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A New Murine Model of Endovascular Aortic Aneurysm Repair
Published on: July 7, 2013
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.
Objective:
Dilatation of the aorta at the landing zone site may be exaggerated by the radial force of stent grafts potentially limiting long-term results of endovascular therapy. We evaluated growth patterns and morphology of the thoracic aorta in young piglets after thoracic stent-graft placement.
Methods:
Eight domestic piglets (37+/-2 kg) had an endovascular stent graft placed in the proximal descending thoracic aorta using retroperitoneal access. At implantation, the stent was oversized by 10%. Aortic size was documented after thoracotomy by intraoperative measurement and angiography. Subsequently the piglets were grown to adult size (181+/-42 kg). At explantation 6-15 months later, CT scan and surgical evaluation for endoleaks, defined as perigraft flow, was performed. Histopathological assessment of the explanted aorta was performed in stented and non-stented segments and compared to five normal porcine aortas.
Results:
No endoleak (perigraft flow) or stent migration occurred even in 230kg pigs. The stent grafts expanded to full size, but there was no further growth in the stented area. The aortic diameter increased significantly by 32+/-9% 1cm proximal to the stents (p=0.0012) and by 45+/-13% 1cm distal to the stents (p=0.0033). The stented area grew less than the proximal (p=0.0011) and distal aorta (p<0.0001). In all pigs, the distal aorta was larger than the proximal overstented segment. Histology of the stented aorta showed significant thickening of the intima (p=0.018) and media (p=0.006) with neointimal formation and segmental fibrosis of the inner 1/3 of the media with loss of smooth muscle cells and compression of the elastic fibers but normal architecture in the outer 2/3 of the media.
Conclusions:
Endovascular stent grafting may inhibit growth of the nonatherosclerotic normal aorta and lead to intimal hyperplasia and focal fibrosis in the inner media part adjacent to the stent. Stent-graft interaction with aortic tissue over time is important and should receive more detailed evaluation. Testing this interaction in an animal model of nonatherosclerotic dilative aortic disease could be of great interest.

