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Stenting-induced Vasa Vasorum compression and subsequent flow resistance: a finite element study
Andrea Corti1, Annalisa De Paolis1, John Tarbell1
1Department of Biomedical Engineering, The City College of New York, Steinman Hall, 160 Convent Ave, New York, NY, 10031, USA.
Biomechanics and Modeling in Mechanobiology
|August 6, 2020
Summary
Stent overexpansion significantly compresses Vasa Vasorum (VV), reducing blood flow and oxygen delivery. This compression, particularly in the Intima and Media, may drive intimal hyperplasia and restenosis after vascular stenting.
Area of Science:
- Cardiovascular Research
- Biomedical Engineering
- Medical Device Analysis
Background:
- Vascular stenting is crucial for treating atherosclerotic plaques but faces restenosis challenges.
- Restenosis is often linked to intimal hyperplasia, a process not fully understood in relation to stenting mechanics.
Purpose of the Study:
- To investigate if stent overexpansion causes Vasa Vasorum (VV) compression.
- To determine if VV compression contributes to vascular wall hypoxia and subsequent restenosis.
Main Methods:
- An idealized multilayered fibroatheroma model with VV was used.
- Finite element analysis simulated stent expansion (up to 1.3:1 ratio) with three designs.
- Poiseuille's law calculated flow resistance based on VV compression in Intima, Media, and Adventitia.
Main Results:
- Stent overexpansion significantly compressed VV, with highest compression in the Intima (up to 74.8%).
- Flow resistance increased substantially, up to 7.9-fold in the Intima and 5.1-fold in the Media.
- VV compression was most severe in the Intima and Media layers.
Conclusions:
- Stent overexpansion leads to significant VV compression and impaired blood flow.
- Reduced oxygen delivery to the vascular wall likely promotes intimal hyperplasia and restenosis.
- Minimizing stent overexpansion may be critical for preventing post-stenting restenosis.
