Nickel release after implantation of the Amplatzer occluder

Transcatheter closure of atrial septal defects is a new and less traumatic technique than open heart surgery. In recent years, patients with a patent foramen ovale sustaining potential paradoxical embolism have also become candidates for interventional closure devices. One of the more popular occluding devices is the Amplatzer septal occluder, which, like many other occluders, is made of nitinol. Nitinol-based alloys are widely used in medical products, for example, in orthopedics and orthodontics. However, the clinical use of nitinol, which contains 55% nickel, is still controversial because of concerns about its biocompatibility. Therefore, we examined the systemic nickel release after implantation of the Amplatzer occluder.

In 67 patients with no history of nickel sensitivity, blood samples were taken 24 hours before and 24 hours, 1, 3, and 12 months after occluder implantation. Nickel serum concentrations were measured by atomic absorption spectrometry; a value of <2 ng/mL of nickel was considered to be normal. A rise in mean serum levels of nickel was observed, from 0.47 ng/mL before implantation to 1.27 ng/mL (24 hours after), to a maximum of 1.50 ng/mL 1 month after implantation, which was statistically significant (P =.008 and P = 0.022, Wilcoxon Test). During follow-up, the values decreased to those measured before implantation.

Nickel seems to be released from the device, causing a systemic rise in serum levels of nickel, possibly until a calcium-phosphate layer has formed on the passive oxide film of the device or until endothelialization is complete. Possible biological effects should be considered, particularly in young patients or patients with nickel hypersensitivity.