title: Longitudinal structural determinants of atherosclerotic plaque vulnerability: a computational analysis of stress distribution using vessel models and three-dimensional intravascular ultrasound imaging.
abstract: OBJECTIVE
  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 hills 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.
authors.affiliation: Department of Molecular Cardiovascular Biology, Yamaguchi University Graduate School of Medicine, Yamaguchi, Ube, Japan.
authors.forename: Koji
authors.initials: K
authors.lastname: Imoto
authors.forename: Takafumi
authors.initials: T
authors.lastname: Hiro
authors.forename: Takashi
authors.initials: T
authors.lastname: Fujii
authors.forename: Akihiro
authors.initials: A
authors.lastname: Murashige
authors.forename: Yusaku
authors.initials: Y
authors.lastname: Fukumoto
authors.forename: Genta
authors.initials: G
authors.lastname: Hashimoto
authors.forename: Takayuki
authors.initials: T
authors.lastname: Okamura
authors.forename: Jutaro
authors.initials: J
authors.lastname: Yamada
authors.forename: Koji
authors.initials: K
authors.lastname: Mori
authors.forename: Masunori
authors.initials: M
authors.lastname: Matsuzaki
mesh_terms: D050197:Atherosclerosis / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D020342:Finite Element Analysis; D021621:Imaging, Three-Dimensional; D008953:Models, Anatomic; D013314:Stress, Mechanical; D018084:Ultrasonography, Interventional / Q000379:methods