Carotid atheroma rupture observed in vivo and FSI-predicted stress distribution based on pre-rupture imaging

Abstract

Atherosclerosis at the carotid bifurcation is a major risk factor for stroke. As mechanical forces may impact lesion stability, finite element studies have been conducted on models of diseased vessels to elucidate the effects of lesion characteristics on the stresses within plaque materials. It is hoped that patient-specific biomechanical analyses may serve clinically to assess the rupture potential for any particular lesion, allowing better stratification of patients into the most appropriate treatments. Due to a sparsity of in vivo plaque rupture data, the relationship between various mechanical descriptors such as stresses or strains and rupture vulnerability is incompletely known, and the patient-specific utility of biomechanical analyses is unclear. In this article, we present a comparison between carotid atheroma rupture observed in vivo and the plaque stress distribution from fluid-structure interaction analysis based on pre-rupture medical imaging. The effects of image resolution are explored and the calculated stress fields are shown to vary by as much as 50% with sub-pixel geometric uncertainty. Within these bounds, we find a region of pronounced elevation in stress within the fibrous plaque layer of the lesion with a location and extent corresponding to that of the observed site of plaque rupture.

Figure 1

CTA studies showing lumen geometry in the longitudinal plane (left) and transverse to the lumen for slices 1 and 2 (right) at (a) baseline, without plaque rupture distal to the bifurcation. Note the irregular lumen geometry proximal to the bifurcation, suggesting existing ulceration of common carotid artery plaque. (b) Eight-month follow-up. Slice 1 shows increased lumen area in the internal carotid artery consistent with plaque rupture, while slice 2 shows that a portion of the plaque core inferior to the rupture location has emptied after fibrous cap failure

Figure 2

Original and segmented CTA images. Green = fibrous tissue, comprising healthy vessel wall and fibrous plaque; Red = vessel lumen; Yellow = lipid pool

Figure 3

Bounding surface representations of key vessel components. Green = healthy vessel wall; Red = vessel lumen; Yellow = lipid pool; Blue = fibrous plaque

Figure 4

Coronal CTA image slices and corresponding slices through the reconstructed geometrical model. Green = healthy vessel wall; Red = vessel lumen; Yellow = lipid pool; Blue = fibrous plaque

Figure 5

Axial slices at level 1 and 2 as shown in Fig. 1. (a) Raw image (left), segmented image (center), final geometry with fibrous plaque (right) for level 1. (b) Raw image (left), segmented image (center), final geometry with fibrous plaque (right) for level 2. Green = healthy vessel wall; Red = vessel lumen; Yellow = lipid pool; Blue = fibrous plaque. Note that in the segmented images, fibrous plaque boundaries have not yet been established

Figure 6

Outline of the 2-stage method used in this analysis, shown for a simple geometry. (a) A schematic artery with eccentric lumen and small cylindrical inclusion. Intersections of the geometry and two truncation planes are shown by the curves separating region 2 from regions 1 and 3. Region 2 is the region of interest. (b) Regions 1 and 2 shown, with bottom end caps for “wall” and inclusion of region of interest shown. (c) Fine mesh within region of interest used for second stage of two-stage method. (d) Magnified display of region of interest. (e) Bottom plane of region of interest, finely meshed in (c), shown with conforming coarse mesh used in the same region during stage 1 of two stage approach. (f) Full-domain coarse mesh used in stage 1

Figure 7

Computational meshes. (a) Fluid domain. (b) Solid mesh used for 1st stage solution. The region of interest covers the rupture location in the ICA. (c) Coarse mesh cutaway in region of interest for 1st stage solution. (d) Fine mesh cutaway in region of interest (shown with remainder of model) used for 2nd stage solution. Note the dramatic increase in element count throughout the fibrous plaque layer

Figure 8

Flow rates at the CCA inlet and ICA outlet. Flow rates were used to generate time-dependent Womersley-type velocity profiles

Figure 9

Cut planes on which first principal stress results are compared. (a) View of full lumen geometry and lipid pool with cut planes. (b) Zoom view of (a) in region of plaque rupture. Post-rupture lumen geometry shown in transparent gray. Stress results are presented for planes 1–10 only, as these cover the region of plaque rupture. The patient’s neck was positioned slightly differently for baseline and follow-up CTA studies, deforming the carotid geometry. Pre- and post-rupture lumen geometries were aligned for maximum overlap of ICA proximal and distal to the region of rupture

Figure 10

Axial “slices” through the region of interest, as shown in Fig. 9. First principal stresses are displayed for fibrous plaque layer in baseline model and model with 0.2 mm lipid surface offset. “Lu” shows the position of the lumen on each slice, “Li” shows the position of the lipid pool, and the outline of the outer vessel wall is shown for reference

Figure 11

Pre-rupture lumen geometry (left), first principal stress field based on pre-rupture geometry (left center), wall shear stress distribution of pre-rupture geometry (right center), and post-rupture lumen geometry (right). The first principal stress field shown is that within the fibrous plaque layer at the lumen surface

Figure 12

Peak stress magnitudes at slices 1–10 for models with varying lipid pool surface offsets. While slice-to-slice trends do not change qualitatively, stress magnitudes and peak stress locations at each slice change significantly