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High Structural Stress and Presence of Intraluminal Thrombus Predict Abdominal Aortic Aneurysm 18F-FDG Uptake: Insights From Biomechanics.

Published version
Peer-reviewed

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Authors

Huang, Yuan 
Elkhawad, Maysoon 
Tarkin, Jason M 
Joshi, Nikhil 

Abstract

BACKGROUND: Abdominal aortic aneurysm (AAA) wall inflammation and mechanical structural stress may influence AAA expansion and lead to rupture. We hypothesized a positive correlation between structural stress and fluorine-18-labeled 2-deoxy-2-fluoro-d-glucose (18F-FDG) positron emission tomography-defined inflammation. We also explored the influence of computed tomography-derived aneurysm morphology and composition, including intraluminal thrombus, on both variables. METHODS AND RESULTS: Twenty-one patients (19 males) with AAAs below surgical threshold (AAA size was 4.10±0.54 cm) underwent 18F-FDG positron emission tomography and contrast-enhanced computed tomography imaging. Structural stresses were calculated using finite element analysis. The relationship between maximum aneurysm 18F-FDG standardized uptake value within aortic wall and wall structural stress, patient clinical characteristics, aneurysm morphology, and compositions was explored using a hierarchical linear mixed-effects model. On univariate analysis, local aneurysm diameter, thrombus burden, extent of calcification, and structural stress were all associated with 18F-FDG uptake (P<0.05). AAA structural stress correlated with 18F-FDG maximum standardized uptake value (slope estimate, 0.552; P<0.0001). Multivariate linear mixed-effects analysis revealed an important interaction between structural stress and intraluminal thrombus in relation to maximum standardized uptake value (fixed effect coefficient, 1.68 [SE, 0.10]; P<0.0001). Compared with other factors, structural stress was the best predictor of inflammation (receiver-operating characteristic curve area under the curve =0.59), with higher accuracy seen in regions with high thrombus burden (area under the curve =0.80). Regions with both high thrombus burden and high structural stress had higher 18F-FDG maximum standardized uptake value compared with regions with high thrombus burdens but low stress (median [interquartile range], 1.93 [1.60-2.14] versus 1.14 [0.90-1.53]; P<0.0001). CONCLUSIONS: Increased aortic wall inflammation, demonstrated by 18F-FDG positron emission tomography, was observed in AAA regions with thick intraluminal thrombus subjected to high mechanical stress, suggesting a potential mechanistic link underlying aneurysm inflammation.

Description

Keywords

abdominal aortic aneurysm, fluorodeoxyglucose F18, inflammation, mechanical stress, positron-emission tomography, thrombosis, Aged, Aged, 80 and over, Aorta, Abdominal, Aortic Aneurysm, Abdominal, Aortic Rupture, Aortitis, Aortography, Biomechanical Phenomena, Computed Tomography Angiography, Female, Finite Element Analysis, Fluorodeoxyglucose F18, Humans, Linear Models, Male, Middle Aged, Multivariate Analysis, Positron Emission Tomography Computed Tomography, Predictive Value of Tests, Prognosis, Pulsatile Flow, Radiographic Image Interpretation, Computer-Assisted, Radiopharmaceuticals, Regional Blood Flow, Risk Factors, Stress, Mechanical, Thrombosis, Vascular Calcification

Journal Title

Circulation. Cardiovascular imaging

Conference Name

Journal ISSN

1941-9651
1942-0080

Volume Title

9

Publisher

American Heart Association
Sponsorship
TCC (None)
British Heart Foundation (None)
British Heart Foundation (None)
European Commission (224297)
Engineering and Physical Sciences Research Council (EP/N014588/1)
Wellcome Trust (104492/Z/14/Z)
British Heart Foundation (None)
British Heart Foundation (None)
British Heart Foundation (None)
British Heart Foundation (None)
National Institute for Health and Care Research (NIHR/CS/009/011)
This study was supported by the British Heart Foundation Cambridge Centre of Excellence (RE/13/6/30180), Heart Research UK (RG2638/14/16), EPSRC Centre for Mathematical and Statistical Analysis of Multimodal Clinical Imaging (EP/N014588/1), and the National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre. Dr Tarkin is supported by a Wellcome Trust research training fellowship (104492/Z/14/Z). Dr Rudd is part-supported by the NIHR Cambridge Biomedical Research Centre, the British Heart Foundation, the Wellcome Trust, and Higher Education Funding Council for England (HEFCE). Dr Newby is supported by the British Heart Foundation (CH/09/002) and is the recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA).