Nickel elution properties of contemporary interatrial shunt closure devices.

OBJECTIVES: We sought to compare nickel elution properties of contemporary interatrial shunt closure devices in vitro. INTRODUCTION: There are two United States Food and Drug Administration (FDA)-approved devices for percutaneous closure of secundum atrial septal defect: the Amplatzer septal occluder (ASO; St Jude Medical Corporation) and Gore Helex septal occluder (HSO; W.L. Gore & Associates). The new Gore septal occluder (GSO) device is in clinical trials. These are also used off-label for patent foramen ovale closure in highly selected patients. These devices have high nickel content. Nickel allergy is the most common reason for surgical device explantation. Nickel elution properties of contemporary devices remain unknown. METHODS: We compared nickel elution properties of 4 devices - ASO, GSO, HSO, and sternal wire (SW) - while Dulbecco's phosphate-buffered saline (DPBS) served as control. Three samples of each device were submerged in DPBS. Nickel content was measured at 14 intervals over 90 days. RESULTS: Nickel elution at 24 hours, compared to control (0.005 ± 0.0 mg/L), was significantly higher for ASO (2.98 ± 1.65 mg/L; P=.04) and SW (0.03 ± 0.014 mg/L; P=.03). Nickel levels at 90 days, compared to control (0.005 ± 0.0 mg/L) and adjusting for multiple comparisons, were significantly higher for ASO (19.80 ± 2.30 mg/L; P=.01) and similar for HSO (P=.34), GSO (P=.34), and SW (P=.34). ASO had significantly higher nickel elution compared to HSO, GSO, and SW (P=.01). CONCLUSION: There is substantial variability in nickel elution; devices with less exposed nickel (HSO and GSO) have minimal elution. The safety of low nickel elution devices in patients with nickel allergy needs to be evaluated in prospective trials.

Cell surface engineering to enhance mesenchymal stem cell migration toward an SDF-1 gradient.

Mesenchymal stem cell (MSC) therapy for the treatment of myocardial infarction (MI) has shown considerable promise in clinical trials. A billion MSCs need to be administered for therapeutic efficacy, however, because only ∼1% of the cells reach the ischemic myocardium after systemic infusion. This is due to the loss of the homing signal on the surface of the MSCs during their expansion in culture. Stromal-derived factor-1 (SDF-1) is up-regulated immediately after infarction and is released into the peripheral blood. This SDF-1 reaches the bone marrow and recruits CXC chemokine receptor 4 (CXCR4)-positive stem cells. The CXCR4/SDF-1 axis plays an important role in MSC homing to the ischemic myocardium. Since SDF-1 is highly expressed for only 48 h after infarction, the current approaches requiring long-term culture of MSCs to induce CXCR4 expression are not clinically useful. To provide a clinically viable means to improve the homing of MSCs, we have developed a surface modification method to incorporate recombinant CXCR4 protein on the membrane of MSCs within 10 min. Using this method, we have confirmed the improved migration of MSCs toward an SDF-1 gradient.