Hemodynamic microenvironment of coronary stent strut malapposition

This study aims to investigate the micro-hemodynamic effects of strut malapposition in patient-specific stented coronary bifurcations.

Using the mapping-back technique, three-dimensional reconstructions of clinical post-stenting artery bifurcations with strut malapposition were accurately generated from optical coherence tomography scans of 9 patients. Computational fluid dynamics (CFD) simulations were then conducted with these models to examine the impact of strut malapposition on various fluid dynamic parameters, including flow patterns, vorticity, strain rates, viscosity, and wall shear stress (WSS). For statistical analysis, virtually apposed models were created to evaluate WSS metrics. Additionally, follow-up data for 5 out of the 9 patients were reviewed to assess evidence of late thrombosis and restenosis.

Malapposed struts induce significant alterations in flow dynamics, including the formation of recirculation regions and the transition from laminar to disturbed flow. The local curvature of the lumen also affects the development of these recirculation regions. Our study demonstrates, for the first time, that the vorticity on the abluminal side of malapposed struts exhibits an opposite sign compared to the surrounding region. The strain rate around these struts shows a distinct transition, with high values at the stent surface that rapidly diminish within the strut-lumen gap. This transition is accompanied by an increase in viscosity within these regions. Furthermore, as the malapposition distance increases, strain rates on the malapposed struts increase while viscosity decreases. Significant differences in WSS metrics were observed between clinically malapposed and virtually apposed scenarios. In clinical follow-up cases, no evidence of thrombosis was found despite the complex micro-hemodynamics in these patients.

There is complex interplay between stent malapposition and hemodynamics within a patient-specific bifurcation. The significant impact of local lumen curvature on flow dynamics underscores the limitations of idealized artery models. Moreover, the absence of thrombosis in subsequent clinical follow-up cases suggests that additional factors, such as antiplatelet medication, may play a significant role in mitigating these risks.