Biocompatibility of Coronary Stents

Abstract

Cardiovascular disease is the dominant cause of mortality in developed countries, with coronary artery disease (CAD) a predominant contributor. The development of stents to treat CAD was a significant innovation, facilitating effective percutaneous coronary revascularization. Coronary stents have evolved from bare metal compositions, to incorporate advances in pharmacological therapy in what are now known as drug eluting stents (DES). Deployment of a stent overcomes some limitations of balloon angioplasty alone, but provides an acute stimulus for thrombus formation and promotes neointimal hyperplasia. First generation DES effectively reduced in-stent restenosis, but profoundly delay healing and are susceptible to late stent thrombosis, leading to significant clinical complications in the long term. This review characterizes the development of coronary stents, detailing the incremental improvements, which aim to attenuate the major clinical complications of thrombosis and restenosis. Despite these enhancements, coronary stents remain fundamentally incompatible with the vasculature, an issue which has largely gone unaddressed. We highlight the latest modifications and research directions that promise to more holistically design coronary implants that are truly biocompatible.

Keywords: biofunctionalization; coronary artery disease; restenosis; stent; thrombosis.

Figure 1.

Coronary stent types, their mechanism of action and innovations: (a) first generation drug eluting stents (DES) impact on vascular biology: Modified from [42], reduced neointima formation (green arrows) but increased thrombogenicity at stent bio-interface. Sirolimus/paclitaxel inhibition of endothelialization, tissue factor induction and endothelial progenitor cells (EPC) homing prevention (red arrows); (b) EPC capture stent mechanism of action: Modified from [59]. The CD-34 antibody immobilized on the stent surface polymer binds the CD-34 antigen on the EPC to promote rapid endothelialization; (c) plasma surface modification for coronary stents: Modified from [60]. Nitrogen, argon and acetylene plasma is introduced into a chamber under a vacuum and ionized by a power source such as an RF electrode. The charged ions in the chamber impact the substrate to modify the surface immersed in the plasma.

Figure 1.

Coronary stent types, their mechanism of action and innovations: (a) first generation drug eluting stents (DES) impact on vascular biology: Modified from [42], reduced neointima formation (green arrows) but increased thrombogenicity at stent bio-interface. Sirolimus/paclitaxel inhibition of endothelialization, tissue factor induction and endothelial progenitor cells (EPC) homing prevention (red arrows); (b) EPC capture stent mechanism of action: Modified from [59]. The CD-34 antibody immobilized on the stent surface polymer binds the CD-34 antigen on the EPC to promote rapid endothelialization; (c) plasma surface modification for coronary stents: Modified from [60]. Nitrogen, argon and acetylene plasma is introduced into a chamber under a vacuum and ionized by a power source such as an RF electrode. The charged ions in the chamber impact the substrate to modify the surface immersed in the plasma.