Abstract
Several previous studies have documented that self-expanding (SE) Nitinol stents implanted in highly mobile peripheral arteries exhibit a fracture rate as high as 30%. The hypothesis of this study is that repetitive mechanical stresses interact synergistically with the atherosclerotic lesion environment to induce corrosive events that ultimately lead to nitinol stent material failure. Using a novel in vitro chamber, electro-polished nitinol coupons were subjected to cyclic defined stress regimens in the presence or absence of adherent acetylated lipoprotein-activated macrophage-like (THP-1) cells over a 5 day period. Nitinol surface corrosion was monitored in real time using open circuit potential (OCP) measurements. Changes in surface chemistry and topography were measured post-stress exposure using X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). The combination of defined bending in the presence of adherent activated macrophages resulted in a significant increase in nitinol surface corrosion as compared to nitinol subjected to either treatment or media exposure alone. Further, a deterioration of the protective oxide layer and an increase in the surface roughness were observed in nitinol specimens exposed to the combined influence of surface-adherent macrophages and repetitive loading. These results demonstrate a significant interaction between the biological and mechanical environment relative to nitinol corrosion potential and provide a basis for design of future studies to improve the long-term performance of peripheral nitinol stents.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 216-224 |
| Number of pages | 9 |
| Journal | Cardiovascular Engineering and Technology |
| Volume | 1 |
| Issue number | 3 |
| DOIs | |
| State | Published - Sep 2010 |
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Keywords
- Activated macrophages
- Corrosion
- Fatigue
- Nitinol
- Open circuit potential
- X-ray photoelectron spectroscopy
ASJC Scopus subject areas
- Biomedical Engineering
- Cardiology and Cardiovascular Medicine
Cite this
Synergistic Effect of Cyclic Mechanical Strain and Activated Macrophage Cells on Nitinol Corrosion. / Marton, Denes; Sprague, Eugene A.
In: Cardiovascular Engineering and Technology, Vol. 1, No. 3, 09.2010, p. 216-224.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Synergistic Effect of Cyclic Mechanical Strain and Activated Macrophage Cells on Nitinol Corrosion
AU - Marton, Denes
AU - Sprague, Eugene A
PY - 2010/9
Y1 - 2010/9
N2 - Several previous studies have documented that self-expanding (SE) Nitinol stents implanted in highly mobile peripheral arteries exhibit a fracture rate as high as 30%. The hypothesis of this study is that repetitive mechanical stresses interact synergistically with the atherosclerotic lesion environment to induce corrosive events that ultimately lead to nitinol stent material failure. Using a novel in vitro chamber, electro-polished nitinol coupons were subjected to cyclic defined stress regimens in the presence or absence of adherent acetylated lipoprotein-activated macrophage-like (THP-1) cells over a 5 day period. Nitinol surface corrosion was monitored in real time using open circuit potential (OCP) measurements. Changes in surface chemistry and topography were measured post-stress exposure using X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). The combination of defined bending in the presence of adherent activated macrophages resulted in a significant increase in nitinol surface corrosion as compared to nitinol subjected to either treatment or media exposure alone. Further, a deterioration of the protective oxide layer and an increase in the surface roughness were observed in nitinol specimens exposed to the combined influence of surface-adherent macrophages and repetitive loading. These results demonstrate a significant interaction between the biological and mechanical environment relative to nitinol corrosion potential and provide a basis for design of future studies to improve the long-term performance of peripheral nitinol stents.
AB - Several previous studies have documented that self-expanding (SE) Nitinol stents implanted in highly mobile peripheral arteries exhibit a fracture rate as high as 30%. The hypothesis of this study is that repetitive mechanical stresses interact synergistically with the atherosclerotic lesion environment to induce corrosive events that ultimately lead to nitinol stent material failure. Using a novel in vitro chamber, electro-polished nitinol coupons were subjected to cyclic defined stress regimens in the presence or absence of adherent acetylated lipoprotein-activated macrophage-like (THP-1) cells over a 5 day period. Nitinol surface corrosion was monitored in real time using open circuit potential (OCP) measurements. Changes in surface chemistry and topography were measured post-stress exposure using X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). The combination of defined bending in the presence of adherent activated macrophages resulted in a significant increase in nitinol surface corrosion as compared to nitinol subjected to either treatment or media exposure alone. Further, a deterioration of the protective oxide layer and an increase in the surface roughness were observed in nitinol specimens exposed to the combined influence of surface-adherent macrophages and repetitive loading. These results demonstrate a significant interaction between the biological and mechanical environment relative to nitinol corrosion potential and provide a basis for design of future studies to improve the long-term performance of peripheral nitinol stents.
KW - Activated macrophages
KW - Corrosion
KW - Fatigue
KW - Nitinol
KW - Open circuit potential
KW - X-ray photoelectron spectroscopy
UR - http://www.scopus.com/inward/record.url?scp=79953295948&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79953295948&partnerID=8YFLogxK
U2 - 10.1007/s13239-010-0021-7
DO - 10.1007/s13239-010-0021-7
M3 - Article
AN - SCOPUS:79953295948
VL - 1
SP - 216
EP - 224
JO - Cardiovascular Engineering and Technology
JF - Cardiovascular Engineering and Technology
SN - 1869-408X
IS - 3
ER -