Stent strut streamlining and thickness reduction promote endothelialization

Abstract

Stent thrombosis (ST) carries a high risk of myocardial infarction and death. Lack of endothelial coverage is an important prognostic indicator of ST after stenting. While stent strut thickness is a critical factor in ST, a mechanistic understanding of its effect is limited and the role of haemodynamics is unclear. Endothelialization was tested using a wound-healing assay and five different stent strut models ranging in height between 50 and 150 µm for circular arc (CA) and rectangular (RT) geometries and a control without struts. Under static conditions, all stent strut surfaces were completely endothelialized. Reversing pulsatile disturbed flow caused full endothelialization, except for the stent strut surfaces of the 100 and 150 µm RT geometries, while fully antegrade pulsatile undisturbed flow with a higher mean wall shear stress caused only the control and the 50 µm CA geometries to be fully endothelialized. Modest streamlining and decrease in height of the stent struts improved endothelial coverage of the peri-strut and stent strut surfaces in a haemodynamics dependent manner. This study highlights the impact of the stent strut height (thickness) and geometry (shape) on the local haemodynamics, modulating reendothelialization after stenting, an important factor in reducing the risk of stent thrombosis.

Coronary Artery Stenting Affects Wall Shear Stress Topological Skeleton

“…ST can be induced by high WSS values, which can lead to platelet activation and triggering of the coagulation cascade [7,8]. High stent strut thickness (e.g., ≥ 150 µm as in the case of the current bioresorbable scaffolds, such as the Magmaris scaffold of Case C) is associated with increased risk of ST [3,7,8,10]. This study confirms that high TAWSS are present at the stent strut top face (Fig.…”

“…Incomplete endothelium promotes the insurgence of ST by exposing potential thrombogenic material, such as the stent material, to the circulating prothrombotic factors [10,30]. Incomplete and dysfunctional endothelium represents a major factor promoting the development of ISR through the increase in permeability, in the expression of chemotactic molecules, in the recruitment and accumulation of monocytes and macrophages, in the smooth muscle cell proliferation and migration, and in the expression of procoagulatory molecules [33][34][35].…”

“…Incomplete and dysfunctional endothelium represents a major factor promoting the development of ISR through the increase in permeability, in the expression of chemotactic molecules, in the recruitment and accumulation of monocytes and macrophages, in the smooth muscle cell proliferation and migration, and in the expression of procoagulatory molecules [33][34][35]. Re-endothelialization rates are affected by the local hemodynamic environment of the stented arterial segment, in particular by the WSS patterns at the stent strut level [9,10]. Low WSS is known to (i) attenuate the endothelial production of nitric oxide, prostacyclin I2, and tissue plasminogen activator, and (ii) inhibit endothelial cell proliferation and delay reendothelialization [7].…”

“…Moreover, the lack of endothelial coverage or delayed re-endothelialization observed in consequence of thicker stent struts, such as in bioresorbable scaffolds, increases the risk of thrombosis [9,10].…”

Development of Innovative Biomaterials and Devices for the Treatment of Cardiovascular Diseases

“…[39] More importantly, endothelialization rate was also lower on the stents with thicker struts. [40] The type of drugs and drug efficacy have a great impact the effectiveness of suppressing the excessive hyperplasia of neointima. Some strategies showed promising via the local release of antioxidants [41] or endogenous molecules (e.g., prostacyclin [42] and nitric oxide [43] ) to either inhibit the oxidative stress or mimic the endothelium function after stent implantation.…”