Effects of Wall Calcifications in Patient-Specific Wall Stress Analyses of Abdominal Aortic Aneurysms

[+] Author and Article Information
Lambert Speelman, Frans N. van de Vosse

Departments of Biomedical Engineering and Medical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands

Ajay Bohra

Departments of Surgery and Bioengineering, McGowan Institute for Regenerative Medicine,  University of Pittsburgh, Pittsburgh, PA 15219

E. Marielle H. Bosboom, Geert Willem H. Schurink

Department of General Surgery, University Hospital Maastricht, Maastricht, The Netherlands

Michel S. Makaroun

Department of Surgery, Division of Vascular Surgery,  University of Pittsburgh, Pittsburgh, PA 15219

David A. Vorp1

Departments of Surgery and Bioengineering, McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA 15219vorpda@upmc.edu


Corresponding author.

J Biomech Eng 129(1), 105-109 (Jul 27, 2006) (5 pages) doi:10.1115/1.2401189 History: Received January 23, 2006; Revised July 27, 2006

It is generally acknowledged that rupture of an abdominal aortic aneurysm (AAA) occurs when the stress acting on the wall over the cardiac cycle exceeds the strength of the wall. Peak wall stress computations appear to give a more accurate rupture risk assessment than AAA diameter, which is currently used for a diagnose. Despite the numerous studies utilizing patient-specific wall stress modeling of AAAs, none investigated the effect of wall calcifications on wall stress. The objective of this study was to evaluate the influence of calcifications on patient-specific finite element stress computations. In addition, we assessed whether the effect of calcifications could be predicted directly from the CT-scans by relating the effect to the amount of calcification present in the AAA wall. For 6 AAAs, the location and extent of calcification was identified from CT-scans. A finite element model was created for each AAA and the areas of calcification were defined node-wise in the mesh of the model. Comparisons are made between maximum principal stress distributions, computed without calcifications and with calcifications with varying material properties. Peak stresses are determined from the stress results and related to a calcification index (CI), a quantification of the amount of calcification in the AAA wall. At calcification sites, local stresses increased, leading to a peak stress increase of 22% in the most severe case. Our results displayed a weak correlation between the CI and the increase in peak stress. Additionally, the results showed a marked influence of the calcification elastic modulus on computed stresses. Inclusion of calcifications in finite element analysis of AAAs resulted in a marked alteration of the stress distributions and should therefore be included in rupture risk assessment. The results also suggest that the location and shape of the calcified regions—not only the relative amount—are considerations that influence the effect on AAA wall stress. The dependency of the effect of the wall stress on the calcification elastic modulus points out the importance of determination of the material properties of calcified AAA wall.

Copyright © 2007 by American Society of Mechanical Engineers
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Grahic Jump Location
Figure 1

(a) CT-slice of an AAA with region of interest indicated by dashed contour and wall calcifications indicated with white arrows. (b) The aortic contour separated from the surrounding tissue. (c) The detected edge of the aorta (white) and the calcifications (dark). (d) The equivalent element representation with material properties of the AAA wall assigned to the white elements and of the calcified wall to the gray elements. The transition of the wall and the calcifications exists from double layered elements.

Grahic Jump Location
Figure 2

The six AAA models studied here, with the calcifications noted in red for fully calcified elements and yellow for semi-calcified elements (a). The in vivo spatial orientation is indicated with A(anterior), P(posterior) or L(left), R(right). Maximum principal stress distribution (in MPa) is shown for the models without calcifications (b), with calcifications with an elastic modulus of 1.47MPa(c), and with calcifications with an elastic modulus of 2.75MPa(d). The “end effects” (i.e., artificial stresses induced by the end fixations) were avoided by excluding stresses in the regions defined by the upper and lower 10% of the model.




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