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Effect of biologically active coating on biocompatibility of Nitinol devices designed for the closure of intra-atrial communications

Authors
Journal
Biomaterials
0142-9612
Publisher
Elsevier
Volume
23
Issue
8
Identifiers
DOI: 10.1016/s0142-9612(01)00304-0
Keywords
  • Nitinol
  • Biologically Active Coating
  • Thrombogenicity
  • Endothelialisation
Disciplines
  • Communication
  • Design

Abstract

Abstract Anti-thrombogenicity and rapid endothelialisation are prerequisites for the use of closure devices of intra-atrial communications in order to reduce the risk of cerebral embolism. The purpose of this study was therefore to assess the effect of bioactive coatings on biocompatibility of Nitinol coils designed for the closure of intra-atrial communications. Nitinol coils (n=10, each) and flat Nitinol bands (n=3, each) were treated by basic coating with poly(amino-p-xylylene-co-p-xylylene) and then coated with either heparin, r-hirudin or fibronectin. Anti-thrombogenicity was studied in vitro in a dynamic model with whole blood by partial thromboplastin time (PTT), platelet binding and thrombin generation, respectively, and cytotoxicity by hemolysis. Endothelialisation was studied on Nitinol bands with human umbilical venous endothelial cells (HUVEC) by 3-(4,5-dimethylthiazole-2yl)-2,5-triphenyl tetrazolium (MTT) assay and immnuofluorescence analysis of Ki67, vinculin, fibronectin and von Willebrand Factor. Uncoated or coated devices did not influence hemolysis and PTT. r-Hirudin (but not heparin) and fibronectin coating showed lower platelet binding than uncoated Nitinol (p<0.005, respectively). Heparin and r-hirudin coating reduced thrombin formation (p<0.05 versus Nitinol, respectively). HUVEC adhesion, proliferation, and matrix formation decreased in the order: fibronectin coating>uncoated Nitinol>r-hirudin coating>heparin coating>basic coating. MTT assay corroborated these findings. In conclusion, r-hirudin and fibronectin coating, by causing no acute cytotoxicity, decreasing thrombogenicity and increasing endothelialisation improve in vitro biocompatibility of Nitinol devices designed for the closure of intra-atrial communications.

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