: None. A. Hill: None. S. Nagpal: None. G. Stotts: None. B. Warren: None. L. Garrard: None. J. DaSilva: None. J. Tardif: None. R.S. Beanlands: None. J. Spence: None.
- © 2015 by American Heart Association, Inc.