Stent malapposition, as a potential mechanism of very late stent thrombosis after bare-metal stent implantation: A case report

Higuma, Takumi; Abe, Naoki; Hanada, Kenji; Yokoyama, Hiroaki; Tomita, Hirofumi; Okumura, Ken

doi:10.1016/j.carrev.2013.09.009

Cited by 1 publication

(8 citation statements)

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“…With non-intact endothelium in our study, the well-apposed strut yielded thrombus formation, which in some cases exceeded that with the largest gap distance. If we assumed that re-endothelialization occurred and that the endothelium was dysfunctional or denuded only at the site from which the strut separated from the wall, in accordance with indications from the clinical studies described in section 4.3 [8, 12], then the well-apposed strut would not produce thrombus because platelets would not adhere to the sustained intact endothelium. Hence, the well-apposed strut would be the least thrombogenic.…”

Section: Discussionmentioning

confidence: 99%

“…Stent malapposition occurs due to unsatisfactory stent deployment [11] or later due to excessive fibrin deposition, positive vascular remodeling, or inflammation [7], causing stent thrombosis in patients [8, 12]. Clinical observations in patients have suggested that stent malapposition caused VLST within both bare-metal stents [8] and drug-eluting stents [12].…”

Section: Discussionmentioning

confidence: 99%

“…Clinical observations in patients have suggested that stent malapposition caused VLST within both bare-metal stents [8] and drug-eluting stents [12]. For example, after treatment of the occurrence of VLST within the left anterior descending artery in a patient with a bare-metal stent, intravascular ultrasound and OCT showed malapposition at the proximal and distal sites of the stent with residual thrombus at these sites [8].…”

Section: Discussionmentioning

confidence: 99%

“…Stent malapposition may occur acutely due to unsatisfactory stent deployment [11] and later due to excessive fibrin deposition, positive vascular remodeling, or inflammation [7]. Stent thrombosis in association with malapposition has been observed clinically in patients [8, 12] and in autopsy settings [7, 13]. Therefore, it is of importance to further study the mechanism of stent thrombosis associated with malapposition.…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies of malapposed stents have suggested that thrombosis may be initiated at the location of stent separation from the wall and initiated by altered hemodynamics due to malapposition [8, 12, 14]. Computational fluid dynamics (CFD) studies, some of which also included experimental testing, examined the fluid flow field near malapposed struts.…”

Section: Introductionmentioning

confidence: 99%

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Computational simulation of platelet interactions in the initiation of stent thrombosis due to stent malapposition

Chesnutt

Han

2016

Phys. Biol.

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Coronary stenting is one of the most commonly used approaches to open coronary arteries blocked due to atherosclerosis. Stent malapposition can induce thrombosis but the microscopic process is poorly understood. The objective of this study was to determine the platelet-level process by which different extents of stent malapposition affect the initiation of stent thrombosis. We utilized a discrete element model to computationally simulate the transport, adhesion, and activation of thousands of individual platelets and red blood cells during thrombus initiation in stented coronary arteries. Simulated arteries contained a malapposed stent with a specified gap distance (0, 10, 25, 50, or 200 μm) between the struts and endothelium. Platelet-level details of thrombus formation near the proximal-most strut were measured during the simulations. The relationship between gap distance and amount of thrombus in the artery varied depending on different conditions (e.g., amount of dysfunctional endothelium, shear-induced activation of platelets, and thrombogenicity of the strut). Without considering shear-induced platelet activation, the largest gap distance (200 μm) produced no recirculation and less thrombus than the smallest two gap distances (0 and 10 μm) that created recirculation downstream of the strut. However, with the occurrence of shear-induced platelet activation, the largest gap distance produced more thrombus than the two smallest gap distances, but less thrombus than an intermediate gap distance (25 μm). A large gap distance was not necessarily the most thrombogenic, in contrast to implications of some computational fluid dynamics studies. The severity of stent malapposition affected initial stent thrombosis differently depending on various factors related to fluid recirculation, platelet trajectories, shear stress, and endothelial condition.

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Section: Discussionmentioning

confidence: 99%