Abstract

Computational models of cerebral aneurysm thrombosis are designed for use in research and clinical applications. A steady flow assumption is applied in many of these models. To explore the accuracy of this assumption a pulsatile-flow thrombin-transport computational fluid dynamics (CFD) model, which uses a symmetrical idealized aneurysm geometry, was developed. First, a steady-flow computational model was developed and validated using data from an in vitro experiment, based on particle image velocimetry (PIV). The experimental data revealed an asymmetric flow pattern in the aneurysm. The validated computational model was subsequently altered to incorporate pulsatility, by applying a data-derived flow function at the inlet boundary. For both the steady and pulsatile computational models, a scalar function simulating thrombin generation was applied at the aneurysm wall. To determine the influence of pulsatility on thrombin transport, the outputs of the steady model were compared to the outputs of the pulsatile model. The comparison revealed that in the pulsatile case, an average of 10.2% less thrombin accumulates within the aneurysm than the steady case for any given time, due to periodic losses of a significant amount of thrombin-concentrated blood from the aneurysm into the parent vessel’s bloodstream. These findings demonstrate that pulsatility may change clotting outcomes in cerebral aneurysms.

Highlights

  • Cerebral aneurysms are localized expansions in cerebral arteries and are caused by structural inadequacies in the arterial wall

  • The methods described give details of the numerical simulations and experimental particle image velocimetry study (PIV), in an idealized symmetrical geometry

  • Results from the PIV studies were used to validate the computational model of thrombin transport in cerebral aneurysms, under steady state conditions

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Summary

Introduction

Cerebral aneurysms are localized expansions in cerebral arteries and are caused by structural inadequacies in the arterial wall. Thrombosis is closely associated with cerebral aneurysms and is defined as blood clotting within the circulatory system, under pathological conditions [1]. Aneurysm rupture is not a prerequisite for thrombosis [2,3,4]. The role of thrombosis is ambiguous, with an increase in rupture risk for some cases and stabilization for others. It is thought that there are similarities and differences between cerebral aneurysm thrombosis and standard physiological clotting [5]. The main differences are thought to arise from geometry-linked local hemodynamics and the behaviour of the vascular endothelium [7,8]

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