2005 Fiscal Year Final Research Report Summary
A Dynamic Approach to Local Mechanism of Coronary Atherosclerotic Plaque Destabilization with Use of Intravascular Ultrasound
| Project/Area Number |
16590690
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Yamaguchi University |
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Principal Investigator |
HIRO Takafumi Yamaguchi University, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (10294638)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Takashi Yamaguchi University, Faculty of Medicine, Associate Professor, 医学部, 助教授 (60228947)
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| Project Period (FY) |
2004 – 2005
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| Keywords | Atherosclerosis / Unstable Plaque / Stress / Plaque Rupture / Intravascular Ultrasound |
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| Research Abstract |
Objectives
This study theoretically examined the longitudinal structural determinants of plaque vulnerability using a color-coded stress mapping technique for several hypothetical vessel models as well as three-dimensional intravascular ultrasound (IVUS) images with use of a finite element analysis.
Background
It has been shown that an excessive concentration of stress is related to atherosclerotic plaque rupture. However, the local determinants of in-plaque longitudinal stress distribution along the coronary arterial wall remain unclear.
Methods
Using a finite element analysis, we performed a color mapping of equivalent stress distribution within plaques for three-dimensional vessel models as well as longitudinal IVUS plaque images (n=15). Then, the effects of plaque size, shape, expansive remodeling, calcification, and lipid core on the equivalent stress distribution were examined.
Results
The color mapping of vessel models revealed a concentration of equivalent stress at the top of the hil
… More
ls and the shoulders of homogeneous fibrous plaques. Expansive remodeling and the lipid core augmented the surface equivalent stress, whereas luminal stenosis and superficial calcification attenuated the equivalent stress. The location of excessive stress concentration was modified by the distribution of the lipid core and calcification. The thickness of the fibrous cap was inversely related to the equivalent stress within the fibrous cap. However, the color mapping of IVUS plaque images showed that the equivalent stress value at the fibrous cap varied with changes in plaque shape and superficial calcification, even when the thickness of the fibrous cap remained constant.
Conclusions
A distribution analysis of longitudinal stress revealed specific effects of plaque shape, size, and remodeling, as well as effects of the interior distribution of tissue components, on the concentration of stress at the plaque surface. Moreover, fibrous caps of the same thickness did not consistently represent the same vulnerability to rupture. Less
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