An investigation of damage mechanisms in mechanobiological models of in-stent restenosis

Abstract

The mechanisms behind in-stent restenosis, the re-narrowing of a stented artery, are poorly understood. However it is known that mechanical damage due to stent implantation plays a major role. This paper investigates the mechanism behind damage-induced cell proliferation using a coupled finite element and agent based model, assuming it is based on a) instantaneous loading, or b) cyclic loading. Furthermore the role of remnant endothelial cells in attenuating in-stent restenosis is examined. Results show that a cyclic damage model predicts a non-physiological, overly proliferative response, whilst the instantaneous model demonstrates that lumen loss may be regulated by re-endothelialisation.