Hemodynamic effect of Neuroform stent on intimal hyperplasia and thrombus formation in a carotid aneurysm

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Abstract

Stents play an important role in management of cerebral aneurysms. A stent reconstructs the parent artery, assists coil embolization, and decreases flow activity within an aneurysm. However, an in-stent stenosis often occurs within the stented artery and compromises the circulation at the parent artery. Hemodynamic basis of re-stenoses from aneurysm stenting is not fully understood. An 8 mm cavernous carotid aneurysm with a wide neck was treated by a Neuroform stent first and by coils five weeks later. A comparison of the difference in morphology during this five-week period reveals the presence of intimal hyperplasia in the internal carotid artery, 1.3 mm thick at the proximal end and 1 mm at the distal end of the stent, and 1 mm thick thrombus at the postero-inferior side of the aneurysm. Computational fluid dynamic analyses show that the site of intimal hyperplasia is exposed to low wall shear with high oscillatory shear index (OSI), and the location of thrombus is subject to high OSI. Intimal hyperplasia and thrombus occur at comparable rates, but at different hemodynamic conditions; however, both prefer regions with high OSIs.

Introduction

Endovascular treatment has become an alternative to the management of cerebral aneurysms. Neuroform stent (Boston Scientific/Target; Fremont, CA) is the first stent designed for treatment of cerebral aneurysms in the United States and allows treatment of wide-necked or complex aneurysms, often with coil embolization [10]. Since then, Neuroform stent has gone through a number of modifications. Complex aneurysms occasionally are treated by stents only [6], and overlapping Neuroform stent can promote thrombosis in fusiform intracranial aneurysms [2]. However, delayed in-stent stenosis at the parent vessel is often observed [11], and, in some cases, the parent vessel could be completely occluded. 6% of cases reported with moderate or severe in-stent stenosis at 2 months [22], and 14% of cases developed in-stent stenosis greater than 50% [28]. These stenoses, often caused by intimal hyperplasia, are found at the proximal [23] and/or distal end of the stent [16] and may require additional intervention.

Both numerical and experimental studies have demonstrated hemodynamic changes within an aneurysm after Neuroform stent placement [8], [21], [29]. Less flow enters the aneurysm after stenting [29], and there is also a reduction of circulation within the aneurysm [1], leading to lower wall shear stresses. However, it is unclear how the stent itself induces thrombus significantly enough to stabilize aneurysm through hemodynamic modification and if the parent vessel is compromised by the in-stent stenosis. As flow diverters are now used increasingly in Europe and South America, how these low porosity device induces thrombus needs to be addressed. We report a study in which both intimal hyperplasia at the parent artery and thrombus within the aneurysm are observed after a Neuroform stent placement. With a patient specific anatomical model and computational fluid dynamics analysis, we are able to determine not only the hemodynamic conditions that these events may occur, but also their rate of development. These data provide valuable clinical information as to how often a patient needs to be monitored and when intervention may be necessary.

Section snippets

Methods

A 34-years-old female was diagnosed by cerebral arteriograms for an 8-mm irregular wide-necked unruptured aneurysm involving the cavernous segment of the right internal carotid artery. A first-generation Neuroform stent (4.5 mm × 30 mm) was deployed across the neck in an attempt to embolize the aneurysm. The patient received a single dose of Clopidogrel and Aspirin daily before and after stenting. Five weeks later, the aneurysm remained opacified so multiple hydrocoils and platinum coils were used

Change of hemodynamics due to stenting

Fig. 2 documents the differences in flow pattern before and after stenting. At the systole (top), blood enters the aneurysm with lower velocity after stenting and decreases its intensity much faster. At the diastole, the flow is extremely slow at the center of aneurysm and near the dome.

Fig. 3 presents the wall shear and OSI before and after stenting. The aneurysm wall, in general, has a very low wall shear except at the proximal and distal necks. There is a greater variation in the OSI on the

Discussion

Intimal hyperplasia and thrombus are two different events. We have demonstrated that these two events can be quantified by two hemodynamic variables, mean wall shear and OSI. Intimal hyperplasia is associated with lower wall shear stress, but thrombus formation prefers a wall shear level between 1 and 3 N/m2 in our case. Higher OSI is related to both intimal hyperplasia and thrombus.

Our results agree with a previous analysis in which intimal hyperplasia occurred at the region with low wall shear

Conflict of interest statement

The authors declare that they have no conflict of interest.

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