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SNIS 9th annual meeting oral poster abstracts
P-024 Stress distribution after intracranial stent by realistic model
  1. M Fujimoto1,
  2. Y Shobayashi1,
  3. S Tateshima1,
  4. H Vinters2,
  5. F Viñuela1
  1. 1Division of Interventional Neuroradiology, Department of Radiological Sciences, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA
  2. 2Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA

Abstract

There is no effective treatment for symptomatic intracranial atherosclerotic stenosis, which has an association with a high rate of recurrent stroke. Percutaneous transluminal angioplasty and stenting (PTAS) has been applied to the intracranial lesion, and only the WingspanTM Stent System (Stryker) was approved by the Food and Drug Administration (FDA) in 2005. However the high incidence of stoke or death (7%–14% at 6 months) and restenosis (25%–32%) have been viewed with suspicion and a randomized trial for intracranial symptomatic severe stenosis (SAMMPRIS Clinical Trial) revealed the superiority of aggressive medical treatments to PTAS. This first-generation intracranial stent can have still room for both procedural and technical improvement. We aimed to explore the cause of stroke complication after stenting in animal model and evaluated the biological response in the Wingspan stent by the fine element method (FEM). Simulation analysis using idealized model showed various stress distribution depended on stent geometries. Although idealized stent analysis has a limitation in its symmetry and uniformity, realistic artery model has been recognized to be essential to prove the correlation with pathobiological response. Some realistic simulation analysis concluded that higher radial stress concentration or non-uniform distribution of wall shear stress could lead to greater neointimal hyperplasia. In this report, we deployed the Wingspan stent at swine ascending pharyngeal artery, and simulated the several stress distribution including radial, circumferential and wall shear stress. We used a realistic arterial model to simulate the clinical situation. As for the radial stress, stress concentration at stent markers and the gradational augmentation of radial stress from proximal to distal were detected. The high wall shear stress gradient at distal stent segment, especially around the stent markers, was also marked. Actually, the excessive intimal hyperplasia was recognized around the distal stent. The radial stress and wall shear stress distribution can have an essential biological implication for intimal hyperplasia. These insights about stress concentration can help us, not only perform the optimal intracranial stenting, but also develop a new endovascular device in future.

Competing interests None.

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