Nitinol Biocompatibility - Influence of Surface Passivation On Biocompatibility

Influence of Surface Passivation On Biocompatibility

Surface passivation techniques can greatly increase the corrosion resistance of nitinol. In order for nitinol to have the desired superelastic and shape memory properties, heat treatment is required. After heat treatment, the surface oxide layer contains a larger concentration of nickel in the form of NiO₂ and NiO. This increase in nickel has been attributed to the diffusion of nickel out of the bulk material and into the surface layer during elevated temperature treatments. Surface characterization methods have shown that some surface passivation treatments decrease the concentration of NiO₂ and NiO within the surface layer, leaving a higher concentration of the more stable TiO₂ than in raw, heat-treated Nitinol.

The decrease in nickel concentration in the surface layer of nitinol is correlated with a greater corrosion resistance. A potentiodynamic test is commonly employed to measure a material’s resistance to corrosion. This test determines the electrical potential at which a material begins to corrode. The measurement is called the pitting or breakdown potential. After passivation in a nitric acid solution, Nitinol stent components showed significantly higher breakdown potentials than those that were unpassivated. In fact, there are many surface treatments that can greatly enhance the breakdown potentials of Nitinol. These treatments include mechanical polishing, electropolishing, and chemical treatments such as, Nitric Oxide submersion, etching of the raw surface oxide layer, and pickling to break down bulk material near the surface.

Thrombogenicity, a material’s tendency to induce clot formation, is an important factor that determines the biocompatibility of any biomaterial that comes into contact with the bloodstream. There are two proteins, fibrinogen and albumin, that first adsorb to the surface of a foreign object in contact with blood. It has been suggested that fibrinogen may cause platelet activation due to a breakdown of the protein structure as it interacts with high energy grain boundaries on certain surfaces. Albumin on the other hand, inhibits platelet activation. This implies that there are two mechanisms which can help lower thrombogenicity, an amorphous surface layer where there will be no grain boundary interactions with fibrinogen, and a surface with a higher affinity to albumin than fibrinogen.

Just as thrombogenicity is important in determining suitability of other biomaterials, it is equally important with Nitinol as a stent material. Currently, when stents are implanted, the patient receives antiaggregant therapy for a year or more in order to prevent the formation of a clot near the stent. By the time the drug therapy has ceased, ideally, a layer of endothelial cells, which line the inside of blood vessels would coat the outside of the stent. The stent is effectively integrated into the surrounding tissue and no longer in direct contact with the blood. There have been many attempts made using surface treatments to create stents that are more biocompatible and less thrombogenic, in an attempt to reduce the need for extensive antiplatelet therapy. Surface layers that are higher in nickel concentration cause less clotting due to albumin’s affinity to nickel. This is opposite of the surface layer characteristics that increase corrosion resistance. In vitro tests use indicators of thrombosis, such as platelet, Tyrosine aminotransferase, and β-TG levels. Surface treatments that have to some extent, lowered thrombogenicity in vitro are:

• Electropolishing
• Sandblasting
• Polyurethane coatings
• Aluminum coatings

Another area of research involves binding various pharmaceutical agents such as heparin to the surface of the stent. These drug-eluting stents show promise in further reducing thrombogenicity while not compromising corrosion resistance.