Biomechanical changes during abdominal aortic aneurysm growth.

Raoul R F Stevens,Andrii Grytsan,Joy Roy,Moritz Lindquist Liljeqvist,T Christian Gasser,Jacopo Biasetti,Jose Manuel Garcia Aznar

doi:10.1371/journal.pone.0187421

Abstract

The biomechanics-based Abdominal Aortic Aneurysm (AAA) rupture risk assessment has gained considerable scientific and clinical momentum. However, such studies have mainly focused on information at a single time point, and little is known about how AAA properties change over time. Consequently, the present study explored how geometry, wall stress-related and blood flow-related biomechanical properties change during AAA expansion. Four patients with a total of 23 Computed Tomography-Angiography (CT-A) scans at different time points were analyzed. At each time point, patient-specific properties were extracted from (i) the reconstructed geometry, (ii) the computed wall stress at Mean Arterial Pressure (MAP), and (iii) the computed blood flow velocity at standardized inflow and outflow conditions. Testing correlations between these parameters identified several nonintuitive dependencies. Most interestingly, the Peak Wall Rupture Index (PWRI) and the maximum Wall Shear Stress (WSS) independently predicted AAA volume growth. Similarly, Intra-luminal Thrombus (ILT) volume growth depended on both the maximum WSS and the ILT volume itself. In addition, ILT volume, ILT volume growth, and maximum ILT layer thickness correlated with PWRI as well as AAA volume growth. Consequently, a large ILT volume as well as fast increase of ILT volume over time may be a risk factor for AAA rupture. However, tailored clinical studies would be required to test this hypothesis and to clarify whether monitoring ILT development has any clinical benefit.

Highlights

Degradation of elastin, collagen and apoptosis of Smooth Muscle Cells (SMC) [1] may lead to Abdominal Aortic Aneurysm (AAA) formation in the infrarenal aorta, which in turn may result in aortic rupture
The present study aims at investigating how geometry, wall stress-related and blood flowrelated biomechanical properties change during AAA expansion
Case D is rather small at baseline (42mm) at a Peak Wall Rupture Index (PWRI) between the cases B and C

Summary

Introduction

Degradation of elastin, collagen and apoptosis of Smooth Muscle Cells (SMC) [1] may lead to Abdominal Aortic Aneurysm (AAA) formation in the infrarenal aorta, which in turn may result in aortic rupture. Elective surgical or endovascular AAA repair is offered to prevent such catastrophic events, and repair is indicated as soon as the risk of aortic rupture exceeds the interventional risks. While the risks of intervention are reasonably predictable, assessing AAA rupture risk remains challenging during clinical decision making. Present clinical guidelines recommend AAA repair as soon as the diameter reaches 55mm or grows faster than. 10mm/year [2,3], and diameter remains the most important surrogate marker of AAA risk [4]. A considerable portion of AAAs rupture below the size of 55mm (especially in female patients and current smokers [5]), whereas many aneurysms larger than 55mm never rupture [6,7,8]. A more robust AAA rupture risk assessment would be of great clinical value

Methods

Results

Conclusion