A.R.T.: concept of a bioresorbable stent without drug elution

Abstract

Why bioresorbable stents? More than 20 years ago, interventional cardiology was launched by Andreas Gruntzig, introducing a revolutionary innovation, i.e., percutaneous balloon angioplasty1. The 316L stainless steel stent was initially introduced to tackle acute closure secondary to dissections following balloon angioplasty. In fact, the stent not only resolved the acute complications, but also appeared to be the appropriate response to the midterm complication, i.e., restenosis2,3. Indeed, the principal mechanism of restenosis after balloon angioplasty appeared to be related to chronic constrictive remodelling as a negative component of the healing process4-6. Nevertheless, the permanent (316L stainless steel) stent was the origin of a new disease, in-stent restenosis, corresponding to a foreign body reaction. Drug eluting stents were conceived to skip this particular healing process via cell cycle-inhibiting drugs in order to prevent in-stent restenosis. However, these drugs were cytotoxic, not only against smooth muscle cells, but also endothelial cells leading to late stent thrombosis and/or restenosis7,8. So, by inhibiting this inescapable healing process, we have delayed the occurrence of complications. The approach of Arterial Remodelling Technologies (A.R.T.) is to consider that the error resides in the discrepancy between the healing duration (i.e., a few months) and the immortal half life of the metallic stent, the source of new complications when it is no longer necessary: the bioresorbable stent acts as a transitory cast, scaffolding the artery wall during the healing process. Moreover, the healing process will induce endothelial coverage, a mandatory step for the midand long-term follow-up that will simplify one of the issues of drug eluting stents, i.e., expensive and prolonged dual antiplatelet therapy reducing the quality of life. The degradation of the bioresorbable stent will result in stent fragmentation, stopping the perpetual mechanico-genic stimulus produced by the stent’s overstretching of the arterial wall after the healing process. This can then restore the remodelling capacities of the artery wall itself, thus preserving its future, avoiding a growing accumulation of metal in the arteries9,10. Last but not least, the bioresorbable stent will not impair vasomotion after healing, namely at its extremities.