Abstract
All vascular implants, including stents, heart valves and graft materials exhibit suboptimal biocompatibility that significantly reduces their clinical efficacy. A range of biomolecules in the subendothelial space have been shown to play critical roles in local regulation of thrombosis, endothelial growth and smooth muscle cell proliferation, making these attractive candidates for modulation of vascular device biointegration. However, classically used biomaterial coatings, such as fibronectin and laminin, modulate only one of these components; enhancing endothelial cell attachment, but also activating platelets and triggering thrombosis. This review examines a subset of extracellular matrix molecules that have demonstrated multi-faceted vascular compatibility and accordingly are promising candidates to improve the biointegration of vascular biomaterials.
Highlights
With advances in technology, implantable cardiovascular devices such as grafts, stents, pacemakers and heart valves are playing an increasingly important role in modern cardiovascular medicine.Despite this, biocompatible and clinically effective synthetic materials for cardiovascular devices areJ
It is currently theorized that tropoelastin deposition on the microfibril is directed toward the inter-bead region and corresponding concentrations of fibrillin-1 [40], implying an important signaling role in elastic fiber assembly
Given that fibulin-5 is known to interact with the elastic fiber molecules, tropoelastin and fibrillin-1 [58] it was proposed to play an important role in fiber assembly, tethering the developing structure to cell surfaces
Summary
Implantable cardiovascular devices such as grafts, stents, pacemakers and heart valves are playing an increasingly important role in modern cardiovascular medicine. Current artificial grafts are predominantly made of either Dacron or expanded polytetrafluoroethylene (ePTFE) These artificial materials lack sufficient elasticity, have poor interactions with vascular cells, are highly thrombogenic and induce chronic inflammation [1]. The problem of innate incompatibility extends beyond graft materials to other vascular devices such as heart valves, pacemaker components and stents. These devices are primarily made of metal alloys, which are highly thrombogenic and induce inflammation at the site of implantation. Injured and diseased vasculature routinely has damaged and compromised endothelium, while the inflammatory response triggers hyper proliferation of smooth muscle cells (SMCs) In this environment, clotting cascade factors are activated and thrombosis is initiated. An optimal medical device will encourage rapid regeneration of the endothelium; inhibit SMC proliferation and migration while having high blood compatibility
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