Heparin coatings for improving blood compatibility of medical devices

Abstract

Blood contact with biomaterials triggers activation of multiple reactive mechanisms that can impair the performance of implantable medical devices and potentially cause serious adverse clinical events. This includes thrombosis and thromboembolic complications due to activation of platelets and the coagulation cascade, activation of the complement system, and inflammation. Numerous surface coatings have been developed to improve blood compatibility of biomaterials. For more than thirty years, the anticoagulant drug heparin has been employed as a covalently immobilized surface coating on a variety of medical devices. This review describes the fundamental principles of non-eluting heparin coatings, mechanisms of action, and clinical applications with focus on those technologies which have been commercialized. Because of its extensive publication history, there is emphasis on the CARMEDA BioActive Surface (CBAS Heparin Surface), a widely used commercialized technology for the covalent bonding of heparin.

Multifunctional coatings combining bioactive peptides and affinity-based cytokine delivery for enhanced integration of degradable vascular grafts

“…13 The heparinbinding peptide FHRRIKA, derived from bone sialoprotein, 14 also mediates cell adhesion by cell surface proteoglycans, but can likewise be used to immobilize soluble heparin. Owing to its excellent anticoagulant properties, 15 heparin grafting itself could reduce thrombogenicity of the scaffold 16 but further exploitation as a delivery system for heparin-binding cytokines could additionally modulate the healing response. 17 Heparin and heparan sulfate bind almost all angiogenic cytokines with high affinity, stabilizing and sequestering them to their respective receptors.…”

Complement activation by gold nanoparticles passivated with polyelectrolyte ligands

“…30,31 Owing to its nature as an anticoagulant, heparin has been reported to minimize complement activation. [33][34][35] However, we found that AuNP-heparin still activated the complement system although their level of complement activation was comparable to PVA and PAA, and much lower than PEI, PSS and PAMAM.…”

Effect of Novel Design Modifications on Fibrotic Encapsulation: An In Vivo Glaucoma Drainage Device Study in a Rabbit Model

“…Microscopic patterned surfaces mimic the extracellular environment; this physical sequestration of stored TGF-b and mechanical reduction of tension may prevent the transdifferentiation of fibroblasts into myofibroblasts. There has been an emergence of research into the non-coagulant use of heparin for various inflammatory disease states such as pulmonary fibrosis, cystic fibrosis, rheumatoid arthritis, and wound healing [20,38]. Beyond its role in the coagulation cascade, heparin has been shown to bind and inhibit various mediators of the inflammatory and scar-formation cascade, notably chemokines, complement, integrins, and angiogenic and growth factors [20,39].…”