Exploring the Biological and Mechanical Properties of Abdominal Aortic Aneurysms Using USPIO MRI and Peak Tissue Stress: A Combined Clinical and Finite Element Study

Noel Conlisk,Barry J Doyle,Calum D Gray,Rachael O Forsythe,Olivia M.B Mcbride,Scott I.K Semple,Tom Macgillivray,Lyam Hollis,Jennifer M.J Robson,Peter R Hoskins,David E Newby,Chengjia Wang,Edwin J.R Van Beek

doi:10.1007/s12265-017-9766-9

Abstract

Inflammation detected through the uptake of ultrasmall superparamagnetic particles of iron oxide (USPIO) on magnetic resonance imaging (MRI) and finite element (FE) modelling of tissue stress both hold potential in the assessment of abdominal aortic aneurysm (AAA) rupture risk. This study aimed to examine the spatial relationship between these two biomarkers. Patients (n = 50) > 40 years with AAA maximum diameters > = 40 mm underwent USPIO-enhanced MRI and computed tomography angiogram (CTA). USPIO uptake was compared with wall stress predictions from CTA-based patient-specific FE models of each aneurysm. Elevated stress was commonly observed in areas vulnerable to rupture (e.g. posterior wall and shoulder). Only 16% of aneurysms exhibited co-localisation of elevated stress and mural USPIO enhancement. Globally, no correlation was observed between stress and other measures of USPIO uptake (i.e. mean or peak). It is suggested that cellular inflammation and stress may represent different but complimentary aspects of AAA disease progression.

Highlights

Each year, over 10,000 deaths in the UK are attributed to rupture of abdominal aortic aneurysms (AAAs) [1]
We have previously demonstrated that ultrasmall superparamagnetic particles of iron oxide (USPIO) can identify areas of mural AAA inflammation, which is associated with more rapid aneurysm expansion [8]
The aim of this study was to explore the spatial relationship between areas of mural cellular inflammation measured by USPIO uptake on magnetic resonance imaging (MRI) and regions of high tissue stress determined through patient-specific finite element (FE) modelling, for a group of 50 patients under surveillance for AAA disease

Summary

Introduction

Over 10,000 deaths in the UK are attributed to rupture of abdominal aortic aneurysms (AAAs) [1]. Various pathobiological processes contributing to AAA development and disease progression have been identified, including infiltration of inflammatory cells such as macrophages, proteolytic degradation of the extracellular matrix (ECM), and neovascularisation. All of these biological processes lead to changes in the mechanical properties of the artery wall including loss of elastin and deposition of collagen that compromises the strength and elasticity of the vessel [3, 4]. It is clear that growth and rupture of AAAs over time occur as a result of complex mechano-biological interactions within the diseased arterial wall [5].

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