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.
- Activated macrophages
- Open circuit potential
- X-ray photoelectron spectroscopy
ASJC Scopus subject areas
- Biomedical Engineering
- Cardiology and Cardiovascular Medicine