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Keywords:

  • abdominal aortic aneurysm;
  • finite element analysis;
  • FDG-PET/CT;
  • inflammation;
  • mechanotransduction;
  • metabolic activity

SUMMARY

Mechanobiological interactions are essential for the adaption of the cardiovascular system to altered environmental and internal conditions, but are poorly understood with regard to abdominal aortic aneurysm (AAA) pathogenesis, growth and rupture. In the present study, we therefore calculated mechanical AAA quantities using nonlinear finite element methods and correlated these to [18F]-fluorodeoxyglucose (FDG)-metabolic activity in the AAA wall detected by positron emission tomography/computed tomography (PET/CT). The interplay between mechanics and FDG-metabolic activity was analyzed in terms of maximum values and the three-dimensional spatial relationship, respectively.

Fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT) data sets of n = 18 AAA patients were studied. Maximum FDG-uptake (SUVmax) in the AAA wall varied from 1.32 to 4.60 (average SUVmax 3.31 ±0.87). Maximum wall stresses and strains ranged from 10.0 to 64.0N∕cm2 (38.2 ±13.8  N∕cm2) and from 0.190 to 0.260 (0.222 ±0.023), respectively. SUVmax was significantly correlated to maximum wall stress and strain (SUVmax to stress: r = 0.71,p = 0.0005; SUVmax to strain: r = 0.66,p = 0.0013). To evaluate the three-dimensional spatial interaction between FDG-uptake and acting wall stress, element-wise correlations were performed. In all but 2 AAAs, positive element-wise correlation of FDG-uptake to wall stress was obtained, with the Pearson's correlation coefficient ranging from −0.168 to 0.738 ( 0.372 ±0.263).

The results indicate that mechanical stresses are correlated quantitatively and spatially to FDG-uptake in the AAA wall. It is hypothesized that unphysiologically increased loading in the AAA wall triggers biological tissue reaction, such as inflammation or regenerative processes, causing elevated FDG-metabolic activity. These findings strongly support experimental hypotheses of mechanotransduction mechanisms in vivo. Copyright © 2011 John Wiley & Sons, Ltd.