Towards a self-reporting coronary artery stent--measuring neointimal growth associated with in-stent restenosis using electrical impedance techniques.

Implantable medical devices have become the standard method for treating a variety of cardiovascular diseases (NICE, 2003, 2009), such as coronary artery disease, where coronary artery stents are the device of choice (Fischman et al., 1994; Babapulle et al., 2004). One post-operative problem with these devices is the long-term monitoring of the device-tissue interface, with respect to the complications that often arise from in-stent restenosis. This monitoring, where it is available, is currently performed using imaging techniques such as contrast angiography, IVUS, CT and MRI. In this study we propose an alternative method for the non-invasive monitoring of restenosis in coronary artery stents. This preliminary study uses impedance spectroscopy to measure the electrical impedance of cells and tissues associated with the neointimal growth that characterises in-stent restenosis in coronary artery stents. An in vitro organ culture model, using a stent implanted in a section of pig coronary artery, simulated tissue growth inside a stent. Impedance measurements were made regularly over a 28-day culture period. In a novel step, the stent itself was employed as an electrode. Differences in electrical impedance could be seen between control (stent alone) and artery-embedded stents in culture, which were associated with the presence of biological tissue. This method could potentially be developed to produce a stent that was capable of self-reporting in-stent restenosis. The advantages of such a device would be that monitoring could be non-invasively and easily carried out, allowing more routine follow-ups and the early identification and management of any device complications.

Simple surface sulfonation retards plasticiser migration and impacts upon blood/material contact activation processes.

BACKGROUND: The use of Di-2-ethylhexyl phthalate (DEHP) plasticised polyvinyl chloride (DEHPPPVC) in medical devices persists despite evidence suggesting that DEHP migration can be harmful. Researchers have shown that a simple surface sulfonation process can retard the migration of DEHP, which may reduce the associated inflammatory response. The present study is designed to investigate the effects of surface sulfonation on DEHP migration and blood contact activation using in vitro and rodent models. METHODS: The study was carried out in two phases: phase 1, in which the migration rate of DEHP from DEHPPPVC and sulfonated DEHP plasticised PVC (SDEHPPPVC) was measured; phase 2 of the study, in which the materials were incorporated into a rat recirculation biomaterial test model and blood samples taken to assess CD11b expression on neutrophils, IL-6 and Factor XIIa. RESULTS: The initial DEHP concentration washed from the surface after storage was 37.19 +/- 1.17 mg/l in the PPVC group and 5.89 +/- 0.81 mg/l in the SPPVC group (p<0.0001). The post-wash migration rate was 3.07 +/- 0.32 mg/l/hour in the PPVC group compared to 0.46 +/- 0.038 mg/l/hour in the SPPVC group (p<0.0001). In phase 2 of the study, CD11b expression increased by 228.9% +/- 37% over the test period in the PPVC group compared to 118.3% +/- 46% in the SPPVC group (p<0.01). IL-6 levels rose from 3.1 +/- 1.4 pg/ml to 263 +/- 26 pg/ml in the PPVC group and 2.2 +/- 1.6 pg/ml to 161 +/- 29 pg/ml in the SPPVC group (p<0.01). Factor XIIa levels rose from 0.22 +/- 0.13 g/ml to 3.7 +/- 0.32 microg/ml and 0.28 +/- 0.09 to 2.71 +/- 0.21 microg/ml in the PPVC and SPPVC groups, respectively (p<0.05 at 90 minutes). CONCLUSIONS: The simple sulfonation process significantly retards the migration of DEHP and is associated with the moderation of contact activation processes.