Increased artery wall stress post-stenting leads to greater intimal thickening

Abstract

Since the first human procedure in the late 1980s, vascular stent implantation has been accepted as a standard form of treatment of atherosclerosis. Despite their tremendous success, these medical devices are not without their problems, as excessive neointimal hyperplasia can result in the formation of a new blockage (restenosis). Clinical data suggest that stent design is a key factor in the development of restenosis. Additionally, computational studies indicate that the biomechanical environment is strongly dependent on the geometrical configuration of the stent, and therefore possibly involved in the development of restenosis. We hypothesize that stents that induce higher stresses on the artery wall lead to a more aggressive pathobiologic response, as determined by the amount of neointimal hyperplasia. The aim of this investigation was to examine the role of solid biomechanics in the development of restenosis. A combination of computational modeling techniques and in vivo analysis were employed to investigate the pathobiologic response to two stent designs that impose greater or lesser levels of stress on the artery wall. Stent designs were implanted in a porcine model (pigs) for approximately 28 days and novel integrative pathology techniques (quantitative micro-computed tomography, histomorphometry) were utilized to quantify the pathobiologic response. Concomitantly, computational methods were used to quantify the mechanical loads that the two stents place on the artery. Results reveal a strong correlation between the computed stress values induced on the artery wall and the pathobiologic response; the stent that subjected the artery to the higher stresses had significantly more neointimal thickening at stent struts (high stress stent: 0.197 ± 0.020 mm vs. low-stress stent: 0.071 ± 0.016 mm). Therefore, we conclude that the pathobiologic differences are a direct result of the solid biomechanical environment, confirming the hypothesis that stents that impose higher wall stresses will provoke a more aggressive pathobiological response.

Computational analysis of mechanical stress–strain interaction of a bioresorbable scaffold with blood vessel

“…ISR is largely a result of neointima formation alone which is composed principally of proliferating smooth muscle cell and accumulated extracellular matrix (Lowe et al, 2002). Stents that induce higher non-physiologic stresses provoke a more aggressive pathobiological response of the artery wall, resulting in a higher degree of neointimal hyperplasia (Timmins et al, 2011). Absorb scaffold is clinically beneficial due to the lower stresses generated in the vessel layers (i.e., lower risks of restenosis, chest pain and arterial dissection or perforation).…”

Multi-objective optimisation of stent dilation strategy in a patient-specific coronary artery via computational and surrogate modelling

“…Such stress differences between models may lead to biomechanical responses which in turn may result in different restenosis rates in the dilated segment. This has been shown in recent studies (Keller et al, 2014;Timmins et al, 2011) reporting localised biological response as a result of mechanical forces imposed by the stent system during deployment and, consequently, the radial compression of the arterial wall. On the other hand, models with low induced mechanical environment are as a result of suboptimal stent and wall interaction or stent under-expansion.…”

Effects of material, coating, design and plaque composition on stent deployment inside a stenotic artery—Finite element simulation

“…The altered solid mechanical environment following stent deployment governs the inflammatory and remodelling response of blood vessels. For instance, Timmins et al (2011) quantified both the solid biomechanical environment and in-vivo porcine arterial response of two stent designs which impose considerably different mechanical stresses and strains on the arterial wall. Stents that induce higher nonphysiologic stresses provoke a more aggressive pathobiological response of the artery wall, resulting in a higher degree of neointimal hyperplasia.…”