Longitudinal Structural Determinants of Atherosclerotic Plaque Vulnerability
A Computational Analysis of Stress Distribution Using Vessel Models and Three-Dimensional Intravascular Ultrasound Imaging
Koji Imoto, MD*,
Takafumi Hiro, MD, PhD*,*,
Takashi Fujii, MD, PhD*,
Akihiro Murashige, MD, PhD*,
Yusaku Fukumoto, MD*,
Genta Hashimoto, MD*,
Takayuki Okamura, MD, PhD*,
Jutaro Yamada, MD, PhD*,
Koji Mori, PhD and
Masunori Matsuzaki, MD, PhD, FACC*
* Department of Molecular Cardiovascular Biology, Yamaguchi University Graduate School of Medicine, Yamaguchi, Ube, Japan
Department of Applied Medical Engineering Science, Yamaguchi University Graduate School of Medicine, Yamaguchi, Ube, Japan
View larger version (52K):
[in a new window]
|
Figure 1 Three-dimensional model. In this vessel model, vessel diameter may vary when a remodeling model is considered.
|
|
View larger version (76K):
[in a new window]
|
Figure 2 Relationship between stress distribution and plaque shape, luminal stenosis, or vessel remodeling. (A1, A2) Color mapping of longitudinal stress distribution within a homogeneous hill-like fibrous plaque model and a complex-shaped model. Relative mapping (A2) was performed in the automatically determined window between the maximum and minimum value of stress. The arrows designate the sites of stress concentration. (B1, B2) Relationship between luminal stenosis and stress distribution. Absolute mapping (B2) represents the distribution of the absolute value of equivalent stress. There was a negative relationship between the equivalent stress and luminal stenosis. (C1, C2) Relationship between vessel remodeling and stress distribution. The equivalent stress at the plaque surface of arteries with expansive remodeling was greater than that of arteries with constrictive remodeling, when the plaque thickness remained constant.
|
|
View larger version (59K):
[in a new window]
|
Figure 3 Effect of lipid core on stress distribution. The arrow indicates the point of stress concentration at a localized surface area just above the lipid core (A2). The size of the lipid core did not influence the value of the surface stress (B2), provided the fibrous cap thickness remained constant. (A1, B1) Plaque models used. (A2, B2) Mapping of stress distribution of the corresponded model.
|
|
View larger version (63K):
[in a new window]
|
Figure 4 Effect of fibrous cap thickness (a, 90 µm; b, 80 µm; c, 40 µm) on stress distribution. When the fibrous cap was thinner than 80 µm, the stress was markedly elevated (arrow). (Aa, Ab, Ac) Plaque models used. (Ba, Bb, Bc) Mapping of stress distribution of the corresponded model.
|
|
View larger version (69K):
[in a new window]
|
Figure 5 The effect of surface calcifications on the distribution of stress in the surrounding tissue. The size and the place of the lipid core remained constant. A superficial calcification adjacent to the lipid core attenuated the peak stress value at the plaque surface just above the lipid core (arrow). (Aa, Ab) Plaque models used. (Ba, Bb) Mapping of stress distribution of the corresponded model.
|
|
View larger version (14K):
[in a new window]
|
Figure 6 Effect of superficial calcifications on the relationship between the fibrous cap thickness and the peak equivalent stress at the plaque surface. The equivalent stress increased dramatically when the fibrous cap thickness became <80 µm. This increase shifted leftward and downward when there was a superficial calcification close to the area of interest.
|
|
View larger version (96K):
[in a new window]
|
Figure 7 Representative examples of the three-dimensional IVUS images and the color mappings of longitudinal stress distribution. The arrows show rupture points. In case 1, the critical thickness of the fibrous cap in terms of rupture was 50 µm (A). However, the thickness in case 2 had to be reduced to <10 µm to reach the critical point in terms of plaque rupture (B). Thus, case 2 seemed to represent a less vulnerable plaque than case 1, although the fibrous cap thickness was the same. (A) Case 1; (B) case 2.
|
|
|
