The pCONUS HPC: 30-Day and 180-Day In Vivo Biocompatibility Results

Abstract

Background Endovascular stents are commonly used during neurointerventional procedures; however, the concomitant use of dual anti-platelet treatment (DAPT) can limit their use. There is a need to develop stent coatings that mitigate requirement for DAPT. Methods The hydrophilic polymer coating is a novel glycan-based multilayer polymer that inhibits platelet adhesion. After Institutional Animal Care and Use Committee approval, 18 New Zealand white rabbits (mean weight 4.02 ± 0.51 kg) were commenced on DAPT (ASA 10 mg/kg/day and clopidogrel 10 mg/kg/day). A bare nitinol pCONUS and coated pCONUS HPC were implanted into the common carotid arteries of each rabbit. Histological examinations were performed at 30 days ( n = 9) and 180 days ( n = 8) to assess the acute and chronic inflammatory reactions to the pCONUS HPC. Wilcoxon/Kruskal–Wallis and ANOVA were used with p value < 0.05 considered as significant. Results There is no statistically significant difference in inflammation within the intima/media or adventitia at 30 days ( p = 0.3901 and p = 1, respectively) or at 180 days ( p = 0.144 and p = 1, respectively) between pCONUS and pCONUS HPC cohorts. There is no significant difference in the presence of granulomas or giant cells between the cohorts at either 30 days ( p = 1 and p = 0.8363) or 180 days ( p = 1.00 and p = 0.149). At 30 days and 180 days, there was near-complete endothelialisation of the stent struts and no significant difference between the pCONUS or pCONUS HPC ( p = 0.7832 and p = 0.334, respectively). Conclusion pCONUS HPC stents do not elicit an acute or chronic inflammatory response in vivo with no significant difference in the tissue response to bare nitinol pCONUS stents or pCONUS HPC stents.

The p48 Flow Modulation Device with Hydrophilic Polymer Coating (HPC) for the Treatment of Acutely Ruptured Aneurysms: Early Clinical Experience Using Single Antiplatelet Therapy

“…It is designed to mimic the biological properties of the glycocalyx, the coverage that can be found on the luminal surface of the endothelium of the arterial wall, making the coated surface hydrophilic and, consequently, less thrombogenic [4]. pHPC has no pharmaceutical effect, is biocompatible with no evidence of acute inflammatory response, and does not interact with the physical properties of the metallic implant [10,11]. Bhogal et al [5] recently reported on the use of the p48MW HPC under SAPT in treating five patients with unruptured aneurysms and reported no thromboembolic complications, with just one patient experiencing a minor hemorrhage from the treated aneurysm 2 weeks postoperatively.…”

Single-Center Experience With the Bare p48MW Low-Profile Flow Diverter and Its Hydrophilically Covered Version for Treatment of Bifurcation Aneurysms in Distal Segments of the Anterior and Posterior Circulation

“…In November 2018, a coated variant of the p48MW obtained CE mark and has been made available for European patients. The HPC has been tested extensively in vitro and ex vivo, and the first clinical experiences have been reported (16)(17)(18)(19)(20)(21). Basically, the coating consists of a covalently bonded pentasaccharide layer at the surface of the device, which prevents platelet and leukocyte adhesion at the surface of the nitinol mesh.…”

Use of the pCONus HPC as an adjunct to coil occlusion of acutely ruptured aneurysms: early clinical experience using single antiplatelet therapy

“…It is designed to mimic the biological properties of the glycocalyx, the coverage that can be found on the luminal surface of the endothelium of the arterial wall, making the coated surface hydrophilic and, consequently, less thrombogenic 7. In vivo studies have shown that the pHPC has no pharmaceutical effect and is biocompatible in both dogs and rabbits, with no evidence of acute inflammatory response 27–29. These in vivo studies comparing coated and uncoated devices showed no difference in the rate of neo-endothelialization, which implies that pHPC reduces the thrombogenicity of the device but does not inhibit its endothelialization.…”