Thoracic endovascular stent grafting inhibits aortic growth: an experimental study

Michael P Siegenthaler1, Ramazan Celik, Joerg Haberstroh

  • 1Division of Cardiac Surgery, Heart Lung Esophageal Surgery Institute, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA. siegenthlaermp@upmc.edu <siegenthlaermp@upmc.edu>

Insights

Thoracic stent grafts inhibited aortic growth and caused intimal hyperplasia in a piglet model. Further research into stent-graft interaction with aortic tissue is crucial for long-term endovascular therapy success.

Area of Science:

  • Cardiovascular Research
  • Biomedical Engineering
  • Surgical Innovation

Background:

  • Radial force from stent grafts may impede aortic growth, potentially limiting long-term endovascular therapy outcomes.
  • Understanding thoracic aorta growth dynamics after stent graft placement is essential.

Purpose of the Study:

  • To evaluate the growth patterns and morphology of the thoracic aorta in young piglets following thoracic stent graft implantation.
  • To assess the impact of stent graft radial force on aortic development in a non-atherosclerotic model.

Main Methods:

  • Endovascular stent grafts were implanted in the proximal descending thoracic aorta of eight piglets, oversized by 10%.
  • Aortic dimensions were measured intraoperatively and post-mortem via CT scans after piglets reached adult size (6-15 months later).
  • Histopathological analysis compared stented and non-stented aortic segments to controls, assessing for endoleaks, migration, and tissue changes.

Main Results:

  • No endoleaks or stent migration were observed.
  • The stented aortic segment showed inhibited growth compared to proximal and distal segments, which significantly dilated.
  • Histology revealed intimal thickening, neointimal formation, and fibrosis in the inner media of the stented aorta.

Conclusions:

  • Endovascular stent grafting can inhibit normal thoracic aorta growth and induce adverse tissue remodeling, including intimal hyperplasia and fibrosis.
  • The interaction between stent grafts and aortic tissue over time warrants further investigation.
  • An animal model of non-atherosclerotic aortic disease is valuable for studying these interactions.
Abstract

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